3.26.2004
http://www.medicalnewstoday.com/index.php?newsid=6755
This research forms a complement to the studies using our technology at Stanford, showing that our technology was sensitive to the detection of APOe4 in patients who showed no others signs.
How genetic factor may increase risk for Alzheimer's disease
24 Mar 2004
Scientists zero in on toxicity of key protein, apoE4
Researchers at the Gladstone Institute of Neurological Disease have identified processes that may explain how a key protein, apolipoprotein E4 (apoE4), contributes to the development of Alzheimer's disease.
Their findings, described in the Journal of Neuroscience (March 10, 2004), include identifying where in the brain apoE4 is broken down into toxic fragments that can impair the function and survival of nerve cells. Results of their study may point the way to a new therapeutic strategy for the prevention and treatment of Alzheimer's disease.
ApoE4 is the best known genetic risk factor for Alzheimer's disease, but, until now, the mechanism by which it increases that risk has remained a mystery. The key finding of the current study relates to apoE4's tendency to be broken down into toxic fragments when it is produced in neurons, the brain cells responsible for cognitive functions.
Proteins can be broken into small pieces by enzymes known as proteases in a process termed proteolysis. While the degradation of proteins is important for many cell processes, it can be harmful when it occurs inappropriately, not only because it destroys the protein, but also because abnormally high levels of fragments can damage cells.
In the new study, involving the examination of genetically engineered mice, Gladstone researchers have established that:
only apoE4 produced by neurons is susceptible to fragmentation, unlike apoE4 produced by other brain cells;
fragmentation is correlated with age, occurring more frequently the older the animal, similar to the effect of age on Alzheimer disease risk in humans;
fragmentation of apoE4 occurs predominantly in the very parts of the brain that are most vulnerable to Alzheimer's disease, the neocortex and hippocampus. In contrast, fragmentation does not occur in the cerebellum, which is much less vulnerable to Alzheimer's disease;
the apoE4 fragments cause an abnormal change to the protein tau, which is also heavily affected by Alzheimer's disease. Both apoE4 fragments and Alzheimer's disease lead to the abnormal attachment of phosphate groups on tau that can end up contorting the shape of brain cells.
The investigators suspect that the fragmentation of apoE4 is caused by a neuron-specific enzyme, which they are now trying to identify and block with drugs.
"From this and our previous studies, we believe that the protease that cleaves apoE4 may serve as a therapeutic target for the prevention and treatment of Alzheimer's disease, especially in patients who are impacted by apoE4," said the senior author of the study, Yadong Huang, MD, PhD, staff research investigator at the Gladstone Institute of Neurological Disease (GIND) and assistant professor of pathology at the University of California, San Francisco (UCSF).
"With this work, we're a significant step closer to solving the key riddle of apoE4, namely, what is occurring at the molecular level that makes this protein so active in causing neurodegenerative disease," explained Dr. Robert Mahley, "Research of this kind is essential for the development of better treatments for Alzheimer's disease."
This work was supported in part by grants from the National Institutes of Health and by a MetLife Foundation award. The paper, "Neuron-Specific Apolipoprotein E4 Proteolysis Is Associated with Increased Tau Phosphorylation in Brains of Transgenic Mice," was co-authored by Gladstone Institute of Neurological DiseaseGIND staff members Walter J. Brecht, senior research associate; Faith M. Harris, research associate; Shengjun Chang, postdoctoral fellow; Ina Tesseur, postdoctoral fellow; Gui-Qiu Yu, senior research associate; Qin Xu, postdoctoral fellow ; Jo Dee Fish, research technologist; Tony Wyss-Coray, former staff research investigator; Manuel Buttini, former research scientist; and Lennart Mucke, GIND director and senior investigator, UCSF professor of neurology, along with Mahley and Huang.
The Gladstone Institute of Neurological Disease is one of three research institutes of The J. David Gladstone Institutes, a private, nonprofit biomedical research institution affiliated with UCSF. For further information, visit www.gladstone.ucsf.edu.
Contact: John Watson
jwatson@gladstone.ucsf.edu
415-695-3833
University of California - San Francisco
[ Wed Mar 24, 01:29:50 AM | michael addic
This research forms a complement to the studies using our technology at Stanford, showing that our technology was sensitive to the detection of APOe4 in patients who showed no others signs.
How genetic factor may increase risk for Alzheimer's disease
24 Mar 2004
Scientists zero in on toxicity of key protein, apoE4
Researchers at the Gladstone Institute of Neurological Disease have identified processes that may explain how a key protein, apolipoprotein E4 (apoE4), contributes to the development of Alzheimer's disease.
Their findings, described in the Journal of Neuroscience (March 10, 2004), include identifying where in the brain apoE4 is broken down into toxic fragments that can impair the function and survival of nerve cells. Results of their study may point the way to a new therapeutic strategy for the prevention and treatment of Alzheimer's disease.
ApoE4 is the best known genetic risk factor for Alzheimer's disease, but, until now, the mechanism by which it increases that risk has remained a mystery. The key finding of the current study relates to apoE4's tendency to be broken down into toxic fragments when it is produced in neurons, the brain cells responsible for cognitive functions.
Proteins can be broken into small pieces by enzymes known as proteases in a process termed proteolysis. While the degradation of proteins is important for many cell processes, it can be harmful when it occurs inappropriately, not only because it destroys the protein, but also because abnormally high levels of fragments can damage cells.
In the new study, involving the examination of genetically engineered mice, Gladstone researchers have established that:
only apoE4 produced by neurons is susceptible to fragmentation, unlike apoE4 produced by other brain cells;
fragmentation is correlated with age, occurring more frequently the older the animal, similar to the effect of age on Alzheimer disease risk in humans;
fragmentation of apoE4 occurs predominantly in the very parts of the brain that are most vulnerable to Alzheimer's disease, the neocortex and hippocampus. In contrast, fragmentation does not occur in the cerebellum, which is much less vulnerable to Alzheimer's disease;
the apoE4 fragments cause an abnormal change to the protein tau, which is also heavily affected by Alzheimer's disease. Both apoE4 fragments and Alzheimer's disease lead to the abnormal attachment of phosphate groups on tau that can end up contorting the shape of brain cells.
The investigators suspect that the fragmentation of apoE4 is caused by a neuron-specific enzyme, which they are now trying to identify and block with drugs.
"From this and our previous studies, we believe that the protease that cleaves apoE4 may serve as a therapeutic target for the prevention and treatment of Alzheimer's disease, especially in patients who are impacted by apoE4," said the senior author of the study, Yadong Huang, MD, PhD, staff research investigator at the Gladstone Institute of Neurological Disease (GIND) and assistant professor of pathology at the University of California, San Francisco (UCSF).
"With this work, we're a significant step closer to solving the key riddle of apoE4, namely, what is occurring at the molecular level that makes this protein so active in causing neurodegenerative disease," explained Dr. Robert Mahley, "Research of this kind is essential for the development of better treatments for Alzheimer's disease."
This work was supported in part by grants from the National Institutes of Health and by a MetLife Foundation award. The paper, "Neuron-Specific Apolipoprotein E4 Proteolysis Is Associated with Increased Tau Phosphorylation in Brains of Transgenic Mice," was co-authored by Gladstone Institute of Neurological DiseaseGIND staff members Walter J. Brecht, senior research associate; Faith M. Harris, research associate; Shengjun Chang, postdoctoral fellow; Ina Tesseur, postdoctoral fellow; Gui-Qiu Yu, senior research associate; Qin Xu, postdoctoral fellow ; Jo Dee Fish, research technologist; Tony Wyss-Coray, former staff research investigator; Manuel Buttini, former research scientist; and Lennart Mucke, GIND director and senior investigator, UCSF professor of neurology, along with Mahley and Huang.
The Gladstone Institute of Neurological Disease is one of three research institutes of The J. David Gladstone Institutes, a private, nonprofit biomedical research institution affiliated with UCSF. For further information, visit www.gladstone.ucsf.edu.
Contact: John Watson
jwatson@gladstone.ucsf.edu
415-695-3833
University of California - San Francisco
[ Wed Mar 24, 01:29:50 AM | michael addic
// posted by neurofuture1:26 AM permanent link
tags:
tags:
tags: help build archive | brain games | more brain games 
3.24.2004
This research forms a complement to the studies using our technology at Stanford, showing that our technology was sensitive to the detection of APOe4 in patients who showed no others signs.
How genetic factor may increase risk for Alzheimer's disease
24 Mar 2004
Scientists zero in on toxicity of key protein, apoE4
Researchers at the Gladstone Institute of Neurological Disease have identified processes that may explain how a key protein, apolipoprotein E4 (apoE4), contributes to the development of Alzheimer's disease.
Their findings, described in the Journal of Neuroscience (March 10, 2004), include identifying where in the brain apoE4 is broken down into toxic fragments that can impair the function and survival of nerve cells. Results of their study may point the way to a new therapeutic strategy for the prevention and treatment of Alzheimer's disease.
ApoE4 is the best known genetic risk factor for Alzheimer's disease, but, until now, the mechanism by which it increases that risk has remained a mystery. The key finding of the current study relates to apoE4's tendency to be broken down into toxic fragments when it is produced in neurons, the brain cells responsible for cognitive functions.
Proteins can be broken into small pieces by enzymes known as proteases in a process termed proteolysis. While the degradation of proteins is important for many cell processes, it can be harmful when it occurs inappropriately, not only because it destroys the protein, but also because abnormally high levels of fragments can damage cells.
In the new study, involving the examination of genetically engineered mice, Gladstone researchers have established that:
only apoE4 produced by neurons is susceptible to fragmentation, unlike apoE4 produced by other brain cells;
fragmentation is correlated with age, occurring more frequently the older the animal, similar to the effect of age on Alzheimer disease risk in humans;
fragmentation of apoE4 occurs predominantly in the very parts of the brain that are most vulnerable to Alzheimer's disease, the neocortex and hippocampus. In contrast, fragmentation does not occur in the cerebellum, which is much less vulnerable to Alzheimer's disease;
the apoE4 fragments cause an abnormal change to the protein tau, which is also heavily affected by Alzheimer's disease. Both apoE4 fragments and Alzheimer's disease lead to the abnormal attachment of phosphate groups on tau that can end up contorting the shape of brain cells.
The investigators suspect that the fragmentation of apoE4 is caused by a neuron-specific enzyme, which they are now trying to identify and block with drugs.
"From this and our previous studies, we believe that the protease that cleaves apoE4 may serve as a therapeutic target for the prevention and treatment of Alzheimer's disease, especially in patients who are impacted by apoE4," said the senior author of the study, Yadong Huang, MD, PhD, staff research investigator at the Gladstone Institute of Neurological Disease (GIND) and assistant professor of pathology at the University of California, San Francisco (UCSF).
"With this work, we're a significant step closer to solving the key riddle of apoE4, namely, what is occurring at the molecular level that makes this protein so active in causing neurodegenerative disease," explained Dr. Robert Mahley, "Research of this kind is essential for the development of better treatments for Alzheimer's disease."
This work was supported in part by grants from the National Institutes of Health and by a MetLife Foundation award. The paper, "Neuron-Specific Apolipoprotein E4 Proteolysis Is Associated with Increased Tau Phosphorylation in Brains of Transgenic Mice," was co-authored by Gladstone Institute of Neurological DiseaseGIND staff members Walter J. Brecht, senior research associate; Faith M. Harris, research associate; Shengjun Chang, postdoctoral fellow; Ina Tesseur, postdoctoral fellow; Gui-Qiu Yu, senior research associate; Qin Xu, postdoctoral fellow ; Jo Dee Fish, research technologist; Tony Wyss-Coray, former staff research investigator; Manuel Buttini, former research scientist; and Lennart Mucke, GIND director and senior investigator, UCSF professor of neurology, along with Mahley and Huang.
The Gladstone Institute of Neurological Disease is one of three research institutes of The J. David Gladstone Institutes, a private, nonprofit biomedical research institution affiliated with UCSF. For further information, visit www.gladstone.ucsf.edu.
Contact: John Watson
jwatson@gladstone.ucsf.edu
415-695-3833
University of California - San Francisco
How genetic factor may increase risk for Alzheimer's disease
24 Mar 2004
Scientists zero in on toxicity of key protein, apoE4
Researchers at the Gladstone Institute of Neurological Disease have identified processes that may explain how a key protein, apolipoprotein E4 (apoE4), contributes to the development of Alzheimer's disease.
Their findings, described in the Journal of Neuroscience (March 10, 2004), include identifying where in the brain apoE4 is broken down into toxic fragments that can impair the function and survival of nerve cells. Results of their study may point the way to a new therapeutic strategy for the prevention and treatment of Alzheimer's disease.
ApoE4 is the best known genetic risk factor for Alzheimer's disease, but, until now, the mechanism by which it increases that risk has remained a mystery. The key finding of the current study relates to apoE4's tendency to be broken down into toxic fragments when it is produced in neurons, the brain cells responsible for cognitive functions.
Proteins can be broken into small pieces by enzymes known as proteases in a process termed proteolysis. While the degradation of proteins is important for many cell processes, it can be harmful when it occurs inappropriately, not only because it destroys the protein, but also because abnormally high levels of fragments can damage cells.
In the new study, involving the examination of genetically engineered mice, Gladstone researchers have established that:
only apoE4 produced by neurons is susceptible to fragmentation, unlike apoE4 produced by other brain cells;
fragmentation is correlated with age, occurring more frequently the older the animal, similar to the effect of age on Alzheimer disease risk in humans;
fragmentation of apoE4 occurs predominantly in the very parts of the brain that are most vulnerable to Alzheimer's disease, the neocortex and hippocampus. In contrast, fragmentation does not occur in the cerebellum, which is much less vulnerable to Alzheimer's disease;
the apoE4 fragments cause an abnormal change to the protein tau, which is also heavily affected by Alzheimer's disease. Both apoE4 fragments and Alzheimer's disease lead to the abnormal attachment of phosphate groups on tau that can end up contorting the shape of brain cells.
The investigators suspect that the fragmentation of apoE4 is caused by a neuron-specific enzyme, which they are now trying to identify and block with drugs.
"From this and our previous studies, we believe that the protease that cleaves apoE4 may serve as a therapeutic target for the prevention and treatment of Alzheimer's disease, especially in patients who are impacted by apoE4," said the senior author of the study, Yadong Huang, MD, PhD, staff research investigator at the Gladstone Institute of Neurological Disease (GIND) and assistant professor of pathology at the University of California, San Francisco (UCSF).
"With this work, we're a significant step closer to solving the key riddle of apoE4, namely, what is occurring at the molecular level that makes this protein so active in causing neurodegenerative disease," explained Dr. Robert Mahley, "Research of this kind is essential for the development of better treatments for Alzheimer's disease."
This work was supported in part by grants from the National Institutes of Health and by a MetLife Foundation award. The paper, "Neuron-Specific Apolipoprotein E4 Proteolysis Is Associated with Increased Tau Phosphorylation in Brains of Transgenic Mice," was co-authored by Gladstone Institute of Neurological DiseaseGIND staff members Walter J. Brecht, senior research associate; Faith M. Harris, research associate; Shengjun Chang, postdoctoral fellow; Ina Tesseur, postdoctoral fellow; Gui-Qiu Yu, senior research associate; Qin Xu, postdoctoral fellow ; Jo Dee Fish, research technologist; Tony Wyss-Coray, former staff research investigator; Manuel Buttini, former research scientist; and Lennart Mucke, GIND director and senior investigator, UCSF professor of neurology, along with Mahley and Huang.
The Gladstone Institute of Neurological Disease is one of three research institutes of The J. David Gladstone Institutes, a private, nonprofit biomedical research institution affiliated with UCSF. For further information, visit www.gladstone.ucsf.edu.
Contact: John Watson
jwatson@gladstone.ucsf.edu
415-695-3833
University of California - San Francisco
// posted by neurofuture3:00 PM permanent link
tags:
tags:
tags: help build archive | brain games | more brain games
25,000 page views...for a small piece of March, not bad, we'll hit 1 million page views easy over at cognitivecare.com. The world's first interactive memory assessment program...with 15.3 million people (officially) diagnosed with Alzheimers at the moment and an enormous multiple at the edge, the time is critical to start monitoring. If you don't check yourself, who will?
// posted by neurofuture1:29 AM permanent link
tags:
tags:
tags: help build archive | brain games | more brain games
3.22.2004
We call them "senior moments," those times we forget in mid-sentence what we intended to say, misplace something we just had in our hands or can't remember why we walked into the kitchen.
We tend to think of memory loss as a natural consequence of aging, something that, unlike gray hair or wrinkles, we can't do anything about.
"But that's not true," said Dr. Gary Small, a geriatric psychiatrist at the University of California, Los Angeles, and director of the school's Center on Aging.
The lifestyle choices we make now -- what we do for fun and relaxation, how active we are, what we eat -- can have a major impact on mental performance and overall brain health for years to come, he said.
Small covers the topic in his book, "The Memory Bible: An Innovative Strategy for Keeping Your Brain Young" (Hyperion, $16.95). A growing body of research in memory and brain function is showing that there are many ways to improve mental sharpness, prevent dementia or even delay the onset of Alzheimer's disease.
"It is never too early to start protecting our brain," Small said.
Memory matters strike a special chord in America's baby boomers, the generation of people now in their early 40s to late 50s who are fueling an explosion of self-help books on memory improvement such as "Keep Your Brain Alive" by Lawrence Katz, "Total Memory Workout" by Cynthia Green and "Saving Your Brain" by Dr. Jeff Victoroff.
Dr. Kathleen W. Wilson, a senior internist at Ochsner Clinic in New Orleans, has an upcoming book, "Maintain Your Brain: Prevent Stroke and Dementia," that looks at things people can do to protect their brains.
"In the last few years, doctors have figured out how to prevent a lot of cases of dementia," Wilson said. "The many people who may be affected in the future need these facts now."
We all experience some forgetfulness as we age, Small notes in "The Memory Bible." Difficulties with memory become more common when we hit middle age, when we notice problems such as forgetting people's names, where we parked the car or what movie we saw last weekend.
Lay some of the blame on our busy lifestyles.
"Our lives have become more frenetic and chaotic," Small said.
"A woman I know who is a real estate agent was multitasking while she was driving. She was talking to her husband on the phone and she said, `I can't find my cell phone. Let me hang up and you call me back so I can find it."'
One memory technique Small recommends can be summed up in three words: "Look, snap and connect."
"It boils down to actively observing what you want to remember, focusing your attention, rehearsing it and being able to pull it out of your memory stores," he said.
"We need to create a mental snapshot. Most people find it easier to remember visual information.
"The story method also is effective. It's a good way to remember errands, to arrange them in a logical order. If I need to go to the market and to pick up the laundry, I might imagine the grocer waving to me from the laundry.
"By adding detail, we're giving it meaning. If it has meaning, it fixes in your memory stores, into the brain cells that organize information, and makes it more permanent."
Small and other researchers stress the importance of physical activity and a healthful diet in maintaining healthy brains. Antioxidants, which occur naturally in many fruits and vegetables, can protect brain cells, Small said, as can foods rich in omega-3 fatty acids, such as fish and nuts. Excess body fat increases the risk of diabetes and high blood pressure, which increase the risk of small strokes in the brain, Small says.
We can keep brain cells active and making those all-important new connections by participating in stimulating activities, Small said. "These can be things like working crossword puzzles or jigsaw puzzles, learning a new language or brushing your teeth with your left hand" if you're right-handed.
When it comes to mental fitness, he said, the phrase "use it or lose it" holds true.
March 22, 2004
We tend to think of memory loss as a natural consequence of aging, something that, unlike gray hair or wrinkles, we can't do anything about.
"But that's not true," said Dr. Gary Small, a geriatric psychiatrist at the University of California, Los Angeles, and director of the school's Center on Aging.
The lifestyle choices we make now -- what we do for fun and relaxation, how active we are, what we eat -- can have a major impact on mental performance and overall brain health for years to come, he said.
Small covers the topic in his book, "The Memory Bible: An Innovative Strategy for Keeping Your Brain Young" (Hyperion, $16.95). A growing body of research in memory and brain function is showing that there are many ways to improve mental sharpness, prevent dementia or even delay the onset of Alzheimer's disease.
"It is never too early to start protecting our brain," Small said.
Memory matters strike a special chord in America's baby boomers, the generation of people now in their early 40s to late 50s who are fueling an explosion of self-help books on memory improvement such as "Keep Your Brain Alive" by Lawrence Katz, "Total Memory Workout" by Cynthia Green and "Saving Your Brain" by Dr. Jeff Victoroff.
Dr. Kathleen W. Wilson, a senior internist at Ochsner Clinic in New Orleans, has an upcoming book, "Maintain Your Brain: Prevent Stroke and Dementia," that looks at things people can do to protect their brains.
"In the last few years, doctors have figured out how to prevent a lot of cases of dementia," Wilson said. "The many people who may be affected in the future need these facts now."
We all experience some forgetfulness as we age, Small notes in "The Memory Bible." Difficulties with memory become more common when we hit middle age, when we notice problems such as forgetting people's names, where we parked the car or what movie we saw last weekend.
Lay some of the blame on our busy lifestyles.
"Our lives have become more frenetic and chaotic," Small said.
"A woman I know who is a real estate agent was multitasking while she was driving. She was talking to her husband on the phone and she said, `I can't find my cell phone. Let me hang up and you call me back so I can find it."'
One memory technique Small recommends can be summed up in three words: "Look, snap and connect."
"It boils down to actively observing what you want to remember, focusing your attention, rehearsing it and being able to pull it out of your memory stores," he said.
"We need to create a mental snapshot. Most people find it easier to remember visual information.
"The story method also is effective. It's a good way to remember errands, to arrange them in a logical order. If I need to go to the market and to pick up the laundry, I might imagine the grocer waving to me from the laundry.
"By adding detail, we're giving it meaning. If it has meaning, it fixes in your memory stores, into the brain cells that organize information, and makes it more permanent."
Small and other researchers stress the importance of physical activity and a healthful diet in maintaining healthy brains. Antioxidants, which occur naturally in many fruits and vegetables, can protect brain cells, Small said, as can foods rich in omega-3 fatty acids, such as fish and nuts. Excess body fat increases the risk of diabetes and high blood pressure, which increase the risk of small strokes in the brain, Small says.
We can keep brain cells active and making those all-important new connections by participating in stimulating activities, Small said. "These can be things like working crossword puzzles or jigsaw puzzles, learning a new language or brushing your teeth with your left hand" if you're right-handed.
When it comes to mental fitness, he said, the phrase "use it or lose it" holds true.
March 22, 2004
// posted by neurofuture11:09 AM permanent link
tags:
tags:
tags: help build archive | brain games | more brain games
3.05.2004
Study: Plant Extracts May Ease Dementia Symptoms
Fri Mar 5, 6:28 AM ET Add Health - Reuters to My Yahoo!
LIVERPOOL, England (Reuters) - Extracts of sage and lemon balm may help to improve memory and behavioral problems in people with Alzheimer's disease (news - web sites) and other types of dementia, scientists said Friday.
Professor Elaine Perry, of the University of Newcastle upon Tyne in northern England, told a medical conference that the plant extracts produced promising results in studies.
"In controlled trials in normal volunteers, both extracts improved memory, and lemon balm improved mood. Lemon balm reduced agitation and improved quality of life in people with Alzheimer's disease," Perry said in a statement.
Preliminary data showed that sage also had a significant effect on attention and behavior. The impact of sage on Alzheimer's are still being investigated but preliminary data indicate significant effects on attention and behavior, she added.
Perry, who presented the results to a two-day meeting on the psychiatry of old age, selected and prepared the extracts after studying different plant species used in traditional and herbal remedies and identifying the main chemical components.
The extracts produced minimal or no side effects in the patients and volunteers.
"Extracts of both sage and lemon balm are clearly worth pursuing as potential treatments..," Perry added.
Millions of people worldwide suffer from dementia, which is characterized by memory loss and a progressive decline in thinking, comprehension and judgment. Alzheimer's disease is the leading type of the disorder in the elderly.
Fri Mar 5, 6:28 AM ET Add Health - Reuters to My Yahoo!
LIVERPOOL, England (Reuters) - Extracts of sage and lemon balm may help to improve memory and behavioral problems in people with Alzheimer's disease (news - web sites) and other types of dementia, scientists said Friday.
Professor Elaine Perry, of the University of Newcastle upon Tyne in northern England, told a medical conference that the plant extracts produced promising results in studies.
"In controlled trials in normal volunteers, both extracts improved memory, and lemon balm improved mood. Lemon balm reduced agitation and improved quality of life in people with Alzheimer's disease," Perry said in a statement.
Preliminary data showed that sage also had a significant effect on attention and behavior. The impact of sage on Alzheimer's are still being investigated but preliminary data indicate significant effects on attention and behavior, she added.
Perry, who presented the results to a two-day meeting on the psychiatry of old age, selected and prepared the extracts after studying different plant species used in traditional and herbal remedies and identifying the main chemical components.
The extracts produced minimal or no side effects in the patients and volunteers.
"Extracts of both sage and lemon balm are clearly worth pursuing as potential treatments..," Perry added.
Millions of people worldwide suffer from dementia, which is characterized by memory loss and a progressive decline in thinking, comprehension and judgment. Alzheimer's disease is the leading type of the disorder in the elderly.
// posted by neurofuture10:00 AM permanent link
tags:
tags:
tags: help build archive | brain games | more brain games
3.01.2004
Today is the first day of the new month which promises to be extraordinarily busy. The good news is that we are rapidly growing our site traffic and hope to, after a series of glitches in the middle of the month of February strive onward to greater utility and stability. The usual start-up growing pains.
We also want to explore establishing communities where support groups can access our tools and use it in a less individualistic way, where groups will be able to compare their own scorecards while also getting understanding and help from those around them. We hope to get to that soon.(as possible) Next week, we will be meeting at a prominent Bay Area university and discussing further ways of leveraging our technology with their research goals....there are some pretty exciting developments coming down the pike. Oh yeah, and over to your right ------>>> please see the XML feed which we are testing and if anyone using a blog reader let us know how it is working so far (Atom format)
Also, we intend to post on some of the growing steps of the company as a means of looking back where we have been at a particular time, which is one of the cool things about start-ups ( the progression down and uncertain path) who knows where it will end up?
Regards,
MA
We also want to explore establishing communities where support groups can access our tools and use it in a less individualistic way, where groups will be able to compare their own scorecards while also getting understanding and help from those around them. We hope to get to that soon.(as possible) Next week, we will be meeting at a prominent Bay Area university and discussing further ways of leveraging our technology with their research goals....there are some pretty exciting developments coming down the pike. Oh yeah, and over to your right ------>>> please see the XML feed which we are testing and if anyone using a blog reader let us know how it is working so far (Atom format)
Also, we intend to post on some of the growing steps of the company as a means of looking back where we have been at a particular time, which is one of the cool things about start-ups ( the progression down and uncertain path) who knows where it will end up?
Regards,
MA
// posted by neurofuture1:44 PM permanent link
tags:
tags:
tags: help build archive | brain games | more brain games
