I try to stay on topic here, but as we end 2004 it's perhaps time for a retrospective, which we will cover in a few separate posts. Blogging has become a big part of what we do at cognitive labs. Recently we've done some interviews for WebFollowing.com, Slate, and we've got other publications calling. Mainly we circulate the freshest information with some commentary and editorial, pick out what's important and also what's interesting, and try to provide the context for the service we are offering. For example, I got this from Biz Stone at Blogger(Google):
People of the Year: Bloggers
According to ABC News, you guys are People of the Year. Good work. "This week, their influence has become readily apparent. Dozens of bloggers have been filing firsthand reports from the areas devastated by southern Asia's deadly tsunamis." (Note to ABC: It's time for a new screenshot.)
People of the Year: Bloggers
Internet Phenomenon Provides Unique Insight Into People's Thoughts
Dec. 30, 2004 - A blog - short for "web log" - is an online personal journal that covers topics ranging from daily life to technology to culture to the arts. Blogs have made such an impact this year that Merriam-Webster named it the word of the year.
"There's a blog for every niche. There's a blog for every interest," said technology writer Xeni Jardin, who co-edits the blog boingboing.net.
Dylan Verdi, an 11-year-old known as the world's youngest videoblogger, says she covers "things that I've seen that I like or that I've heard of, or just anything that happened to me that day that I'm thinking."
There are millions of blogs on the Internet - a new one is created every seven-and-a-half seconds. More than 10,000 new additions are added to the "blogosphere" each day.
Firsthand Reporting on Asian Tsunami Catastrophes
This week, their influence has become readily apparent. Dozens of bloggers have been filing firsthand reports from the areas devastated by southern Asia's deadly tsunamis.
"There is kind of an immediacy that people can relate to - can't help but relate to that in a very intimate way," said Jardin.
"Day three," one blogger writes from the scene, "this may be an unexpected challenge and responsibility, and it hurts to see people in pain. But it's also a remarkable experience to be on hand to do something modest, but useful, in the aftermath of a disaster."
Bloggers around the world have made themselves useful, encouraging donations to relief groups, posting the names of the missing and expressing sympathy for the victims.
Expanding Political Coverage
As a driving force in politics this year, bloggers covered the 2004 presidential campaigns and election. Political candidates also used them as valuable campaign tools.
"The Internet taught us, rather than the other way around," said former Democratic presidential candidate Howard Dean.
This year, for the first time, bloggers were permitted to cover the national political conventions firsthand...."Suddenly the mainstream media, the nightly news, on all three networks and on cable, picked up the story and the papers picked up the story and the next thing you know, Trent Lott's resigning and gone," said Democratic strategist Joe Trippi, who masterminded Dean's groundbreaking online campaign efforts.
Person of the Week: Complete Coverage
2004: The Year in Review
Some of the most compelling images of 2004 found their way to blogs first, from the Florida hurricanes to the war in Iraq. It was a blogger who got the first photographs of coffins carrying U.S. soldiers arriving in the United States from Iraq.
But for Verdi, it is the simple pleasure of knowing that someone is listening that makes blogging worthwhile.
"On my blog it allows people to post comments, and I have gotten comment upon comment upon comment," she said. "It makes me feel really good that somebody else cares about what I have to say."
ABC News' Elizabeth Vargas filed this report for "World News Tonight."
Something very exciting is happening in the midst of the challenging close to the year 2004. Our knowledge and ability to help ourselves is increasing. Since we have more access to information, we have more tools to learn and modify our behavior and environment then ever before. Did you know that I can pick up a phone and say whatever I want, and in the background, a technical engine converts those bits of data randomly flowing through twisted copper or as packets through the air into a MP3 file and posts it here. This is due to a service called audioblogger.com which means anyone can record their own 30 second or 60 second spot and play it back to millions.
The growth of Sirius and XM Radio to 1.5 and 3 million subscribers each means that alternatives to AM and FM radio are taking hold, eventually their will be even more options including MP3 radio - in fact this has been around for years but has proven difficult to turn into a profit-making business, even with the inroads of bittorrent, the service that makes short-work of all downloads.
2005 could be the year where this changes, based on always-cheaper bandwidth. Imagine a radio channel 24 hours per day 7 days per week that focuses only on the mind, memory, and cognition, support for people with Alzheimer's and caregivers, and, helpful tips to prevent memory loss. Now imagine a cable channel (on the internet) that does the same thing. We've already had a million people who are interested in memory loss sign-up. We added over 5,000 people in the past 30 days. In January we'll aim for 6,000 new members. As always, thanks for your support here at cognitive labs' headquarters, where your purchases of MemCheck keep the lights on.
People advanced more quickly than other forms of life on Earth in terms of mental capacity. Why? Recent research provides clues....
The genes that regulate brain development and function evolved much more rapidly in humans than in nonhuman primates and other mammals because of natural selection processes unique to the human lineage. Researchers reported their findings in the cover article of the Dec. 29, 2004, issue of the journal Cell.
"Humans evolved their cognitive abilities not due to a few accidental mutations, but rather, from an enormous number of mutations acquired though exceptionally intense selection favoring more complex cognitive abilities," said lead scientist Bruce Lahn, an assistant professor of human genetics at the University of Chicago and an investigator at the Howard Hughes Medical Institute.
"We tend to think of our own species as categorically different - being on the top of the food chain," Lahn said. "There is some justification for that."
From a genetic point of view, some scientists thought that human evolution might be a recapitulation of the typical molecular evolutionary process, he said. For example, the evolution of the larger brain might be due to the same processes that led to the evolution of a larger antler or a longer tusk. It's just a particular feature that is exaggerated in the human species.
"We've proven that there is a big distinction. Human evolution is, in fact, a privileged process because it involves a large number of mutations in a large number of genes," Lahn said. "To accomplish so much in so little evolutionary time - a few tens of millions of years - requires a selective process that is perhaps categorically different from the typical processes of acquiring new biological traits."
Generally speaking, the higher up the evolutionary tree, the bigger and more complex the brain becomes (after scaling to body size). But this moderate trend became a huge leap during human evolution. The human brain is exceptionally larger and more complex than the brains of nonhuman primates, including man's closest relative, the chimpanzee.
One way to study evolution at the molecular level is to examine changes of when and where proteins are expressed in the body. "But there are many challenges to study the evolution of protein expression. Instead, we chose to track structural changes in proteins," said graduate student Eric Vallender, lead author of the article along with former graduate student Steve Dorus, both of Lahn's laboratory.
Researchers examined the DNA of 214 genes involved in brain development and function in four species: humans, macaques (an Old World monkey), rats and mice. (Primates split from rodents about 80 million years ago; humans split from macaques 20 million to 25 million years ago; and rats split from mice 16 million to 23 million years ago.)
For each of these brain-related genes, they identified changes that altered the structure of the resulting protein, as well as those that did not affect protein structure. Only those genetic changes that alter protein structure are likely to be subject to evolutionary selection, Lahn said. Changes in the gene that do not alter the protein indicate the overall mutation rate - the background of random mutations from which evolutionary changes arise, known as the gene's molecular clock. The ratio of the two types of changes gives a measure of the pressure of natural selection driving the evolution of the gene.
Researchers found that brain-related genes evolved much faster in humans and macaques than in rats and mice. Additionally, the human lineage has a higher rate of protein changes than the macaque lineage. Similarly, the human lineage has a higher rate than the chimpanzee lineage.
"For brain-related genes, the amount of evolution in the lineage leading to humans is far greater than the other species we have examined," Lahn said. "This is based on an extensive set of genes."
They argue that a significant fraction of genes in the human genome were impacted by this selective process. The researchers estimate there may have been thousands of mutations in thousands of genes that contributed to the evolution of the human brain. This "staggering" number of mutations suggests that the human lineage was driven by intense selection process.
To further investigate the role of selection on brain development, the researchers compared the evolutionary rate of brain-related genes against a control group of 95 genes, which are involved in basic functions necessary for each cell in the body to survive.
"If there is something inherently different about humans in the evolution of their genes - not related to selection - the control genes should reveal it too. These basic, conserved genes are the last to change," Vallender said.
The control genes looked the same. The researchers did not find an excess of changes in these genes during human evolution. This provides a sharp contrast to the tremendous excess of changes in the brain-related genes.
The study also revealed two dozen "outliers" - those genes with the fastest evolutionary rates in the human lineage. Of these, 17 are involved in controlling brain size and behavior, arguing that genes that affect brain size and behavior are preferential targets of selection during human evolution. Lahn and his colleagues now are focusing on these outlier genes, which may reveal more about how the human brain became bigger and better.
For two of these outliers, ASPM and Microcephalin, previous work from Lahn's group already has implicated them in the evolutionary enlargement of the human brain. Loss-of-function mutations in either ASPM or Microcephalin cause microcephaly in humans - a severe reduction in the size of the cerebral cortex, the part of the brain responsible for planning, abstract reasoning and other higher cognitive function.
The researchers found that both the ASPM and Microcephalin genes showed clear evidence of accelerated changes due to intensified evolutionary pressure in the lineage leading to humans. For ASPM, the acceleration is particularly prominent in recent human evolution after humans parted way from chimpanzees. By contrast, the researchers' analyses of ASPM and Microcephalin in the more primitive monkeys and in cows, sheep, cats, dogs, mice and rats, showed no evidence of accelerated evolutionary changes.
Lahn also is considering the wider impact of this research. "Are the genes involved in the evolution of the human brain more likely to be linked to diseases of the human brain? What happens when something goes wrong in these genes? Does it create neurological and psychiatric problems such as mental retardation or addiction? Could these genes contribute to IQ differences in humans? Do people with a particular mutation in one of these genes study better?"
According to Lahn, data from the Cell paper secures humans' privileged position in the evolutionary tree. "Human brain evolution required a major overhaul of the genetic blueprint - perhaps much more so than the evolution of other biological traits," he said.
But how did human ancestors encounter an environment where selection for better brains suddenly became such a prominent force? Lahn suggests that because humans have become a progressively more social species, greater cognitive abilities have become more of an advantage.
"As humans become more social, differences in intelligence will translate into much greater differences in fitness," he said, "because you can manipulate your social structure to your advantage.
"Even devoid of the social context, as humans become more intelligent, it might create a situation where being a little smarter matters a lot.
"The making of the large human brain is not just the neurological equivalent of making a large antler. Rather, it required a level of selection that's unprecedented," Lahn said. "Our study offers the first genetic evidence that humans occupy a unique position in the tree of life. Simply put, evolution has been working very hard to produce us humans."
Source: University of Chicago Medical Center
Now you can check your memory, anytime, anywhere with MemCheck and your wireless Internet Service Provider: AOL, Comcast, Earthlink, Roadrunner, T-Mobile (and at Starbucks), BT-Yahoo Broadband. Try a green tea or grande coffee and see how that enhances your cognitive performance! Special thanks to AOL which is our largest referrer of new users!!! Thanks!
The Lafsers near their home in LaQuinta, CA Los Angeles Times/photo: Orlando Sentinel
Early detection is ever more important and with time, will grow more important. MRI and PET scans offer a way to detect anomalies in people suspected of early memory loss. The research indicated below, and cognitive's own research, suggests that scanning be deployed earlier than it has been up to now. Still, the costs to administer PET or a less expensive MRI could add to topline healthcare expenses in the short-run, even if the outcome is eventually less costly for the healthcare system. Non-interventional methods also exist, such as MemCheck, which can offer assistance to individuals and practitioners in the form of monitoring over time and provide a very inexpensive, point-to-point system for managing and observing cognitive performance objectively over time.
Brain scans may reduce the guesswork involved in diagnosis, offering some patients and their families a chance to prepare.
By Shari Roan | Los Angeles Times
Posted December 28, 2004
For almost three years, Janelle Lafser pleaded with doctors to order a PET scan for her husband, Frank.
He had been experiencing memory and mood problems -- beginning at age 45 -- and was having trouble in his job as an executive at a paint company. The doctors said he was depressed, but Janelle was unconvinced.
She suspected Alzheimer's disease and wanted the positron emission tomography test because it can provide physical evidence of the disease.
Physicians steadfastly refused, telling her that Frank was too young to have Alzheimer's, which occurs mostly in people age 65 and older.
Finally, when his doctors recommended electric shock treatments for depression, Janelle made it contingent upon a PET scan that showed no abnormalities. Only then did the Lafsers, who live in La Quinta, Calif., get the scan. As Janelle suspected, Frank had Alzheimer's disease.
Until recently, PET scanning has been seldom used in the diagnosis and treatment of Alzheimer's, even though it is billed as "a window to the brain" and is the only test, other than an autopsy, to offer physical proof of the disease. At about $1,500 per exam, doctors have deemed it too expensive and too experimental, with many saying a scan would be of little practical benefit to a patient with an incurable disease.
But some families have increasingly countered that they need a specific diagnosis of Alzheimer's -- backed by a PET scan -- to ensure proper treatment and to plan for their loved ones' gradual deterioration.
Now, more of them will know what type of treatment to pursue. In October, Medicare announced that it would begin to pay for PET scans in some patients with signs of the disease, a move that is expected to lead to increased coverage by private insurers.
That move could be just the beginning. Many experts predict that, within the next decade, PET scanning also may be recommended for healthy people who lack symptoms but who are at high risk for developing the disease. Alzheimer's physicians and researchers say PET scanning will lead to better diagnoses in the short term and -- with other brain-imaging techniques and blood tests in development -- to preventive treatment of Alzheimer's in the long term.
"PET scanning is going to be a very powerful tool in the future," says Dr. Richard Powers, a trustee of the Alzheimer's Foundation of America and chief of the bureau of general psychiatry for the Alabama Department of Mental Health.
Alzheimer's disease is a progressive brain disorder that causes declines in memory, cognition and functioning.
About 10 percent of Americans older than 65 and half of all people older than 85 have the disease, according to the Alzheimer's Association. No one knows what causes Alzheimer's, although most researchers think there are genetic influences.
PET produces images of the brain's activity; most other imaging devices show only structures in the brain. During a scan, a radioactive substance is injected into the body and a scanner tracks the resulting signals. The procedure is considered extremely safe because only a small amount of radiation is required.
The majority of people with Alzheimer's disease don't undergo the scans, says Robert J. Schumacher, vice president of the western region for Molecular Imaging Corp., a major provider of PET services, based in San Diego. Most are diagnosed after a comprehensive work-up that essentially rules out other causes of dementia. This approach includes a physical exam, lab tests and extensive psychological and cognitive tests.
The traditional office assessment for Alzheimer's disease can take months or years and is less accurate than PET scanning, advocates of the scan say.
Widely accepted research shows that traditional methods diagnose Alzheimer's accurately only 60 percent to 70 percent of the time, said Dr. Daniel Silverman, director of the University of California, Los Angeles Alzheimer's Disease Center, Imaging Core. PET scanning, meanwhile, is about 91 percent accurate, he says.
Early warning system
In ruling that it would pay for PET scans for some people suspected of having Alzheimer's, the Centers for Medicare and Medicaid Services stopped short of endorsing the scans as a general diagnostic test for the disease. Instead, Medicare and Medicaid will cover the test only for those patients whose symptoms are not typical and who doctors think may have Alzheimer's disease or one of several other brain disorders known as fronto-temporal dementia.
But it's a significant first step, says Dr. William Bradley Jr., chairman of the department of radiology at the University of California, San Diego.
"If you can use diagnostic imaging equipment like PET earlier and either slow a disease or cure it altogether," he says, "that is going to save money in the long run."
Experts agree the best use for PET in the Alzheimer's arena is to help doctors figure out whether a patient has the disease when the standard work-up has not produced a clear answer.
But for many patients, Silverman says, an earlier diagnosis offers several advantages, such as the opportunity to take one of several medications for Alzheimer's disease. The drugs typically work better the earlier they are started.
"What the data show is that you not only make an accurate diagnosis, but you make that accurate diagnosis three years ahead of time," Silverman says.
Some leaders in the field suggest that PET scanning eventually could be used to follow the progression of the disease and assess whether medications are working. And, although current drugs can only do so much, an earlier diagnosis can help families plan for the future.
The Lafsers found Frank's diagnosis both devastating and a relief.
"Once we knew the answer, all of my anger went away," says Janelle. "I could love him and accept that this is where we're going now. For Frank, it was like a ton of bricks was lifted off his shoulders. He had been beating himself up about why he was acting this way."
Window to the brain
Researchers acknowledge they still have much to learn about PET scans and Alzheimer's disease.
The National Institute on Aging announced plans for a five-year study on how PET, MRI and biological markers, such as blood and cerebral spinal fluid, can be combined to measure the progression of mild cognitive impairment and Alzheimer's disease.
Other researchers are also studying how PET can be used to assess progression of the disease.
Still other doctors are studying families with a strong incidence of the disease to see whether PET scanning can reveal changes in the brain well before any symptoms occur. This knowledge could lead to drugs that disrupt the disease process, says Bill Thies of the Alzheimer's Association. And a few scientists are using different imaging agents to detect the development of amyloid plaques -- protein deposits that disrupt brain-cell function and that may be one of the primary causes of the disease.
All agree that people with Alzheimer's will increasingly benefit from technology that reveals --objectively -- what is happening in the brain.
"Now we have a way of following the disease," says UC San Diego's Bradley. "That will spur the development of additional drugs. We do have a chance to cure this disease in some way. But we need an accurate way of imaging it first."
Our news stories resume today. Thanks to all who have joined over the Holidays. It's not too late to purchase a gift subscription for a friend or family member.
Biopharmaceutical company Axonyx Inc. reported Tuesday that it completed the last treatment period for its Alzheimer's disease drug candidate Phenserine in late stage clinical trials.
Shares of Axonyx rose 35 cents, or 5.7 percent, to $6.45 in morning trading on the Nasdaq.
The company said it plans to spend the next several weeks analyzing data from the Phase III clinical trial and report study results by March.
The study enrolled more than 375 Alzheimer's patients who were either treated with 15 milligrams of Phenserine twice a day, or 10 milligrams of Phenserine twice a day or placebo, and then given standard memory and cognition tests. The trial started in June 2003.
Phenserine is an enzyme and inhibitor being developed to treat patients with mild-to-moderate Alzheimer's disease. The company said two additional Phase III clinical trials were initiated for the treatment in the second half of 2004.
Did the 1979-vintage arcade game asteroids enhance cognitive performance..wouldn't it be great to know?
MARINA DEL REY -If Dr. James Rosser Jr. had his way, every surgeon in America would have three indispensable tools on the operating room tray: a scalpel, sutures, and a video game controller.
Rosser looks like a football player and cracks jokes like a comic, but his job as a top surgeon and director of the Advanced Medical Technologies Institute at Beth Israel Medical Center in New York is to find better ways to practice medicine. At the top of his list - video games.
"Traditional academic surgeons look at what I do and thumb their noses," Rosser said at the first Video Game/Entertainment Industry Technology and Medicine Conference, sponsored by the U.S. Army's Telemedicine and Advanced Technology Research Center (TATRC), in early December.
Surgeons who play video games three hours a week have 37 percent fewer errors and accomplish tasks 27 percent faster, he says, basing his observation on results of tests using the video game "Super Monkey Ball."
To devise better systems for training physicians, Rosser and his colleagues brought together surgeons, movie makers and video game designers to discuss ways the three groups can develop better tools.
While the systems are aimed mostly at medical training, he also does classroom demonstrations so kids can get a taste of what it's like.
More than 5,000 people, from schoolchildren to surgeons, have done training exercises on a system Rosser calls "Top Gun," designed to train laparoscopic surgeons, doctors who use minimally-invasive techniques to repair injuries.
Rosser has had subjects play "Super Monkey Ball" as well as practice techniques of laparoscopic surgery by suturing a sponge with long probes and dropping a pea into a hole. In all, he has done "Top Gun" training for more than a decade.
Video games also have much to offer the military, said Greg Mogel, a radiologist and director of the West Coast arm of TATRC, who spoke alongside Rosser at the conference held in Marina del Rey.
"You train as you fight and you fight as you train," he said.
TATRC demonstrated a program called "STATCare," a virtual simulator for combat medics that lets them bandage wounds, apply tourniquets, administer intravenous fluids, inject medications and make all of the other assessments they would be required to do in an actual battlefield.
The program is proven to work, said TATRC's J. Harvey Magee, but "on the negative side, it doesn't respond like a really cool video game yet."
That is where Rosser said he hoped the conference would be of value.
One of the other titles he helped demonstrate was "The Journey to Wild Divine," a $160 game that relies on biofeedback.
Players with heart-rate and skin-conduction monitors hooked to their fingers must calm the body and mind to bring responses in line with the demands of the game.
In a demonstration, players had to control their heart rate and stress levels in order to make a balloon float through a mystical environment.
Another product on display was a system developed by researcher Walter Greenleaf that applies technology to hand rehabilitation -- patients wear a special sensor-laden glove and control a video game by doing exercises. In the classic game "Asteroids," rotating the wrist moves a spaceship left and right, while making a fist fires cannons.
All of that game play may sound like a waste of time to some people, but for Rosser, it's all part of the job.
"You have to be a Nintendo surgeon," he said.
a new graphic on our site under enterprise sales
You probably know that MemCheck can help individuals monitor and track their memory and cognitive health, but, did you know that the same principles can have a ripple effect when applied to a large group of people, like your friends, your social and community groups, or, even the workplace? Yes, it is probable that by helping people individually we also help our larger society stay focused and alert.
This is particularly important as we live longer than ever before, and we can assume, people are going to want to stay engaged in work longer than ever before -- making the mandatory retirement age a relic of the past. Already, we know many individuals who work circles around other people, belying the old mythology. Still, there are actions one can take to create an environment supportive of long-term mental acuity: MemCheck is a component, exercise is a component, arts, music, and socializing are other components of this grand tapestry....
Image shows trace of the IDE   image on right depicts an enyzme
Low Fat Diet may have a protective effect against Alzheimer's - researchers find
UCLA/VA Research Explains Alzheimer's Link To Diabetes; Shows Protective Effect Of Low-fat Diet
Insulin-degrading enzyme (IDE) is a protein known to play a role in eliminating amyloid peptides that cause destructive plaques and tangles in the brains of Alzheimer's patients. Until now, little has been known about the cellular and molecular regulation of IDE.
Using animal models and human tissue, the research team 1) identified a shortfall of IDE protein in the brains of Alzheimer's disease patients; 2) found a cause-effect relationship between insulin signaling and increased production of IDE, and 3) demonstrated that a low-fat diet high in fish and soy can increase production of IDE.
The findings for the first time explain the association between insulin-resistant Type 2 diabetes and Alzheimer's disease, and demonstrate the ability to manipulate levels of the protective IDE protein through diet.
The lead author was Greg M. Cole, professor of medicine and neurology at the David Geffen School of Medicine at UCLA, associate director of the UCLA Alzheimer's Disease Research Center, and associate director of the Geriatric Research and Education and Clinical Center at the VA Greater Los Angeles Healthcare System, Sepulveda.
You are. Because we are growing pretty fast, we put an Alexa Internet graph on this page at the very bottom that shows our traffic.
We analyzed some of your emails and we find that people from all walks of life are concerned with memory loss including the 1st Marine Air Wing.
This is from the 1st Marine home page:
1st MAW boasts a broad spectrum of aircraft and equipment that can be configured to any mission requirement or task. We build airfields where none exist, fly assault or support missions regardless of time or weather, and we control the skies in the area we inhabit. All our personnel are highly trained and motivated and committed to the challenge of maintaining the "Tip of the Spear" in Marine aviation. Dependable, determined, and always prepared, we are the powerful right arm of the III Marine Expeditionary Force.
Mitochondria, the tiny power plants inside all plant and animal cells, play a critical role in the health and well-being of synapses, neuroscientists at MIT's Picower Center for Learning and Memory report in the Dec. 17 issue of the journal Cell.
Each living cell is a miniature breathing, eating, waste-expelling organism. Hundreds or thousands of little footprint-shaped mitochondria generate energy for cell functions from sugar and oxygen. They are particularly important in brain cells, where they perform additional jobs related to signaling and programmed cell death, but little is known about how their distribution and movement relates to the synaptic activity crucial for learning and memory, said Morgan Sheng, Menicon Professor of Neuroscience at MIT and an investigator with the Howard Hughes Medical Institute.
Compared with most cells, neurons are more elongated and complex. Neurons are divided into different sections: the long, thin axon and the branching, tree-like dendrites that receive signals from other neurons via the suction cup-shaped synapses. Synapses, tiny gaps separating neurons, consist of a presynaptic ending at the very tip of an axon that contains neurotransmitters; a postsynaptic ending that contains neurotransmitter receptor sites; and the space between the two endings. Both presynaptic and postsynaptic endings require the energy generated by mitochondria.
Critical functions, such as synapses' transmission of information and ability to change rapidly in response to stimuli, are managed by distant cellular compartments that can become isolated from their nearest mitochondria. Sheng and postdoctoral fellow Zheng Li explored whether having the power source far away, like a too-distant room heater, would effect synaptic function.
The researchers looked at mitochrondria in living hippocampal neurons. The hippocampus, a seahorse-shaped brain region in the temporal lobe, is known to play a critical role in memory.
When synapses are stimulated, the researchers found, mitochrondria in the dendrites changed from being long and thin to more aggregated, collecting in globules near the enlarged dendritic spines, as if the mitochondria were reporting for duty at the active part of the neuron.
"Our studies reveal that mitochrondria dynamically redistribute into dendritic protrusions in response to synaptic excitation SThe dendritic distribution of mitochondria appears to be an essential and limiting factor for synaptic density and plasticity," the authors wrote. If mitochondria don't migrate into the distant reaches of the dendrites-where most synapses are present-the synapses become less numerous and lose some of their ability to respond to external input. Enhancing mitochondria with the nutrient creatine also promoted synaptic density, the study showed.
These findings on mitochondrial function correlate with the fact that neurodegenerative diseases such as Alzheimer's and Parkinson's are associated with abnormal mitochondria. The synapse loss characteristic of these diseases may stem in part from mitochondrial dysfunction, the authors write.
In addition to Li and Sheng, authors include Picower Center researchers Yasunori Hayashi, assistant professor of brain and cognitive sciences, and postdoctoral associate Ken-Ichi Okamoto.
This work is funded by the Howard Hughes Medical Institute.
Older adults who get daily social and physical activity -- even for brief periods -- sleep better and have improved cognition, says a Northwestern University study in the Dec. 15 issue of Sleep.
"Many of the health changes associated with aging, including the decline in sleep and cognitive abilities, can be attributed to sedentary lifestyles and social disengagement among older individuals," lead researcher Susan Benloucif, an associate professor in the Ken and Ruth Davee Department of Neurology and Clinical Neurological Sciences at Northwestern's Feinberg School of Medicine, said in a prepared statement.
"Evidence suggests that maintenance of social engagement and avoidance of social isolation are important factors in maintaining cognitive vitality in old age," Benloucif said.
The study of 12 health older men and women between 67 and 86 years old found that 14 weeks of a daily 90-minute social and physical activity program improved cognitive performance by 4 percent to 6 percent, and also improved sleep quality.
The daily sessions included 30 minutes of stretching, walking, and stationary upper and lower body exercises. That was followed by 30 minutes of social interaction. The final 30 minutes consisted of mild to moderate physical activity such as rapid walking, calisthenics, or dancing. That was followed by a 10-minute cool-down.
The U.S. National Institute on Aging has more about older adults and exercise.
The Amidha Buddha, commisioned by the priest Jomo from 'clean funds' - Kamakura, Japan C. 1250
Calorie Restriction has been proven effective in extending human life - just think of Buddhist monks or Indian yogis, who often are centenegarians. Could the same approach to slowing down biologic processes help to stem memory loss?
A restrictive diet in mice reduces the build-up of a substance linked to memory loss. But can the findngs be applied to humans?
Restricting the diets of mice reduces the build-up of plaques in the brain that are linked to Alzheimer's disease, according to a USC study.
With obese people generally considered to be at a higher risk for developing Alzheimer's, the research raises questions about whether the findings are potentially applicable to humans.
"This is the first indication that modest changes in the normal diet can slow some aspects of Alzheimer's disease," said Caleb Finch, co-author of the study published in the online version of the journal Neurobiology of Aging.
"But that is far and away yet to be proven for humans. It's a big jump to say that what's true for a mouse in a cage is relevant to people living in our complex world," Finch said.
In the study, conducted with collaborators at the University of South Florida in Tampa, researchers used mice whose DNA had been altered with human genes from two families with early onset hereditary Alzheimer's.
The mice were then split into two groups as young adults: one that could eat all it desired ("ad libitum") and the other that had its food intake reduced by 40 percent over a four-week period (diet- restricted).
The researchers were looking specifically at the formation of plaques caused by a build-up of the fiber-like substance called beta-amyloid.
Made up of proteins and polysaccharides, amyloid plaques are deposited in the brain during Alzheimer's disease. Specifically, plaques accumulate in the hippocampus and frontal cortex of Alzheimer's sufferers - areas responsible for memory.
In the diet-restricted mice, both the amount and size of plaque was about 50 percent less than in mice that ate as much as they wanted.
"The power of this study is that two different sets of [human] family mutations were equally sensitive to the effect of diet and slowing the Alzheimer's-like change," said Finch, holder of the ARCO-William F. Kieschnick Chair in the Neurobiology of Aging at USC.
The next goal is to find out why diet restriction has such profound and rapid effects, Finch said.
"We are going to look into the details of metabolism to try and isolate which of the consequences of diet restriction is at work," Finch said. "Is it the blood glucose? Is it the lowered insulin? Those are two targets."
The other USC researchers on this study were Nilay V. Patel, a former USC postdoc who is now a staff scientist at City of Hope Medical Center, and Todd E. Morgan, a research assistant professor in the Andrus Gerontology Center at USC.
The researchers at the University of Southern Florida are Marcia Gordon, Karen E. Connor, Robert A. Good, Robert W. Engelman, Jerimiah Mason and David G. Morgan.
How come we sometimes feel sympathy for animated characters who are 'robotic'? While other times we do not. This process has to do with the perception of reality in the mind, with genetic, pre-wired factors, and our own experiences logged in looking at thousands of people from infancy to present. Since some aspects of detecting memory loss revolve around facial recognition, for example, Stephen Ferris' work at NYU, if we look at the commercial phenomenon of animated films as 'lab' experiment on human perception held at arm's length, we may begin to understand the underlying mechanisms....
By Neil Parmar
Computer-animated films may be grounded in fantasy but one of the secrets behind making them blockbusters remains buried deep within human psychology.
From "Toy Story' to "Finding Nemo,' Pixar Animation Studios has trumped its rivals for almost a decade by using computer graphics to generate cartoon characters that look real -- but not too real. Artists at DreamWorks Animation have followed suit and stuck to anthropomorphically lucrative heroes like Shrek, and Oscar from "Shark Tale.'
So when execs at Warner Bros. Animation gambled more than $265 million to produce and promote the lifelike cast of "The Polar Express' only to watch them get derailed by Pixar's "The Incredibles,' psychologists weren't all that surprised with the film's initially lackluster box-office performance.
According to the "uncanny valley' theory developed in the late 1970s by Masahiro Mori, a Japanese roboticist, we increasingly empathize with a robot the more it looks like a human being (recall C-3PO from "Star Wars'). Yet if a robot appears too humanlike, our compassion peaks, then plummets into a chasm of emotional detachment and disgust. That's because we can usually still detect a robot's eerie, machinelike movement or cold, mechanistic facial expressions -- no matter how much it resembles us. Once a robot becomes completely lifelike, however, our emotional guards melt and we may actually feel affection toward, say, the more lifelike androids in Steven Spielberg's "A.I Artificial Intelligence.'
The uncanny valley theory has yet to be proved -- or disproved -- by a scientific study. But it may exist because our eyes pick up subtle differences between things that appear similar but are not quite identical, says Donald Norman, author of "Emotional Design' and a professor of psychology and cognitive science at Northwestern University in Evanston, Ill. Experts say that it's during this process of mental nitpicking that we notice off-putting features: cheeks that fail to bulge, eyes without shadows beneath them, wrinkles that don't crease across the forehead and oddly textured skin.
Norman notes that the uncanny valley phenomenon is equally applicable to video games and computer-generated films like "The Polar Express' because the more a character seems real, "the more we expect them to behave like us.' When a computer carbon copy of Tom Hanks, for instance, falls short of impressing us or creeps us out, we're left disappointed and buzz quickly fades for a film.
Although a captivating story is obviously crucial in holding our interest at the theater, Norman argues that the emotion-based region of our brain places more importance on trying to "identify with a movie's actors,' he says. "How are we going to identify with a computer-generated character, or a physical or virtual robot?'
Marian Bartlett, an assistant research professor at the Machine Perception Lab at the University of California, San Diego, has studied human facial expressions and recently helped design an animated, computer-based tutor for children. She says the problem with films like "The Polar Express' and certain video game characters is that artists often fail to capture subtle changes in facial expressions.
"If you just capture the movement of facial features -- and not the surface changes in shadows -- characters are less appealing,' says Barlett. "The onset of facial expressions and how that coordinates with speech are also important. If you don't get the timing right things really look bad.'
Indeed, the time between when a character speaks and when their coinciding facial expression changes is vital in sidestepping the uncanny valley. Our eyes shift, for example, a fraction of a second before our head moves when we turn to talk to our neighbor. Yet, in many scenes from "The Polar Express,' the Christmas-happy protagonist moves his head about and chats with his conductor friend while his eyes remain scarily frozen in place.
Most animation companies now employ full-time "localization translators' who determine how much and in what way a character's mouth will move when it speaks. One such employee is Kristopher Tan, a 25-year-old video game designer at the Canadian-based company BioWare. He acknowledges that numerous animators have been trained to avoid the uncanny valley by perfecting the fine dynamics of speech.
In fact, Tan studied the theory in a computer graphics class when he attended university and now spends his days at BioWare translating character-speak into languages other than English. He then sends text codes to animators so that they can realistically alter the facial expression of characters when they converse. That way, international gamers won't be put off.
What's groundbreaking about "The Polar Express' is that director Robert Zemeckis attempted to create a world that intersected films, video games and reality. That's why he purposefully combined old-fashioned human acting, motion-capture technology and computer graphics so that he could get a look "somewhere in between.' Unfortunately, it appears as though he left his latest creation parked in the middle of the uncanny valley.
Rolipram may offer promise in the fight
Alzheimer's disease is the most common form of dementia in the elderly with typical symptoms being memory loss, speech deterioration, and behavioral changes. An early study of the drug rolipram in mice shows promise for possible use in treating Alzheimer's disease in people, according to a new study.
Researchers say they found that treatment of a mouse form of AD with rolipram improves memory in long-term potential and contextual learning -- two measurements of brain function.According to researchers Rolipram works by modifying gene expression, making brain synapses more resistant to the damage caused by accumulating beta amyloid.
Results showed rolipram's protective benefit lasted at least two months after the drug course was stopped. The benefits of the treatment also were not limited to the early stages of AD, with behavioral changes occurring in older mice as well as younger mice.
Thus in conclusion researchers suggest that drugs, such as rolipram, that inhibit phosphodiesterase have the potential to prevent the memory loss characteristic of Alzheimer's disease.
For families, Alzheimer's is a challenge, when a father or mother or grandparent has the disease, everyone needs to adjust to the circumstances. It is a difficult process. Maria Shriver, the First Lady of California has done a good job in her book, which comes highly recommended, just look at the reviews on Amazon.com.
Dec. 10, 2004 - For Grisette Ducos the pain of watching her father struggle with Alzheimer's Disease was heartbreaking. She helped to care for him at home while caring for her two young children, "I literally went from changing my father's undergarments or feeding him to feeding my baby. And, that's heart wrenching."
Grisette's father died last year. Her oldest child Brianna has fond memories of her beloved Papa, but the changes, particularly toward the end, were difficult, "He didn't really remember me because of the sickness."
The effects of Alzheimer's can touch an entire family, and experts say for children the disease can be confusing, even scary. Jed Levine of the Alzheimer's Association says, "I think it can be very confusing for a child who normally has a sense of what an adult should be and what that adult role is. When that changes, it is very upsetting."
Levine encourages parents to talk with their kids about the changes to help them deal with their feelings. He says parents should educate them about the disease in age appropriate ways, like with children's books.
Parents can also find activities kids and grandparents can do together, even if it's just watching a video or looking at old pictures.
But, he warns, don't let children supervise a person. Levine says it can be risky and overwhelming, "Psychologically it's very demanding on a child and very stressful on a child."
Grisette says she worried about what Brianna would remember, "I didn't want her to remember him as just Papa, that person curled up in bed who didn't interact. I wanted her to remember those great times."
To keep those great times alive, Grisette put together a book, "When Papa Remembered Me," full of illustrations done by her husband showing the children's grandfather in better days, so the entire family to hold onto the man they loved.
Brianna says, "I remember when he was on his chair he used to put me on his lap and swing me around like an airplane, and he used to buy me ice cream and sneak another cone."
Levine says it's helpful for some kids to take positive action through things like public awareness activities. If they are old enough, they may want to write about how Alzheimer's has affected their family.
We have been traveling, including some meetings in Chicago, which has slowed down our reporting, but, on the other hand, shows us the national and global scope of the crisis of Alzheimer's. Rest assured we will resume today. The weather has been pleasantly warm. Above is the Wrigley Building of chewing gum fame. As usual, there have been many developments in the field of Alzheimer's and Memory Loss, and we will do our best to bring them to you.
The answer is: Yes.
Here are the findings of a 60 year study on the long term study health of the brain in connection with smoking. While some studies show that smoking can improve concentration, for example in studies of military pilots by Dr. Jerome Yesavage at Stanford, there are long term effects.
LONDON, Dec 8 (Reuters) - Smoking not only damages health, it is bad for the brain too, according to a Scottish study spanning nearly 60 years.
Professor Lawrence Whalley and his team looked at how the cognitive abilities of 465 people, half of them smokers, changed over their lifetime.
They were first tested in 1947, at 11 years old and examined again between 2000 and 2002 when they were 64.
Smokers performed significantly worse in five different cognitive tests than did both former smokers and those who had never smoked.
When social and health behaviour was taken into account -- factors like education, occupation and alcohol consumption -- smoking still appeared to contribute to a drop in cognitive function of just less than 1 percent.
The link between cognitive ageing and impaired lung functions could be that smoking subjects the vital organs, including the brain, to oxidative stress, suggests Whalley, of the Department of Mental Health at the University of Aberdeen.
The study he and colleagues at the University of Edinburgh produced appears in New Scientist magazine.
What can you do to track your memory - buy MemCheck of course. It's easy. Just go here and you can get started right away. Come on, give it a try - it's the right thing to do.
Part 2 - While it's unclear exactly how the antioxidants affected the dogs, Joseph, co-author of "The Color Code: A Revolutionary Eating Plan for Optimum Health," says many fruits and vegetables primarily valued for their powerful antioxidants may in fact provide multiple benefits for the aging brain. They may not only slow oxidation, but may also act as anti-inflammatory agents, make the brain less vulnerable to amyloid plaque, improve communication between neurons and allow the brain to regenerate — all of which contribute to better memory in old age.
Purple fruits and vegetables, such as blueberries, cranberries and Concord grapes, may be especially beneficial for the brain, says Joseph. In a study on aging mice genetically engineered to develop Alzheimer's, Joseph was able to improve their cognitive function by feeding the animals a diet high in blueberries.
In addition to better memory and motor skills, Joseph found that the mice had fewer signs of damage from oxidation and inflammation in their brain tissue than did mice fed a standard diet. They also had higher levels of chemicals necessary for brain cells to regenerate and communicate.
While it's still too early to tell if the animal studies apply to humans, it's quite possible that "what's going on in the rat may be what's going on in a human," says Joseph, who published the results of the study last year in the journal Nutritional Neuroscience.
In addition to particular fruits and vegetables, scientists believe that curcumin, a spice used in India and known for its anti-inflammatory effects, may prevent memory loss. Curcumin is what gives yellow curry its bright color and is frequently used as a natural food dye.
In a study on genetically engineered mice, Dr. Greg Cole, associate director of the Alzheimer's Center at the University of California, Los Angeles, found that curcumin helped reduce amyloid plaque in the animals, and also limited damage from oxidation and inflammation. The results of the study were published in 2001 in the Journal of Neuroscience. A clinical trial is now under way at UCLA to test curcumin in people and find an effective dose.
New research has also shown that B vitamins, such as niacin and folic acid, are vitally important to brain function and may help keep the mind sharp. Found in a range of foods, including lean meat, fish, legumes, dairy products, grains and green, leafy vegetables, B vitamins appear to help control inflammation and may play a role in the development of new brain cells.
Supplements may not do the same
Given the growing evidence of the benefits of antioxidants and other chemicals on the brain, why not just take specific supplements to prevent memory loss?
Most researchers caution that sources of antioxidants from food are far more effective - and safer - than supplements. Although it isn't precisely known how the chemicals work, it's believed that they act in combination with one another.
In addition, different chemicals in plants protect against different kinds of damage, and there may be additional but as yet undiscovered substances in plants that work with antioxidants to provide the protective effects.
Fruits + Vegetables
- Red grapes
- Red apples - Kale
- Brussels sprouts
- Alfalfa sprouts
- Red bell peppers
photo credit: MSNBC.com
This article provides an excellent overview of healthy living and the best practices and actions you can take to take charge of your memory's health. I thought I should share it to kick off our monday.
Molly Masland, MSNBC Health Editor
As concern over Alzheimer's disease grows, more Americans are turning to expensive and potentially unsafe supplements that claim to enhance memory. But prevention of age-related memory loss may be no further away than your refrigerator, and no more expensive than a bag of groceries, experts say.
With the aging population of baby boomers in the United States, more research is being done than ever before on diseases such as Alzheimer's and other forms of dementia. Scientists are developing a better understanding of why memories fade, and along the way they are finding new ways to combat the decline.
For one thing, research increasingly suggests that diet may be important in preventing Alzheimer's.
Inside the aging process
As the brain ages, it loses the ability to protect itself from the barrage of commonplace dangers it faces every day, particularly inflammation and oxidation, a process which allows damaging free radicals to attach themselves to cells.
While it's not entirely clear what causes Alzheimer's disease, amyloid plaque — a goopy, fibrous substance akin to fur balls in the brain — plays a key role. As the plaque builds up, it causes more oxidation and inflammation, and begins to kill off brain cells.
In addition, brain cells often stop communicating with each other as people age, making it harder for the brain to process thoughts, retain short-term memory and create new cells.
"Old neurons are like old married couples - they don't talk to each other very much anymore. They just sit in the room with the remote and stare at the TV," says Dr. James Joseph, director of the Neuroscience Lab at the Human Nutrition Research Center on Aging at Tufts University in Boston.
Older dogs can learn new tricks
While research in the field of aging and nutrition is still in its infancy, scientists have found that diet may help minimize the brain's sensitivity to oxidation and inflammation, as well as improve brain cells' ability to communicate with each other.
One of the most intriguing areas of research involves the role of antioxidants, potent chemicals in plants that protect against free radicals, highly active molecules that damage cells. Antioxidants are what give fruits and vegetables their bright colors. Plants produce these chemicals to protect themselves from environmental insults, such as pollution, and when humans eat plants, they also reap the protective benefits.
In a study involving about 70 beagles, Dr. Carl Cotman, director of the Institute for Brain Aging and Dementia at the University of California, Irvine, found that older dogs fed a diet rich in antioxidants over several years were able to perform tasks — and learn new tricks — far better than fellow canines fed a normal diet.
"We rejuvenated a capacity in the aging brain which wasn't there in the beginning and wasn't coming back on its own," says Cotman. "It indicated the brain has a capacity to recover some age-related loss of cognitive function."
Moreover, MRI scans later revealed structural changes in the brains of the dogs on the antioxidant diet, most notably a decrease in the buildup of amyloid plaque.
Part 2 will be run later in the day
Different approaches are used in individuals with just the beginnings of memory loss, where an early screen such as MemCheck can be extremely helpful, and later stages, where different memory centers are targeted and individuals are trying to re-learn.
Harry Shultz vividly recalls the day he met his wife, Harriet, more than 60 years ago, "I took my friends over to see her in my car, and all of a sudden it switched around. She was going with me."
But, what Harry can't remember is how to pay his bills. He suffers from the early stages of Alzheimer's Disease, but a new program is helping Harry improve his short-term memory.
Cognitive Rehabilitation uses real-life skills to target different areas of the brain. One exercise helps patients link names with faces by more than 100 percent. Another improved patients' ability to make change by more than 70 percent.
A recent study by neuropsychologist David Loewenstein showed mental exercises like crossword puzzles did not improve memory in Alzheimer's patients, but the targeted exercises had a big impact, "People with Alzheimer's Disease can learn. You just have to present them with the type of tasks that bypass certain areas of the brain, which are problematic for these individuals."
As part of the Cognitive Rehabilitation program patients were required to bring a family member. Harry brought Harriet, "We help each other. I probably help her more with dishes and stuff like that." Harry's happy to hold onto those small memories.
The patients in the study met with therapists twice a week for 45 minutes over three months. Both groups also took standard medications to treat their disease.
Doctor Loewenstein says the greatest benefit of the Cognitive Rehab program is there are no side effects.
I forgot to mention that Wes technically could not classify as a high tech hunk, not being in technology but has a very remarkable resemblance to Stephen Speilberg.
Another new member of the team is Dr. Wes Ashford, senior scientist at the Stanford/VA NIH Alzheimer's Center, whose expertise is neuropsychological testing and the early incidence of Alzheimer's Disease.
Wes has a B.S. from UC-Berkeley, M.D. from UCLA-Geffen School of Medicine, and a Ph.D. in Neuroscience, also from UCLA.
Here is a summary of Dr. Ashford's AlzForum' presentation on genetic risk factors for Alzheimer's Disease:
ApoE's Strong Genetics :
J. Wesson (Wes) Ashford of the Stanford/VA Alzheimer's Center in Palo Alto, California, set the stage with a general review of the effect the ApoE genotype has on the epidemiology and onset of AD. He suggested that the onset of AD, like that of mortality and most age-related diseases, follows a descriptive, fundamental aging theory developed in 1825 by the British actuary Benjamin Gompertz. It holds that the death rate of a population doubles every set number of years. For humans aging without AD, this number has evolved to be 7.5 years for women and 8.2 for men. The specific Gompertz parameters underlying AD are not understood, but even so, it is clear that ApoE genotype changes this curve, Ashford said. Despite regional and ethnic variation in its prevalence, the ApoE4 allele overall is likely responsible for half of all nonfamilial AD cases in the US. First identified as a major AD risk factor by Allen Roses and colleagues, then at Duke University, in 1993 (Corder et al., 1993) , this allele occurs in 22 percent of the population, but in 60 percent of AD cases, whereas the E2 and E3 alleles together occur in 78 percent of the population, but only 40 percent of AD cases. ApoE exerts its main effect by influencing when people get AD, Ashford said. In a clinic population, the E4/4 genotype reduces the mean age of onset to 68 from 74 in E3/3 carriers.
Environmental factors and nonspecific genes also play a role in determining AD risk and may, in fact, have a relatively greater effect in very old age (see also Silverman et al., 2003). Ashford suggested that the E2 and E3 alleles, which evolved from the ancestral E4, better support the remodeling of dendrites and minimize neuronal stress over time (see also Live Discussion). E4 also has an inferior ability to handle (excess) animal fat, and its exposure to contemporary environmental conditions with its Western diet and longer lifespans could have made it a susceptibility allele for coronary heart disease and AD (see Corbo and Scacchi, 1999). Allen Roses of GlaxoSmithKline in Research Triangle Park recalled earlier attempts at studying AD in populations that have high E4/4 rates, including African pygmies, Australian aborigines and native Brazilian tribes. The study was difficult, in part because these groups tended to die too young to develop AD in significant numbers, but the few who were available for study had massive neurodegeneration.
List of publications from PUBMED search
ARTICLES REFERENCED ON "PUBMED" to Ashford JW
- some PDF files available (5/22/2004) (52 references)
and 2 papers in press and 1 book chapter
Raber J, Huang, Y, Ashford JW, ApoE genotype accounts for the vast majority of AD risk and AD neuropathology.
Neurobiology of Aging 2004. PDF
Ashford JW. APOE genotype effects on Alzheime's disease onset and epidemiology.
Journal of Molecular Neuroscience 23:155-163, 2004. PDF
Mendiondo MS, Ashford JW, Kryscio RJ, Schmitt FA. Designing a brief Alzheimer screen (BAS).
J Alzheimers Dis. 2003 Dec 5:391-398. PDF
Teter B, Ashford JW.
Neuroplasticity in Alzheimer's disease.
J Neurosci Res. 2002 Nov 1;70(3):402-37. PDF
Ashford JW, Mortimer JA.
Non-familial Alzheimer's disease is mainly due to genetic factors.
J Alzheimers Dis. 2002 Jun;4(3):169-77. PDF
ApoE4: is it the absence of good or the presence of bad?
J Alzheimers Dis. 2002 Jun;4(3):141-3. No abstract available. PDF
Ashford JW, Schmitt FA.
Modeling the time-course of Alzheimer dementia.
Curr Psychiatry Rep. 2001 Feb;3(1):20-8. PDF
Schmitt FA, Davis DG, Wekstein DR, Smith CD, Ashford JW, Markesbery WR. Preclinical" AD revisited: neuropathology of cognitively normal older adults.
Neurology. 2000 Aug 8;55(3):370-6. PDF
Mendiondo MS, Ashford JW, Kryscio RJ, Schmitt FA. Modelling mini mental state examination changes in Alzheimer's disease.
Stat Med. 2000 Jun 15-30;19(11-12):1607-16. PDF
Ashford JW, Shih WJ, Coupal J, Shetty R, Schneider A, Cool C, Aleem A, Kiefer VH, Mendiondo MS, Schmitt FA. Single SPECT measures of cerebral cortical perfusion reflect time-index estimation of dementia severity in Alzheimer's disease.
J Nucl Med. 2000 Jan;41(1):57-64.
Shih WJ, Ashford JW, Coupal JJ, Ryo YU, Stipp V V, Magoun SL, Gross K. Consecutive brain SPECT surface three-dimensional displays show progression of cerebral cortical abnormalities in Alzheimer's disease
Clin Nucl Med. 1999 Oct;24(10):773-7.
Shih WJ, Wilson D, Stipp V, Ashford JW.Heterogenous uptake on brain SPECT.
Semin Nucl Med. 1999 Jan;29(1):85-8. No abstract available.
Ashford JW, Mattson M, Kumar V. Neurobiological systems disrupted by Alzheimer's disease and molecular biological theories of vulnerability.
In Advances in the Diagnosis and Treatment of Alzheimer's Disease. Kumar V. Eisdorfer C. eds, Springer Publishing Company, New York, 1998:85-8. PDF
Ashford JW, Soultanian NS, Zhang SX, Geddes JW. Neuropil threads are collinear with MAP2 immunostaining in neuronal dendrites of Alzheimer brain.
J Neuropathol Exp Neurol. 1998 Oct;57(10):972-8.
Piecoro LT, Wermeling DP, Schmitt FA, Ashford JW. Seizures in patients receiving concomitant antimuscarinics and acetylcholinesterase inhibitor.
Pharmacotherapy. 1998 Sep-Oct;18(5):1129-32.
Pettigrew LC, Bieber F, Lettieri J, Wermeling DP, Schmitt FA, Tikhtman AJ, Ashford JW, Smith CD, Wekstein DR, Markesbery WR, Orazem J, Ruzicka BB, Mas J, Gulanski B. Pharmacokinetics, pharmacodynamics, and safety of metrifonate in patients with Alzheimer's disease.
J Clin Pharmacol. 1998 Mar;38(3):236-45.
Shih WJ, Davis DG, Stipp V, Ashford W, Magoun S. Bilateral perfusion defect/hypoperfusion in temporal and parietal regions on brain SPECT.
Semin Nucl Med. 1998 Apr;28(2):192-3. No abstract available.
Schmitt FA, Ashford W, Ernesto C, Saxton J, Schneider LS, Clark CM, Ferris SH, Mackell JA, Schafer K, Thal LJ. The severe impairment battery: concurrent validity and the assessment of longitudinal change in Alzheimer's disease. The Alzheimer's Disease Cooperative Study.
Alzheimer Dis Assoc Disord. 1997;11 Suppl 2:S51-6.
Geddes JW, Tekirian TL, Soultanian NS, Ashford JW, Davis DG, Markesbery WR. Comparison of neuropathologic criteria for the diagnosis of Alzheimer's disease.
Neurobiol Aging. 1997 Jul-Aug;18(4 Suppl):S99-105.
Butler SM, Ashford JW, Snowdon DA. Age, education, and changes in the Mini-Mental State Exam scores of older women: findings from the Nun Study.
J Am Geriatr Soc. 1996 Jun;44(6):675-81.
Ashford JW, Shan M, Butler S, Rajasekar A, Schmitt FA. Temporal quantification of Alzheimer's disease severity: 'time index' model.
Dementia. 1995 Sep-Oct;6(5):269-80.
Semla TP, Cohen D, Freels S, Paveza GJ, Ashford JW, Gorelick P, Luchins D, Eisdorfer C. Psychotropic drug use in relation to psychiatric symptoms in community-living persons with Alzheimer's disease.
Pharmacotherapy. 1995 Jul-Aug;15(4):495-501.
Smith CJ, Lippiello PM, Ashford JW. Smoking, Alzheimer's disease, and confounding with genes.
Lancet. 1995 Apr 22;345(8956):1054. No abstract available.
Mark RJ, Ashford JW, Goodman Y, Mattson MP. Anticonvulsants attenuate amyloid beta-peptide neurotoxicity, Ca2+ deregulation, and cytoskeletal pathology.
Neurobiol Aging. 1995 Mar-Apr;16(2):187-98.
Cohen D, Eisdorfer C, Gorelick P, Paveza G, Luchins DJ, Freels S, Ashford JW, Semla T, Levy P, Hirschman R. Psychopathology associated with Alzheimer's disease and related disorders.
J Gerontol. 1993 Nov;48(6):M255-60.
Coburn KL, Ashford JW, Moreno MA. Delayed late component of visual global field power in probable Alzheimer's disease.
J Geriatr Psychiatry Neurol. 1993 Apr-Jun;6(2):72-7.
Semla TP, Cohen D, Paveza G, Eisdorfer C, Gorelick P, Luchins D, Hirschman R, Freels S, Levy P, Ashford JW, et al. Drug use patterns of persons with Alzheimer's disease and related disorders living in the community.
J Am Geriatr Soc. 1993 Apr;41(4):408-13.
Cohen D, Eisdorfer C, Gorelick P, Luchins D, Freels S, Semla T, Paveza G, Shaw H, Ashford JW. Sex differences in the psychiatric manifestations of Alzheimer's disease.
J Am Geriatr Soc. 1993 Mar;41(3):229-32.
Hargrave R, Ashford JW. Phenelzine treatment of depression in Parkinson's disease.
Am J Psychiatry. 1992 Dec;149(12):1751-2. No abstract available.
Freels S, Cohen D, Eisdorfer C, Paveza G, Gorelick P, Luchins DJ, Hirschman R, Ashford JW, Levy P, Semla T, et al. Functional status and clinical findings in patients with Alzheimer's disease.
J Gerontol. 1992 Nov;47(6):M177-82.
Brewer GJ, Ashford JW. Human serum stimulates Alzheimer markers in cultured hippocampal neurons.
J Neurosci Res. 1992 Nov;33(3):355-69.
Paveza GJ, Cohen D, Eisdorfer C, Freels S, Semla T, Ashford JW, Gorelick P, Hirschman R, Luchins D, Levy P. Severe family violence and Alzheimer's disease: prevalence and risk factors.
Gerontologist. 1992 Aug;32(4):493-7.
Luchins DJ, Cohen D, Hanrahan P, Eisdorfer C, Paveza G, Ashford JW, Gorelick P, Hirschman R, Freels S, Levy P, et al. Are there clinical differences between familial and nonfamilial Alzheimer's disease?
Am J Psychiatry. 1992 Aug;149(8):1023-7.
Eisdorfer C, Cohen D, Paveza GJ, Ashford JW, Luchins DJ, Gorelick PB, Hirschman RS, Freels SA, Levy PS, Semla TP, et al. An empirical evaluation of the Global Deterioration Scale for staging Alzheimer's disease.
Am J Psychiatry. 1992 Feb;149(2):190-4.
Ashford JW, Kumar V, Barringer M, Becker M, Bice J, Ryan N, Vicari S. Assessing Alzheimer severity with a global clinical scale.
Int Psychogeriatr. 1992 Summer;4(1):55-74.
Coburn KL, Ashford JW, Moreno MA. Visual evoked potentials in dementia: selective delay of flash P2 in probable Alzheimer's disease.
J Neuropsychiatry Clin Neurosci. 1991 Fall;3(4):431-5.
Cohen D, Paveza G, Levy PS, Ashford JW, Brody JA, Eisdorfer C, Gorelick P, Hirschman R, Luchins D, Trozzolo T, et al. An Alzheimer's disease patient registry: the Prototype Alzheimer Collaborative Team (PACT).
Aging (Milano). 1990 Sep;2(3):312-6. No abstract available.
Coburn KL, Ashford JW, Fuster JM. Visual response latencies in temporal lobe structures as a function of stimulus information load.
Behav Neurosci. 1990 Feb;104(1):62-73.
Ashford JW, Kolm P, Colliver JA, Bekian C, Hsu LN. Alzheimer patient evaluation and the mini-mental state: item characteristic curve analysis.
J Gerontol. 1989 Sep;44(5):P139-46.
Small GW, Kuhl DE, Riege WH, Fujikawa DG, Ashford JW, Metter EJ, Mazziotta JC. Cerebral glucose metabolic patterns in Alzheimer's disease. Effect of gender and age at dementia onset.
Arch Gen Psychiatry. 1989 Jun;46(6):527-32.
Ashford JW, Sherman KA, Kumar V. Advances in Alzheimer therapy: cholinesterase inhibitors.
Neurobiol Aging. 1989 Jan-Feb;10(1):99-105.
Parks RW, Crockett DJ, Tuokko H, Beattie BL, Ashford JW, Coburn KL, Zec RF, Becker RE, McGeer PL, McGeer EG. Neuropsychological "systems efficiency" and positron emission tomography.
J Neuropsychiatry Clin Neurosci. 1989 Summer;1(3):269-82. Review.
Small GW, Kuhl DE, Fujikawa DG, Ashford JW. Clinical characterization of Alzheimer's disease: reliability of 'age at onset' and a new descriptor, 'age at shift'.
J Geriatr Psychiatry Neurol. 1988 Oct-Dec;1(4):207-11.
Kumar V, Smith RC, Sherman KA, Ashford W, Murphy J, Giacobini E, Colliver J. Cortisol responses to cholinergic drugs in Alzheimer's disease.
Int J Clin Pharmacol Ther Toxicol. 1988 Oct;26(10):471-6.
Ashford JW, Fuster JM. Occipital and inferotemporal responses to visual signals in the monkey.
Exp Neurol. 1985 Nov;90(2):444-66.
Ashford JW, Coburn KL, Fuster JM. The elgiloy microelectrode: fabrication techniques and characteristics.
J Neurosci Methods. 1985 Sep;14(4):247-52.
Ashford JW, Jarvik L. Alzheimer's disease: does neuron plasticity predispose to axonal neurofibrillary degeneration?
N Engl J Med. 1985 Aug 8;313(6):388-9. No abstract available.
Fuster JM, Willey TJ, Riley DM, Ashford JW. Effects of ethanol on visual evoked responses in monkeys performing a memory task.
Electroencephalogr Clin Neurophysiol. 1982 Jun;53(6):621-33.
Ashford JW, Soldinger S, Schaeffer J, Cochran L, Jarvik LF. Physostigmine and its effect on six patients with dementia.
Am J Psychiatry. 1981 Jun;138(6):829-30. No abstract available.
Ashford JW, Schulz C, Walsh GO. Violent automatism in a partial complex seizure. Report of a case. Arch Neurol. 1980 Feb;37(2):120-2.
Ashford JW, Ford CV. Use of MAO inhibitors in elderly patients.
Am J Psychiatry. 1979 Nov;136(11):1466-7. No abstract available.
That's what we say to our delay in posting...but we'll be updating shortly. The reference above is the one of the several original Trek parallel universe episodes, where Spock was an emotional enforcer/Vin Diesel type of character...
100 new members by 11:56 AM. After you have taken the free test, go here to enroll...only 18 cents a day, one-eigth the cost of your daily coffee. You get the dashboard to track and monitor your memory...
The cognitive labs brain trust continues to expand as Dr. Elan Amir and Dr. Wes Ashford have joined our management advisory team.
Elan has co-founded three companies, ProxiNet, Puma Technology, and Fast Forward. All were acquired, the last by Inktomi. We think there are some things we can do to our huge database to make it even more dynamic, mobile-accessible, and able to thrive as we progress into the 21st century. He is currently CEO of Bivio Networks Here's a cool map of cyberspace
Here's the full bio.
Dr. Elan Amir brings to Bivio broad technology and leadership experience in the networking industry. Dr. Amir joined Bivio Networks in 2003 as CTO. Prior to joining Bivio Networks, Dr. Amir served as CTO for OmniSky Corporation, one of the pioneers in the wireless data applications, software and services sectors. At OmniSky, Dr. Amir oversaw all aspects of the company’s technology development, it's direction and strategy, intellectual property development, and M&A due diligence.
Prior to OmniSky, Dr. Amir was CTO and VP of Engineering at ProxiNet, one of the first developers of web browsing solutions for mobile devices. ProxiNet was aquired by Puma Technology (now Intellisync corporation) in 1999. Before ProxiNet, Dr. Amir co-founded FastForward Networks, a developer of broadcast media distribution software. FastForward Networks was acquired by Inktomi Corporation in August 2000.
Dr. Amir received his Doctoral and Masters degree in Computer Science from the University of California at Berkeley, and a B.S. in Electrical Engineering and Computer Science from Berkeley.
He also made the top 10 list of High Tech Hunks according to the SF Chronicle, with, notably, Sergey Brin.
We'll get to Wes next.
Food for thought...
By ROGER DOBSON
Take a 50-year-old IQ test and it's likely that you will emerge a genius. In fact, most of the population would almost certainly be classed as super-intelligent if they were scored on tests set half a century ago.
"If people taking an IQ test today were scored with the norms of their grandparents' performances 50 years ago, more than 90 per cent of them would be classified as geniuses, while, if our grandparents were scored today, most of them would be classed as borderline mentally retarded," says Dr Stephen Ceci, who is professor of developmental psychology at Cornell University.
Average IQ has increased around 20 points a generation over the past 60 or so years, an increase that has been seen in more than a dozen countries, including New Zealand, Britain, the United States, Japan, Africa, and Australia.
Just why is unclear. Genetic factors, better-educated parents, more sophisticated toys, television and computers have all been given the credit, but with little supporting evidence.
Now, new research has given a considerable boost to the idea that nutrition and diet are largely responsible for the huge rise in IQ. It is suggested that the right nutrition at the right time increases intelligence, possibly by boosting the physical growth of the brain.
Although average intelligence has increased, it is not clear whether everyone has benefited. Have the very intelligent pushed up the average by becoming even brighter, has the increase in IQ been across the board, or have those at the lower end benefited the most?
Many of the explanations that have been put forward require either an across-the-board increase, or for those at the top end to have pulled further ahead. But if nutrition is the explanation, then the increase in IQ would be mainly in deprived groups who, over time, have gained access to better diets.
Novelist Showed Signs of Alzheimer's in Final Book
Iris Murdoch unwittingly showed in black and white that she was suffering from the disease before she was diagnosed, a new study contends.
Neuroscientists have confirmed what literary critics have long suspected: that Dame Iris Murdoch's final novel revealed signs of the Alzheimer's disease that would eventually take her life.
Jean Iris Murdoch published her first novel, Under the Net, in 1954 and went on to win the Booker Prize for The Sea, The Sea in 1978. Her final novel, Jackson's Dilemma, however, did not receive resounding praise when it was released in 1995. Not long after its release, when she was 76, Murdoch was diagnosed with Alzheimer's disease. She died in 1999 and donated her brain to science.
A.S. Byatt compared the structure of Jackson's Dilemma to "an Indian rope trick," leaving the work with "no story and no novel." Another reviewer likened it to "the work of a 13-year-old schoolgirl who doesn't get out enough."
With all of her works, Murdoch was notorious for not allowing anyone to edit her writing. This trait provided the current researchers a unique opportunity to analyze the early effects of Alzheimer's in a person who was unaware she had the disease. They published their findings Dec. 1 in the online issue of Brain.
Given postmortem analysis of Murdoch's brain, there seemed little doubt that the early signs of the disease were already interrupting her cognitive abilities when she embarked on her last novel, the researchers found.
Dr. Peter Garrard, a senior lecturer at the Institute of Cognitive Neuroscience in London and the lead author of the study, said he approached the project with both trepidation and excitement.
"I've always been a keen reader of her work," he said. "What I was hoping to find -- which was what we did find -- was that this change might in some way be translatable into the language of neuroscience, and that was a very exciting prospect."
Garrard and his colleagues used specialized software to analyze these three novels, representing Murdoch's early, middle and later career. In comparing Under the Net, The Sea, The Sea, and Jackson's Dilemma, they found two major differences that were consistent with changes that would be under way in the brain at this early stage of Alzheimer's.
"First, the variety of vocabulary that Iris Murdoch used was much greater in the earlier works than in the later works," said Garrard, who is clinical senior lecturer in neurology at the Institute of Cognitive Neuroscience. "It appeared that she was working with a more limited, more restricted vocabulary. And not only did she appear to be working with that restriction, but the rate at which she introduced new words was much slower, so it was more repetitive, if you like."
The second main difference was that the words used in the final novel were more ordinary or common words than those used in the earlier novels, Garrard said. There was also a progression evident between the Under the Net and The Sea, The Sea, that later dropped off.
Garrard and his colleagues found no change, however in the syntactic structure of sentences. "All were equally complex and long," Garrard said. "It's interesting because there's a suggestion, not completely established, that syntax is preserved while word meaning and vocabulary is lost in early Alzheimer's."
The use of common words and "simplification of speech in the absence of overt grammatical errors are the known features that occur as Alzheimer's disease progresses," said Mony de Leon, a professor of psychiatry and director of the Center for Brain Health at New York University School of Medicine.
Garrard pointed out that the study also sheds light on language and how it is organized in the brain. "That's important not only to Alzheimer's but to the understanding of the brain as a whole," he explained.
At some point in the future, however, it may be beneficial to pick up on the very earliest signs of Alzheimer's, such as those found in this study, he said.
John Bayley, Iris Murdoch's husband, said in a statement, "When I was first contacted about this study by the research team, I told them that I had felt all along that there was something different about Iris's last novel, that it was moving but strange in many ways. I felt sure that Peter Garrard would find something unusual in her writing."
When asked if he could identify anything quintessentially Murdoch in her final novel, Garrard replied, "Not much would make me think it was an Iris Murdoch."
"Because the study is so poignant -- because of this individual writer -- it brings to life the concept of what it is to lose this capacity," de Leon said.
Remember to eat dark green leafy 'cruciferous' vegetables...
Along with its many other functions in the body, magnesium may also help maintain learning and memory in middle age and beyond, according to a study in the Dec. 2 issue of Neuron. Scientists already knew that magnesium helps build bones, regulate body temperature, produce proteins and release energy stored in muscles.
The new study by Massachusetts Institute of Technology researchers found that magnesium also helps regulate a key brain receptor that plays an important role in learning and memory. The finding indicates that magnesium deficiency may result in reduced ability to learn and memorize, while cognitive function may be improved by an abundance of magnesium.
"Our study shows maintaining proper magnesium in the cerebrospinal fluid is essential for maintaining the plasticity of synapses," the study authors wrote.
Synapses are the connections among brain cells. Plasticity, which refers to the ability to change, is vital to the brain's ability to learn and remember.
"Since it is estimated that the majority of American adults consume less than the estimated average requirement of magnesium, it is possible that such a deficit may have detrimental effects, resulting in potential declines in memory function," the authors wrote.
Magnesium is found in foods such as dark green, leafy vegetables. The adult daily requirement for magnesium is about 400 milligrams a day. It's estimated that about half of all Americans don't get enough magnesium.
Anxiety, heart disease, muscle cramps, asthma, allergies, attention-deficit disorder and other health problems have been linked to lack of sufficient magnesium.