UCLA Study: Fish may help to protect the brain against the memory loss and cell damage caused by Alzheimer's disease, scientists reported yesterday.

Salmon may be more than heart healthy and rich in Omega-3 fatty acids, known to lower cholesterol - it may help your memory. In fact bears, eating berries and salmon, have perhaps a naturally optimized diet...

Fish may help to protect the brain against the memory loss and cell damage caused by Alzheimer's disease, scientists reported yesterday.

A study of mice carrying a human gene that causes Alzheimer's disease suggests that a diet rich in an omega-3 fatty acid called DHA slows progression of the disorder in its later stages.

"This is the first proof that our diets affect how our brain cells communicate with each other under the duress of Alzheimer's," said Prof Greg Cole of the University of California, Los Angeles, senior author of the paper in the journal Neuron. "

A diet rich in DHA, or docosahexaenoic acid, dramatically reduces the impact of the Alzheimer's gene.

"Consuming more DHA is something the average person can easily control. Anyone can buy DHA in its purified form, fish-oil capsules, high-fat fish or DHA-supplemented eggs."

In the study, his team focused on Alzheimer's damage to synapses - the chemical connections between brain cells that facilitate memory and learning. The team bred mice with genetic mutations that cause brain lesions linked to advanced Alzheimer's disease. But, though the mice developed the lesions, they showed little memory loss or synaptic brain damage.

"The mice lived on a nutritious diet of fish, which is chock-full of omega-3 fatty acids," said co-author Dr Sally Frautschy. "We realised that the mice's diet could be countering the very thing we were trying to accomplish - showing the progression of the Alzheimer's-related brain damage."

Subsequent studies found high amounts of synaptic damage in the brains of the Alzheimer's-diseased mice that ate a DHA-depleted diet. "After adjusting for all variables, DHA was the only factor remaining that protected the mice against the damage," said Prof Cole.

The human brain absorbs DHA rapidly, making a constant supply critical for proper cognitive function, eye development and mental tasks. Sources of DHA include salmon, halibut, mackerel, sardines and herring.


Jury still out on Alzheimer's and vitamins, according to the Berkeley Wellness Letter, but hints suggest that intervention brings benefits

The excerpt below is a view from Canada (Canoe.CA)

Can C and E prevent Alzhimer's? Nearly five million people in North America have Alzheimer's disease. Though prevention is not yet within our grasp, claims are made daily as to the power of various vitamin and mineral supplements -- most of them expensive and a waste of money.

According to the September issue of the Berkeley Wellness Letter, evidence for supplements has been missing or mixed. But a recent, credible study of 5,000 people over the age of 65 suggests that taking a combination of vitamins C and E may show some promise.

I say "may" because the study was based on what people remembered taking, not a clinical trial, and it was done for only three years, while Alzheimer's can take more years to develop. Those in the study also took large amounts of the vitamins -- at least 500 mg of C and at least 400 IU of E each day.

In a larger 19-year study of 13,388 women out of Harvard University, it was found high fruit and vegetable intake was associated with less mental decline.

So C plus E plus plenty of salad may be tomorrow's recipe for brain food.

Are you too sweet?

The World Health Organization has declared diabetes an epidemic: An aging, overweight population means that type 2 diabetes is a threat to millions worldwide.

High blood sugar eventually damages many of the body's organs and causes everything from blindness to heart disease and stroke.

According to the September issue of the Johns Hopkins Medical Letter, pre-diabetes is also a growing issue with more than 41 million North Americans affected. Pre-diabetes is defined by blood sugar levels that are higher than normal but not yet in the diabetic range.

However, symptoms are silent -- which is why anyone over the age of 45 (particularly if they're overweight) should be routinely tested by a fasting blood glucose test that measures the level of blood sugar. Even if you're younger, you should ask for such a test if you have high blood pressure, high cholesterol, a family history of diabetes, had diabetes during pregnancy or gave birth to a baby weighing more than nine pounds.

How to minimize your risk of prediabetes? Eat a healthy diet, exercise at least 150 minutes a week and lose weight if you need to.


Financial planning can help kin cope with Alzheimer's

Early detection of memory loss is very important for more than health reasons. The financial burden on family, caregivers, and society as a whole can be quite overwhelming. The earlier the condition is detected, the more likely it is that outpatient treatment will be effective. Of course, it is best to avoid altogther by making lifestyle changes that have proven effective in numrous studies, coupled with ongoing monitoring.

Financial planning can help kin cope with Alzheimer's
Dallas Morning News

DALLAS - Sharon McIver spends a good part of her days stretching her 86-year-old mother's dollars as far as she can. In the morning, the Dallas woman looks for sales on personal items her mother needs. After lunch, she makes a call to dispute an unusually large medical bill. And by evening, she has searched for the highest interest rate for her mother's bank certificates.

"I feel as though I'm running two households," she explains. "It overwhelms me some days."

That's a common feeling among people who care for parents with Alzheimer's disease. Adult children like McIver shoulder many tasks as caregivers, but overseeing their parents' finances can be among the most difficult.

The bills are staggering - they average $25,000 a year for home care and $50,000 a year for nursing homes. And financial resources often are limited - Medicare doesn't pay for long-term care.

Alzheimer's patients with retirement nest eggs can exhaust their savings within several years.

After having her mother live with her, McIver moved her to an assisted-living center this spring.

"I just couldn't keep her with me anymore," she says. "Her dementia had become too severe."

McIver's mother pays for her $118-a-day room with her savings and Social Security check. Yet as hard as McIver tries to stretch those dollars, she expects her mother to run out of money within three years.

"After that," the daughter predicts, "her only option will be to go on Medicaid."

Managing the money of aging parents is always a big responsibility, but it's especially true of Alzheimer's patients. Sons and daughters can't talk finances with parents whose mental faculties have dimmed. A person with Alzheimer's lives an average of eight years and sometimes as long as 20 after the onset of symptoms.

Geriatric care manager Kay Paggi of Richardson, Texas, has found that families often don't understand the financial implications when a parent is diagnosed with Alzheimer's.

"Every week I hear from sons or daughters who think Medicare will cover their parents' long-term care," she says. "It's up to me to tell them the bad news - Medicare will cover hospital stays but not extended care."

Financial advisers agree that families who think early about how to pay for an aging parent's care will have more options.

"Money can be a touchy subject in any family - children are afraid to pry, and parents value their privacy," says Kevin Pittman of American Express Financial Advisers in Addison, Texas. "Still, I can't emphasize enough the importance of coming up with a financial plan as early as possible."

Here are some points that experts say adult children should cover when they sit down with Mom or Dad to talk about their financial future and Alzheimer's care.

Be tactful.

Virginia Morris, author of "How to Care for Aging Parents," advises treading gently when you raise the issue of managing your parent's money.

"Letting someone else take charge of your finances is a clear indication you're losing control of your life," she says. "It can be demeaning and hurt your self-esteem. Children must be mindful of that and always act respectfully."

Put one person in charge.

Elder law attorney Janet Boyanton of DeSoto, Texas, says your parent should execute a document known as a durable power of attorney, which gives an individual of your parent's choosing the legal authority to act on his or her behalf until death. An attorney can help with the paperwork.

Boyanton advises against delay. If your parent becomes mentally incapacitated, you may need to go through the cumbersome process of gaining legal guardianship to manage financial affairs.

Gather important documents and study them.

Paggi says providing for your parent's care requires having a full understanding of the financial assets and liabilities.

That includes checking and savings accounts, Social Security income, certificates of deposit, stocks and bonds, real estate deeds, insurance policies and annuities, pension benefits, credit card debts, home mortgages and loans, and so forth. And don't forget your parent's legal documents, including wills and living wills.

Ask some basic questions. And consider consulting professionals.

What are your parent's current financial needs and potential needs?

Morris says most families try to keep a parent with Alzheimer's at home as long as possible, hiring home care aides to help. But for many, a nursing home eventually becomes necessary.

Is your parent able to pay for that care?

Calling on a financial adviser or geriatric care manager may help in answering those questions and identifying community resources to defray the expenses.

Think long and hard before cracking into your own nest egg.

Paggi says she often has clients who spend their own retirement nest eggs on their parents' care. "There's no right or wrong choice - everyone needs to make the decision that works best for him," she says.

Carefully evaluate nursing home options.

Experts say it's never too soon to start looking at nursing homes.

"Some have waiting lists, and you may need one for your parent before you think you do," Morris says. "And because Medicaid patients tend to have fewer choices, it's better to apply before your parent has exhausted his savings and your family still can pay."

Know Medicaid's requirements.

Families should become familiar with Medicaid's limits on the income and assets someone can have and still qualify for assistance, Boyanton says.

Think about long-term care insurance for yourself.

Pittman says it may be too late to buy long-term coverage for a parent already diagnosed with Alzheimer's, but it's not too late for you.

The earlier you purchase such insurance, the lower the premiums will be (and the longer you'll pay them, of course). He says a policy will help guarantee good care for yourself, if you ever need it, and give your children some peace of mind.

Be a model child.

Finally, financial planners point out that how well you look after your parents' finances today is likely to be the model for how well your children will treat you when your turn comes.

As Morris says, "Instead of titling my book 'How to Care for Aging Parents,' maybe I should have called it: Be Nice, You're Next!"


Morphing with MemCheck?

Reading a post by Michael S. Malone at Silicon Insider got me to thinking about interconnections. Malone's piece "Shape-Shifting Microchip Technology Could Reorganize the Corporate World" from abcnews.com basically makes the argument that the future will belong to morphing technology that can change shape and function based on a specific application, and that these changes ultimately will lead to a world where chips and corresponding devices can rapidly alter their use.

The idea was attributed to the man who led the team that built the world's first microprocessor, the Intel 4004: Dr. Federico Faggin. Faggin saw that chips could reorganize themselves architecturally, in real time, so in the one day day, a single chip in your hand might wirelessly download music and e-mails, then turn into a cellphone, then check your blood pressure, then control the thermostat and air conditioner in your home. As Malone points out, today these are all handled by independent devices with their own custom processors - leaving us to lug around cell phones, game players, laptops, PDAs, GPS devices, iPods, etc. What if one chip could do all of these things? What Faggin was describing was a single chip - a "protean chip," that could do all of these things.

In the news recenty,IBM announced a revolutionary new chip "morphing" technology that, in the words of Big Blue, can produce semiconductor devices "that can monitor and adjust their functions to improve their quality, performance and power consumption without human intervention."

Specifically, the technology is called "eFuse." It is a combination of software algorithms and microscopic hardware fuses on the chip surface that senses declining performance by the chip and automatically changes the configuration and efficiency of the surrounding circuits for improved operation.

In conception eFuse sounds like MemCheck - that it, a system to monitor and report on performance and ultimately re-route all of us to more productive cognitive-related activities, general exercise and an experts' advice included.


MemCheck Pro Alpha - Web Service

If you are physician, and we know that many of our readers are - clearly it is less than 640,000 but more than fourscore have already expressed interest in getting MemCheck for your practice - you need something more accurate, that's faster, can be used remotely or from home, than the current paper-based tests like the MMSE when someone comes to your office with a memory concern.

One of the things I did awhile ago is the old HP MBWA "management by walking around" and talking to people in scanning centers, not the owners, but the people who greeted you and actually had to do the work. So, we got some feedback and that's what we are putting into the alpha. Sometimes the real intel starts at the loading dock and gets smaller as you get towards the 50th floor.

That's where we come in and if you move quickly you can join our 'alpha' (here's an ad on Yahoo) on the next generation web service for cognitive monitoring which will be called MemCheck Pro. Well, we had a product that we felt made us beholden to the people of Redmond and the (unbeknownst to us) future plans for Windows XP.

Why is all this important, you may ask?

Well, it is very important. Since we know our tests can detect cognitive impairment (Stanford, Scripps, UC-Irvine)and have even shown significant correlation with MRI results, what it means is that we have a chance of catching the early stages of cognitive decline which some researchers have suggested could start as early as 18 and certainly in the 30's. Usually there is no reason to get an MRI as you or I wouldn't even think we had a problem; when in fact it exists but is beneath the threshold of sensitivity. What our software does then, and puts in your hands, is added granularity so that those early onsets might be detected. If so, drugs like Aricept show a much better result and can slow down Alzheimer's. Also, exercise and mental stimulation (e.g. Alz.org's train your brain campaign) can reduce memory loss, particularly when combined with aerobic exercise. Rather than a triangulated approach to detect memory loss, we enable a triangulated campaign to prevent and rollback memory loss like a heatshield on a descending spacecraft.


Here is a new study from University of Pennsylvania and Stanford involving the venture-backed firm Eunoe which i think was funded by a firm right down the street.

Editor's Note: You'll notice that paper and pencil tests were used to assess performance. As an alternative, try the CognitiveLabs beta.

For a limited time you can sign up for free. We're not reporting yet on the activity over at cognitivecare.com, but it's in the hundreds of thousands.


Decreasing toxins in brains of Alzheimer's patients keep cognitive deficits at bay
Pilot study shows that selectively draining isoprostanes from cerebrospinal fluid stabilizes cognitive decline

Philadelphia, PA – The ever-slowing capacity to clear the build-up of such toxins as isoprostanes and misfolded proteins that accumulate in the brains of Alzheimer's disease patients causes the death of cells involved in memory and language. Domenico Pratico, MD, Associate Professor of Pharmacology at the University of Pennsylvania School of Medicine, and colleagues have shown in a preliminary study that reducing the levels of isoprostanes, which specifically reflect oxidative damage in the brain, by draining cerebral spinal fluid (CSF) can stave off future reductions in cognitive abilities. This work appears in the August issue of the Journal of Alzheimer's Disease.

As measured by a paper-and-pencil cognitive test, the researchers found that scores of the eight patients who had the specially designed shunt continuously operating for one year stayed stable. However, the scores of patients who did not get the shunt declined by 20 percent after 12 months. "What's interesting is that the patients without the shunt didn't stop taking their regular Alzheimer medication, such as anti-cholinesterase," says Pratico.

Over 12 months, the isoprostanes were reduced by about 50 percent compared to Alzheimer's patients taking standard anti-Alzheimer oral medications alone. "We were very happy to see this amount of reduction," says Pratico, who adds that the research team predicted reductions only half that size. Additionally, the normal components of CSF like glucose and immunoglobulins did not change after the shunt was placed in patients. The shunt has a selective capacity to filter out toxins of a specific molecular weight and size, in this case isoprostanes.

Applying a treatment for hydrocephalus to Alzheimer's disease, the microns-wide shunt, or catheter, is placed subcutaneously in a space at the base of the cerebellum. It runs under the skin to the peritoneum, a space in the belly where body fluids accumulate before flowing to the kidney to be filtered and eventually eliminated in the urine. The shunt is put in once, drains continuously, and is cleaned out periodically by a neurologist.

The eight patients still have their shunts and there are now almost 100 patients recruited into the next phase of the study, which is being conducted at Stanford University. Other collaborators on this paper are: Yuemang Yao from Penn; Joshua Rokach, Florida Institute of Technology; Gerald G. Silverberg, Stanford University School of Medicine; Martha Mayo and Dawn McGuire, University of California, San Francisco Medical Center and Enroe Inc. This study was funded in part by the Alzheimer's Association. Pratico has no financial interest in Enroe Inc.

This release can also be found at: http://www.uphs.upenn.edu/news.

PENN Medicine is a $2.5 billion enterprise dedicated to the related missions of medical education, biomedical research, and high-quality patient care. PENN Medicine consists of the University of Pennsylvania School of Medicine (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System (created in 1993 as the nation's first integrated academic health system).

Penn's School of Medicine is ranked #3 in the nation for receipt of NIH research funds; and ranked #4 in the nation in U.S. News & World Report's most recent ranking of top research-oriented medical schools. Supporting 1,400 fulltime faculty and 700 students, the School of Medicine is recognized worldwide for its superior education and training of the next generation of physician-scientists and leaders of academic medicine.

The University of Pennsylvania Health System includes three owned hospitals [Hospital of the University of Pennsylvania, which is consistently ranked one of the nation's few "Honor Roll" hospitals by U.S. News & World Report; Pennsylvania Hospital, the nation's first hospital; and Presbyterian Medical Center]; a faculty practice plan; a primary-care provider network; two multispecialty satellite facilities; and home care and hospice


Drug Shows Promise Against Alzheimer's

Researchers are racing to find a way to stop the spread of Alzheimer's. The Government projects 16 million people will have the disease by 2050. A unique experiment at the Mayo Clinic is sparking a lot of interest on the subject right now.

There are at least five major drugs being tested around the country. All the experiments are trying to find ways to modify brain chemistry to alter the course of the disease. But one drug in particular had some unusual results when given to a special breed of mice.

The mice are genetically programmed at birth to develop a memory deficit. The experiment involved a partnership between Utah-based Myriad Genetics and the Mayo Clinic.

Dr. Adrian Hobden, Myriad Genetics: "But it was modeled on the same genetic background as human disease. So we know if you over express this toxic peptide in mice, they develop cognitive deficits."

So a mouse, with its own version of Alzheimer's, swims aimlessly in a circle trying to find a hidden platform. Though taught how to find the platform to get out of the water, it never remembers.

For humans at this stage of the disease, they may not remember where they parked a car or how to get home.

But then the mouse is given this new drug which goes after a toxic molecule in the brain, believed to be the primary trigger for Alzheimer's. It's an astonishing turnaround. Though the platform has been removed so the mouse can't see it, it swims to the location. Even when it swims away, it goes back, remembering that is where that platform was located.

Results of the Phase Two human trials should be available by next year. Even though this drug has a new application in these experiments, it's been used in the past to treat prostate cancer. In those patients it's had no ill side effects.


Jurassic-Era Gingko to Get Dementia Test

Scientists are to test whether the ancient Chinese remedy gingko can combat Alzheimer's disease and other forms of dementia, it emerged today.

The trial will involve 250 patients over the age of 55 with memory loss, an early dementia symptom.

It is the first study to test gingko as an "at home" treatment rather than giving it to more seriously afflicted patients in hospital.

Chief researcher Dr James Warner, from Imperial College London, said: "We believe gingko may prove more effective if prescribed in a community setting where patients' symptoms are usually less severe.

"This trial will help us to find out whether with gingko it's a case of 'the sooner the better' for patients who may benefit from taking it"

Gingko, extracted from the Gingko biloba tree, is traditionally used to treat circulatory problems.

The remedy, which has been used in traditional Chinese medicine for at least 5,000 years, is believed to cause blood vessels to dilate.

It is thought to improve blood flow to the brain, and reduce clotting by thinning the blood. Gingko may also have antioxidant powers that protect nerve cells from damage.

"All of these effects would suggest that gingko might slow down a degenerative process such as dementia," said Dr Warner.

An estimated 700,000 people in the UK are affected by dementia, 60% of whom are diagnosed with Alzheimer’s disease.

It is hoped gingko might provide a cheaper alternative to conventional medicines, with fewer side effects such as nausea, loss of appetite, tiredness and diarrhoea.

A quality gingko extract costs around £200 for a year's supply and can be obtained over the counter.

Conventional medicines for memory loss are based upon drugs known as cholinesterase inhibitors, which cost around £1,000 a year and are restricted to certain groups of patients.

Participants in the double-blind trial will continue to take conventional medicines for age-associated memory loss.

For six months they will be given 60mg of gingko extract or a non-active "dummy" treatment daily.

Each volunteer will be assessed for mental functioning, memory, quality of life and behaviour.

The research team is recruiting individuals in London and the home counties over the age of 55 whose GPs suspect may have dementia.

Fossilised remains of Gingko biloba trees have been found dating back 200 million years, which places the Gingko in the middle of Earth's Jurassic period.

Four of the trees survived the Hiroshima atom bomb blast in 1945, leading local people to name the tree "The Bearer of Hope".

In Germany, gingko is of the top 10 prescription medicines for the treatment of circulatory problems. Germans spent £153 million on ginkgo in 1993.


Here's a story from the ever popular Dr. Dean Edell at KGO (ABC-Disney) in San Francisco, home of the SF 49ers and the Cal Bears (Go Bears knock off the USC Trojans again (this time in tinseltown) just like last season.

New Blood Test For Alzheimer's
Aug. 17 - Currently, the only definitive test for Alzheimer's disease is an autopsy. So to diagnose early Alzheimer's, doctors are stuck using a series of physical and cognitive exams. But as Dr. Dean Edell reports, there's a promising new way to identify Alzheimer's using a simple blood test.

Neurobiologists have developed a blood test they hope will lead to early diagnosis and more effective treatment. The blood test measures levels of two antibodies.

Jerry Bucchafusco, PhD, pharmacologist: "The Alzheimer's individuals have between three and five fold higher levels of these antibodies."

The antibodies develop when the immune system responds to a combination of proteins linked to Alzheimer's. During the study, researchers looked at blood samples in 75 people with the disease and without, and conducted memory tests.

Jerry Bucchafusco, PhD, pharmacologist: "The blood sample was used to determine the levels of these particular antibodies, and the cognitive testing was done to determine how far along their disease was."

A year later, researchers did the same thing. And they found something incredibly significant in those with Alzheimer's - even though their memory had declined, their levels of antibodies were the same. This suggests the antibodies are present well before symptoms are seen. This could be critical for effective treatment.

Jerry Bucchafusco, PhD, pharmacologist: "The earlier you diagnose that patient, the better chance you have of slowing that process. Most of the patients that come in for treatment come in so far advanced for this disease that the drugs that we have right now are not very effective."

The hope is patients can be tested during standard medical visits.

Kathleen Wilson, MD, neurologist: "If it provides a simple blood test for Alzheimer disease and we develop treatment for it, which we are in the process of doing, then you could have this test done at midlife and initiate aggressive treatment to prevent it."

The study also provides promise for new drugs that attack the antibodies. Some are already in clinical trials to see if they delay the onset of Alzheimer's.

PET scans help determine presence of Alzheimer's disease

Aug. 17, 2004 - A test being developed by WUSM researchers could more definitively tell doctors whether or not a patient has Alzheimer's disease. The process involves the use of PET scan technology. Health reporter Kay Quinn describes the test in the following St. Louis Post-Dispatch article.

Alzheimer's test is being developed at WU

(Republished with permission from the St. Louis Post-Dispatch. This article originally ran in the Health & Fitness section on Monday, July 12, 2004)

By Kay Quinn

It's a heartbreaking conundrum. Medical science is struggling to find a way to detect Alzheimer's disease before it slowly erases a lifetime of memories in its victims.

Yet, doctors have no definitive test that can tell patients and families whether early signs of memory loss are Alzheimer's or some other disease.

Now, researchers at Washington University School of Medicine believe they may be closer to developing just such a test.

In fact, local scientists have already made an important breakthrough they believe will help doctors diagnose, and eventually cure, Alzheimer's. They've done it by using PET scan technology.

PET stands for positron emission tomography. It's a way of looking at the function and biochemistry of the body and the brain.

Specifically, doctors with Washington University's Memory and Aging Project are focusing on a protein known as amyloid.

Everyone has traces of amyloid in the brain, but the protein forms deposits in the brains of Alzheimer's patients.

When a compound known as a tracer is injected into a patient intravenously, it adheres to the amyloid deposits in the brains of those with the disease, but washes away in disease-free patients.

PET scans allow doctors to view the deposits and determine who has them.

The question now is whether all patients who show traces of amyloid deposits eventually develop the disease.

Over the next few years, researchers will study several hundred patients, with and without Alzheimer's, to find the answer.

Two groups they hope to target: those 75 and older and the adult children of Alzheimer's patients.

But the researchers already face some serious ethical questions. Right now, if healthy study volunteers show signs of amyloid deposits in their brains, doctors won't inform them of the finding.

The reason? Doctors still can't be sure it's a definite indicator that the volunteers will develop the disease, and perhaps more important, there is no treatment.

Along with studying PET scans of the brain, researchers are also looking at other factors, such as genetics, personality changes, cognitive performance over time and changes in the protein levels of the blood or spinal fluid.

The eventual hope is to diagnose Alzheimer's disease early in life, before symptoms occur and much of the damage has already been done.


Beginning today we will begin linking to all significant news sources that provide us with the interesting content that we share with you. Links will be featured in the right hand margin, along with our testing and links to our partners. Of course, thanks for your support by becoming a member at cognitivecare.com . Join the tens of thousands of other concerned people that have signed up in the past few months.


Use it or Lose it

Your editor has just returned from a few days fishing and hiking on the Fall, Gallatin, and Yellowstone Rivers in Montana, all part of the "Greater Yellowstone" area wisely set aside by the U.S. government in the 19th Century in an effort led by Presidents Ulysses S. Grant (1872) and later popularized by Teddy Roosevelt who frequently roughed it in the area. The experience was beneficial for body and mind, including a hike to a remote hot spring where an underground river of boiling mineral water emerges from the earth and joins a snowmelt fed river, an amazing place. The area was seen in the film Legends of the Fall starring Brad Pitt and Anthony Hopkins.

For today's post, we touch on the importance of socialization and continued interaction for a fast growing part of the populace:

Senior citizens living alone and independently in apartments should interact often with others---both friends and family members---if they want to maintain their ability to communicate, a new University of Michigan study showed.

A lifestyle with organized activities seems to provide the best social opportunities for the elderly, said Deborah Keller-Cohen, a U-M professor of women's studies and linguistics.

Much is known about the association between declines in cognitive function among the elderly and the ability to communicate, but little has been explored about what role social engagement might play in that relationship. The U-M research targeted people 85 and older---the fastest growing segment of the U.S. population, Keller-Cohen said.

U-M researchers examined the relationships among social engagement, cognition and communicative skills. They reviewed notebooks kept by the study's participants, who tracked the frequency, purpose and quality of interactions. The participants were tested on their ability to name objects in pictures, a common measure of language skill ability.

Individuals who experienced less cognitive decline were involved in a wider range of relationships, each of which challenges individuals to speak and listen to others on a range of topics. Thus, this diversity in interaction would seem to keep one's linguistic skills activated, she said.

When the elderly limited their contact solely to family members, they didn't fare as well as they could have with communications skills had they also interacted with others, Keller-Cohen said. Although additional research is required, this might have implications for how senior living centers structure programming and activities.

"It's possible that as individuals decline cognitively, they become less able to handle social contact and become more dependent on family members who by virtue of kin obligations, will continue to interact with them," she said.

This research, "Social contact and communication in people over 85," was presented at the recent American Psychological Association conference in Hawaii. Other U-M researchers for this study are Amanda Toler, Diane Miller, Katherine Fiori and Deborah Bybee.

For more information on Keller-Cohen, visit http://www.lsa.umich.edu/ling/people/Deborah_Keller-Cohen.htm
For more on the American Psychological Association, visit http://www.apa.org/


Boomers worry about Alzheimer's

The recent death of an American icon from Alzheimer's disease, and aggressive marketing of products intended to treat it, are contributing both to public understanding of age-related dementia and to individual anxiety over what may be normal signs of aging.

By all indications, Ronald Reagan's public announcement of his Alzheimer's diagnosis in 1994 spiked a first wave of national interest in the disease. The former president's death in June pushed public concern to the flood stage.

"The hysteria factor has set in," says Lois Schneider, 56, a volunteer for the Alzheimer's Association in Sarasota.

"Every time I can't remember a word or a name, or I can't remember what the French and Indian War was all about, I get that sinking feeling in the pit of my stomach," Schneider says.

At a conference she attended on Alzheimer's recently in Tallahassee, recalls Schneider, "A woman about my age got up and said, 'I'm one scared cookie.' That's the way we all feel, I think."

First studied by a task force of the American Psychological Association in 1998, the fear of Alzheimer's, clinicians say, has grown at a faster rate than the disease itself, which now now afflicts 4.5 million Americans.

"When I started here seven years ago, we saw maybe 120 people a year," says Nancy Teten, clinical coordinator of the memory disorder clinic on the University of South Florida campus in Tampa, one of the first such facilities in the state when it opened in 1986.

"Last year, we saw 1,200," says Teten, 50, who admits to moments of concern about her own occasional memory lapses.

Pfizer, the drug giant whose Aricept is the most widely prescribed of the four drugs believed to temporarily forestall memory loss and dementia for some Alzheimer's sufferers, recorded a threefold increase in the number of people seeking information in June and July. Company spokesman Alison Lehanski would not disclose actual numbers, beyond quantifying the increase as in "the tens of thousands."

Read more from The Herald Tribune Story


Return to the Planet of the Apes?
SIGN of high IQ? Chimps yawn like humans

INUYAMA, Aichi Prefecture-Monkey see, monkey yawn.

That's right, adult chimpanzees yawn right after seeing others yawn, just like adult humans, according to research conducted mainly by the Primate Research Institute of Kyoto University.

The study will be a useful tool for deciphering the evolution of emotion, the researchers say.

``The `transmission' of yawning requires considerably high intelligence,'' says Tetsuro Matsuzawa, professor of comparative cognition at the institute.

``It does not occur without an ability to distinguish oneself from others and a sort of sympathy toward the behavior of others. The study proved that the intelligence of chimpanzees is high enough for the transmission,'' he said.

Researchers, including Matsuzawa and James Anderson, professor of psychology at the University of Stirling in Britain, studied nine chimps at the institute, including three young chimps and six aged 19 or older. Among the older chimps were Ai, known for her ability to recognize words and numbers, and Mari.

The team showed the chimps a videotape of chimps yawning about 10 times, and another tape of chimps just opening their mouths, each for 3 minutes. The team observed the chimps while the tapes played and for 3 minutes after.

They found that the six older chimps yawned 10 times on average when the tape showed yawning chimps. Their yawning averaged only 4.7 times when they saw the other tape.

The ``transmission'' of yawning was especially high for Ai and Mari. Ai yawned 24 times and Mari 25 times during and after the ``yawning'' tape.

But yawning does not transmit to young chimps-the same result as for human children. All three chimps aged 3 did not yawn once.

Source: Asahi.com


Diet, lifestyle changes could give breakthrough in Alzheimer's Press Trust of India

Diet, lifestyle and various medicines are being explored in the fight against Alzheimer's disease, a devastating neuro-degenerative condition that affects almost one in 50 people in industrialised countries.

An article in the issue of Nature due out today says that although the incidence of the disease is predicted to increase threefold in the next half century, the prospects of preventing and treating it are not entirely gloomy.

According to the study, carried out by Mark Mattson of the National Institute on Aging in Baltimore, Maryland, recent research has indicated ways of defending against the disease and treating patients already suffering from its symptoms.

"Rapid progress towards understanding the cellular and molecular alterations that are responsible for the demise of neurons may soon help in developing effective preventative and therapeutic strategies," Mattson said.

In the meantime, according to Mattson, the same kind of measures that may prevent cardiovascular disease, including modifications of diet and exercise, also seem to have a beneficial effect against Alzheimer's.

These include increased physical exercise and diets low in calories, cholesterol and saturated fats. In addition, the article said mental stimulation may also help prevent the demise of neurons responsible for Alzheimer's symptoms.

Mattson said other promising therapies include vitamins, B, C and E; cholesterol-reducing drugs known as statins, aspirin and other anti-inflammatory agents, anti-oxidants and substances that neutralize excesses of iron and copper in the brain.

from the Hindustan Times


Early Detection, Early Treatment

Aug. 4, 2004 -- Early removal of plaque in the brain is the key to treating Alzheimer's disease, mouse studies suggest.

That's easier said than done, although several anti-plaque treatments are in the pipeline. But the new findings seem to resolve the chicken-or-egg question at the heart of Alzheimer's research.

That crucial question: Which of the two brain lesions found in Alzheimer's patients causes the disease? Is it the plaque that clogs the brain? Or is it the tangled protein that gums up nerve cells?

Frank LaFerla, PhD, and colleagues at the University of California, Irvine, say they have the answer.

"We've demonstrated in the lab that removing plaques from the brain can indeed lead to a total clearance of tangle pathology," LaFerla says in a news release.

The only downside is that the tangles only go away if treatment starts early. Once the tangles reach a certain stage, they stay stuck in the brain after plaque removal.

Plaque and Tangles

The brain uses protein messengers to send and receive various signals. Badly formed proteins act like a monkey wrench in the brain machinery. That's why the brain has a system for clearing away bad proteins.

But the amyloid proteins that make up Alzheimer's plaque somehow defeat this system. They clog up the works. That, LaFerla says, lets Alzheimer's tangles build up.

To prove it, LaFerla's team used a strain of mice that gets both Alzheimer's plaque and Alzheimer's tangles. When given an antibody that makes the immune system destroy plaque, the mouse brains become completely free of plaque. A little later, the tangles go away, too -- unless you wait too long. Once the tangles reach a certain point, even a plaque-free brain can't clear them.

Anti-tangle antibodies removed early tangles. But that didn't make the plaque go away. And the antibodies didn't work on advanced tangles.

The findings appear in the Aug. 5 issue of Neuron.

LaFerla says it's important to find ways to diagnose Alzheimer's disease in its earliest stages so anti-plaque treatments -- once they're perfected -- can work the best. He also says it's important to look for ways to clear late-stage tangles.

"These findings raise the intriguing possibility that a multi-antibody-based approach -- one targeted against [plaque] and one targeted against [tangles] -- may provide the most significant benefit for the treatment of Alzheimer's disease," LaFerla and colleagues write.

Scientists study how the brain remembers, forgets

WASHINGTON - After decades of studying how memory works, scientists are trying to figure out how we forget.

Their goal is to help people:

Forget painful things they don't want to remember, from an embarrassing moment in high school or a stupid mistake at work on up to a traumatic rape or accident.

Not forget things they do want to remember, such as where they left their keys or the name of the boss's spouse all the way, and slow the devastation of Alzheimer's disease.

Instead of just giving memory tests to people, neuroscientists are using recent technologies that observe the living brain at work, such as fMRI (functional magnetic resonance imaging) and PET (positron emission tomography).

In addition, legions of flies, snails and mice have given up their lives to provide insight into how people remember and forget, since some brain structures and functions are similar in humans and lowly pests.

Forgetting is basically the reverse of remembering. Memories form when new physical and chemical links, called synapses, are created between brain cells, called neurons, or when old synaptic links are strengthened.

An elaborate network of connections, rather like a computer wiring diagram, assembles a memory from separate parts of the brain that process the myriad sights, sounds, words, people, motions and emotions that crowd the senses every waking moment.

This step is known as "consolidation." It occurs when a memory is moved from a short-term holding room - a mental scratchpad called working memory that lasts a few seconds or minutes - to long-term storage elsewhere in the neural network.

When a memory is recalled, the process is called "retrieval." The memory isn't stored in a single place, but reassembled from bits and pieces scattered across the neural network. It never comes back exactly the way it went in because new experiences have reshaped the brain in the interim. Mistaken or garbled memories are common, as detectives and trial jurors learn to their sorrow.

Forgetting can be a failure of either consolidation or of retrieval. In addition, memories may fade or decay over time, or be wiped out by interference from other memories. For example, you probably remember what you had for breakfast yesterday, but not last year. Too many breakfasts have come in between.

Steven Schmidt, a psychologist at Middle Tennessee State University in Murfreesboro, likens forgetting to what happens when a stone is thrown into a lake.

"The lake `remembers' the input of the rock as a series of waves on its surface," he explained in an e-mail. "Consolidation is a process that `holds' that pattern of waves. If consolidation is disrupted, the wave patterns are not retained."

Like a water-skier breaking up the pattern of waves, the release of certain hormones in the brain may halt the process of consolidation. "The memory is simply not fully laid down," Schmidt said.

Interference results when a pattern of activated neurons no longer can be sustained, perhaps because a flood of new information has overwritten the original memory. An analogy would be throwing many rocks into the lake near where the first one hit the water.

"The wave patterns of the more numerous set of rocks will make it difficult to see the waves created by the first rock," Schmidt said.

Failure to retrieve a memory is the inability to access information previously stored in the brain. "In my lake metaphor," he said, "I throw a rock in on one shore and notice the pattern of activation. At a later date I may have difficulty recognizing that pattern on the water if I am standing on the other side of the lake."

Loss of memory also can result from emotional or physical causes, such as a blow to the head, a stroke, an infection or surgery. The brains of Alzheimer's patients are destroyed by plaques and tangles of alien material invading once-healthy neural networks.

This kind of damage "could make old memories inaccessible because the fragments would be present in the cortex, but not connected, so the episode could no longer be reassembled," Joseph LeDoux, a neuroscientist at New York University, wrote in his new book, "Synaptic Self."

"Patients lose memories because they lose the cells and synapses that lead to, or contain, those memories," Ivan Izquierdo, a Brazilian biochemist, said in an e-mail interview from Rio Grande do Sul.

Mansuo Hayashi, a brain researcher at the Massachusetts Institute of Technology in Cambridge, used mutant mice to show what happens when short-term memory isn't consolidated in long-term storage.

By altering a gene, she created a mouse with fewer, but bigger, synapses in the cortex, but left the hippocampus, a region where short-term memories are processed, alone. As a result, her mice learned the location of a platform in their cage, but after a few days they couldn't remember where it was.

"We showed their formation of memories is fine," Hayashi said. "However, their long-term storage is impaired."

In another intriguing experiment, Alison Barth, a neuroscientist at Carnegie Mellon University in Pittsburgh, found a way to make individual mouse neurons glow when they're processing a memory. To accomplish this feat, Barth attached a green fluorescent chemical to a gene that turns on when a nerve cell is activated.

"Our mouse is a novel tool that can be used to visualize, in living brain tissue, a single neuron that has been activated in response to an animal's experience," Barth reported in the July 21 issue of The Journal of Neuroscience. By observing precisely where a memory is forming, she said, scientists will be better able to understand and treat neurological diseases.

Forgetting, or at least reducing, painful memories - known as "therapeutic forgetting" - can be helpful to people such as soldiers or accident or rape victims.

A drug called propranolol can blunt the memory of a trauma, according to James McGaugh, the director of the Center for Neurobiology of Learning and Memory at the University of California, Irvine.

"The drug does not remove the memory - it just makes the memory more normal," McGaugh said in an e-mail report. "It prevents the excessively strong memory from developing, the memory that keeps you awake at night."

"The original memory is not erased," Izquierdo said. "It is literally pushed backstage by other connections. Animals and humans must preserve the memory of frightening events in order to be able to react to them if required, but must keep them sufficiently less accessible if they want to live any life worthy of the name from then on."

Michael Anderson, a psychologist at the University of Oregon in Eugene, used fMRI to find out what happens when people make a conscious effort - without drugs - to forget some words. He discovered that high-level areas of the cortex send signals to suppress low-level activity in the hippocampus, blocking recovery of the words.

"Memory suppression requires people to override or stop the retrieval process," Anderson reported in the Jan. 9 edition of the journal Science. "This work confirms the existence of an active process by which people can prevent awareness of an unwanted past experience. This process causes forgetting."

On the Web:

For more information, go to http://web.mit.edu/picowercenter and type in "memory" as the search term.


Alzheimer's robbing Robinson

More on Eddie Robinson, who was diagnosed with Alzheimer's, which we covered in an earlier post:

Eddie Robinson shuffles into the room, hunched over a cane - a shadow of the charismatic coach who made little Grambling State University famous.

Then he catches the eye of a visitor, and a familiar smile lights his face, just as it always has.

"I feel good," Robinson said, before drifting off into silence.

The smile is almost all that remains of one of the greatest coaches in college football history.

Once the most ebullient of men, Robinson has become quiet and distant as Alzheimer's disease isolates him from all that was once important to him.

Robinson, 85, now sits quietly, answering questions with short replies or looks of consternation.

He retired in 1997 as the winningest coach in college football history with 408 victories at Grambling. Shortly after his 56-year coaching career at the historically Black school ended, symptoms of the disease began to show.

"He just didn't feel too well," his wife, Doris, said. "Then it was like he was just slipping away. Every day a little more was gone."


Dietary Impact on Alzheimer's Disease? Input from the South Pacific

Neurotoxins from blue-green algae present in certain foods or water can accumulate in proteins and might cause brain diseases like Alzheimer's after many years, suggests a new study.

The latest research explains how a devastating neurodegenerative disease common on the remote Pacific island of Guam can still strike people down decades after they have left the island.

The disease, called amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC), has symptoms resembling those of both Parkinson's and Alzheimer's disease. The brain damage it causes is similar to that found in Alzheimer's patients.

The latest theory is that the islanders' taste for flying foxes is to blame. A neurotoxin called BMAA found in the fruit of the cycads on which the flying foxes feed, is thought to become concentrated in the flying foxes' flesh. BMAA, in turn, is made by a blue-green alga, or cyanobacterium, that lives in the roots of the cycads.

But this theory does not explain everything. Many islanders who leave Guam develop ALS/PDC decades later. BMAA is a water-soluble chemical, which means the body should soon get rid of it. So how BMAA caused brain damage so long after exposure had puzzled scientists.

Now a team led by Paul Cox, director of the National Tropical Botanic Garden in Hawaii, has shown that that BMAA is sometimes incorporated into proteins in place of normal amino acids. BMAA's structure was already known to resemble that of the amino acids that make up the proteins in our body.

Levels of this protein-bound form of BMAA in the cycad flour eaten by islanders, in the flesh of flying foxes and in the brains of ALS/PDC victims, are typically around a hundred times higher than that of the free form, the team found.

Protein tangles

This BMAA would slowly be released as proteins are broken down, Cox suggests. So for years after eating contaminated food, people's brains would be exposed to low levels of the neurotoxin. What is more, the abnormal proteins containing BMAA could also damage the brain in several ways, for instance by binding together to form the protein tangles characteristic of both ALS/PDC and Alzheimer's.

The study also raises intriguing new questions. As controls, about 20 brain samples from Canada were also tested for BMAA alongside the eight samples from Guam. As expected, no BMAA was found in the brain of the 13 Canadians who had not died from neurological diseases. But protein-bound BMAA was found in the brains of eight Canadian victims of Alzheimer’s disease.

Cox stresses that the study does not prove that BMAA plays a role in Alzheimer's or other brain diseases. "The sample size that we have studied is too small," he says.

And it still has not been proven conclusively that BMAA is the cause of ALS/PDC on Guam, Cox adds. However, its presence in the brain could be a sign that people have been exposed to other, as-yet-unknown cyanobacterial toxins.

The idea is plausible, says cyanobacteria expert Hans Paerl of the University of North Carolina in Chapel Hill, US. Cyanobacteria are common in freshwaters and seas worldwide, and thrive in polluted, nutrient-rich waters. "Their influence is expanding as we nutrify the environment," he says.

For example, in China there is growing evidence that cyanobacterial contamination of drinking water is to blame for the high rates of liver cancer in some regions, says Paerl. "We are just starting to put the pieces of the puzzle together."

Proceedings of the National Academies of Sciences

Dr. Robert Heller, our Medical Advisor noticed the following article in Diagnostic Imaging which which I wanted to bring to your attention.

Patients in an early stage of Alzheimer's disease can benefit from disease-modifying treatments. Surrogate imaging markers of early AD pathology are needed for testing potential preventive therapies.

Mayo Clinic researchers suggest that FDG-PET distinguishes between patients with amnestic mild cognitive impairment (aMCI) and those with AD.

Dr. Kejal Kantarci and colleagues in Rochester, MN, used FDG-PET to image nine patients with AD, six with aMCI, and 12 healthy controls. FDG uptake was extracted using a 3D stereotactic surface projection technique (3D-SSP). The 3D-SSP maps of each group were compared against one another pixel by pixel.

Compared with normals, people with aMCI had decreased FDG uptake in the frontal pole, orbitofrontal cortices, and frontal, temporal, and parietal association cortices. Compared with normals, subjects with AD had decreased glucose uptake in the frontal and temporal lobes, parietal association cortex, posterior cingulate cortex, and precuneus.

FDG uptake in the primary sensory and motor cortices and in the occipital lobes were similar for all three groups.

An ROC curve analysis showed that FDG uptake in the right temporal lobe was the most accurate marker to differentiate patients with aMCI from normals, with 69% sensitivity and 80% specificity.

The same region distinguished patients with AD from normals with 91% and 85% sensitivity and specificity, respectively. Patients with AD showed the most significant decrease in FDG uptake in the temporal and parietal lobes, with a very high level of accuracy.

FDG uptake in all regions of interest in aMCI patients confirmed that MCI is a transitional stage between normal and AD, Kantarci said.

Using region of interest analysis, researchers unexpectedly found a decrease in FDG uptake in the medial temporal lobe of AD patients, while it remained normal in aMCI. This finding contradicts many structural MR studies showing hippocampal atrophy in MCI, she said. Previous FDG-PET studies also showed decreased FDG uptake in the medial temporal lobe.

One explanation Kantarci offered dealt with a flaw in the ROI analysis. Because of PET's low resolution, images could have included pixels from outside the medial temporal lobe structures, which might have affected the average FDG uptake. In aMCI, structures adjacent to the medial temporal lobe may have normal FDG uptake, and including them in the ROI may mask decreased glucose metabolism in the medial temporal lobe.

In AD, however, pixels adjacent to the medial temporal lobe may have decreased FDG uptake due to the extent of the pathologic temporal lobe involvement in AD. Therefore, medial temporal lobe uptake may be measured lower than normal in AD but not in aMCI.

"We will be using MR coregistration to trace the medial temporal region of interest as a result of this issue," Kantarci said.


Scientists May Have Found New Way to Treat Alzheimer's in Study

Pfizer Inc. and Cleveland Clinic researchers may have uncovered a new route to keep the body from making a substance that clogs the brain in Alzheimer's disease, according to a study in the Aug. 1 Nature Medicine.

Scientists and drug companies have been searching for a way to disable or hamper the body's production of BACE1, an enzyme responsible for the production of beta amyloid, since it was discovered in 1999. Beta amyloid is the main component of the plaque that collects between the nerve cells in the brains of people with Alzheimer's, a central feature of the disease.

Now researchers have found a natural protein in the body that binds to BACE1, probably decreasing amyloid production and perhaps slowing the dementia associated with Alzheimer's. In laboratory tests, increased quantities of the Nogo family of proteins substantially reduced production of beta amyloid, said Riqiang Yan, senior author of the paper.

"We identified a potential therapeutic target that may inhibit the production of amyloid and slow down the progression of Alzheimer's disease," Yan, an associate staff member of the Cleveland Clinic Foundation, said in a telephone interview.

About 4.5 million Americans suffer from Alzheimer's, which claimed the life of former U.S. President Ronald Reagan last month after a decade-long battle with the disease.

One member of the Nogo protein family is responsible for regulating nerve growth, particularly after an injury. Additional studies are under way to confirm that the proteins can inhibit amyloid production in animal models, Yan said.

Yan, a discoverer of the BACE1 enzyme, was working at Pfizer's Pharmacia unit when the study began. Scientists at both locations are now studying the proteins independently. It's still not known how to manipulate the protein levels in the human brain, Yan said.

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