There is currently no cure for Alzheimer's disease
The most common form of dementia may be closely related to another common disease of old-age - type II diabetes, say scientists.
Treating Alzheimer's with the hormone insulin, or with drugs to boost its effect, may help patients, they claim.
The journal Proceedings of the National Academy of Sciences reports insulin could protect against damage to brain cells key to memory.
UK experts said the find could be the basis of new drug treatments.
The most exciting implications are that some diabetes drugs have the potential to be developed as Alzheimer's treatments
Spokesman, Alzheimer's Research Trust
The relationship between insulin and brain disease has been under scrutiny since doctors found evidence that the hormone was active there. More
Study: Diabetes Linked to Cognitive Decline
By ALICE PARK Monday, Jan. 05, 2009
Studies have shown that diabetes may speed up aging-related deficits in mental function and lead to a twofold increase in the risk of dementia. Some researchers have speculated that diabetes could even boost the risk of developing Alzheimer's disease. Roger Dixon, a psychologist at the University of Alberta in Canada, wanted to learn whether this was true and set out to study exactly how uncontrolled blood sugar affected the brain.
Dixon and his colleagues studied 41 adults with diabetes and 424 healthy adults between the ages of 53 and 90, and reported their findings in the journal Neuropsychology. After testing the participants on memory, recall, verbal fluency, executive functions involving critical thinking and the speed of their mental faculties, researchers found the most significant deficits in diabetes patients on tasks of executive function and speed. These problems showed up in the youngest patients as well as the older ones, and once the cognitive symptoms appeared, they did not seem to worsen or change over time. Although Dixon's study failed to add new information on the question of diabetes and Alzheimer's disease, other experts view these results as useful fodder in the growing field of diabetes research.
"This study in general supports what we understand," says Dr. Alan Jacobson, chief of psychiatric services at the Joslin Diabetes Center in Boston. "It's another study adding to our recognition that Type 2 diabetes portends some type of problem in terms of cognitive function." More
Showing posts with label Alzheimer's. Show all posts
Showing posts with label Alzheimer's. Show all posts
Tuesday, February 3, 2009
Sunday, June 22, 2008
New clue to Alzheimer's found
New clue to Alzheimer's found
WASHINGTON (AP) — Researchers have uncovered a new clue to the cause of Alzheimer's disease.
The brains of people with the memory-robbing form of dementia are cluttered with a plaque made up of beta-amyloid, a sticky protein. But there long has been a question whether this is a cause of the disease or a side effect. Also involved are tangles of a protein called tau; some scientists suspect this is the cause.
Now, researchers have caused Alzheimer's symptoms in rats by injecting them with one particular form of beta-amyloid. Injections with other forms of beta-amyloid did not cause illness, which may explain why some people have beta-amyloid plaque in their brains but do not show disease symptoms.
The findings by a team led by Dr. Ganesh M. Shankar and Dr. Dennis J. Selkoe of Harvard Medical School were reported in Sunday's online edition of the journal Nature Medicine.
The researchers used extracts from the brains of people who donated their bodies to medicine.
Forms of soluble beta-amyloid containing different numbers of molecules, as well as insoluble cores of the brain plaque, were injected into the brains of mice. There was no detectable effect from the insoluble plaque or the soluble one-molecule or three-molecule forms, the researchers found.
But the two-molecule form of soluble beta-amyloid produced characteristics of Alzheimer's in the rats, they reported.
Those rats had impaired memory function, especially for newly learned behaviors. When the mouse brains were inspected, the density brain cells was reduced by 47% with the beta-amyloid seeming to affect synapses, the connections between cells that are essential for communication between them.
The research, for the first time, showed the effect of a particular type of beta-amyloid in the brain, said Dr. Marcelle Morrison-Bogorad, director of the division of neuroscience at the National Institute on Aging, which helped fund the research.
It was surprising that only one of the three types had an effect, she said in a telephone interview.
Morrison-Bogorad said the findings may help explain the discovery of plaque in the brains of people who do not develop dementia. For some time, doctors have wondered why they find some brains in autopsy that are heavily coated with beta-amyloid, but the person did not have Alzheimer's.
The answer may lie in the two types of beta-amyloid that did not cause symptoms.
Now, the question is why one has the damaging effect and not others.
"A lot of work needs to be done," Morrison-Bogorad said. "Nature keeps sending us down paths that look straight at the beginning, but there are a lot of curves before we get to the end."
Dr. Richard J. Hodes, director of the National Institute on Aging, said that "while more research is needed to replicate and extend these findings, this study has put yet one more piece into place in the puzzle that is Alzheimer's."
In addition to the Institute on Aging, the research was funded by Science Foundation Ireland, Wellcome Trust, the McKnight and Ellison foundations and the Lefler Small Grant Fund.
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Copyright 2008 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
WASHINGTON (AP) — Researchers have uncovered a new clue to the cause of Alzheimer's disease.
The brains of people with the memory-robbing form of dementia are cluttered with a plaque made up of beta-amyloid, a sticky protein. But there long has been a question whether this is a cause of the disease or a side effect. Also involved are tangles of a protein called tau; some scientists suspect this is the cause.
Now, researchers have caused Alzheimer's symptoms in rats by injecting them with one particular form of beta-amyloid. Injections with other forms of beta-amyloid did not cause illness, which may explain why some people have beta-amyloid plaque in their brains but do not show disease symptoms.
The findings by a team led by Dr. Ganesh M. Shankar and Dr. Dennis J. Selkoe of Harvard Medical School were reported in Sunday's online edition of the journal Nature Medicine.
The researchers used extracts from the brains of people who donated their bodies to medicine.
Forms of soluble beta-amyloid containing different numbers of molecules, as well as insoluble cores of the brain plaque, were injected into the brains of mice. There was no detectable effect from the insoluble plaque or the soluble one-molecule or three-molecule forms, the researchers found.
But the two-molecule form of soluble beta-amyloid produced characteristics of Alzheimer's in the rats, they reported.
Those rats had impaired memory function, especially for newly learned behaviors. When the mouse brains were inspected, the density brain cells was reduced by 47% with the beta-amyloid seeming to affect synapses, the connections between cells that are essential for communication between them.
The research, for the first time, showed the effect of a particular type of beta-amyloid in the brain, said Dr. Marcelle Morrison-Bogorad, director of the division of neuroscience at the National Institute on Aging, which helped fund the research.
It was surprising that only one of the three types had an effect, she said in a telephone interview.
Morrison-Bogorad said the findings may help explain the discovery of plaque in the brains of people who do not develop dementia. For some time, doctors have wondered why they find some brains in autopsy that are heavily coated with beta-amyloid, but the person did not have Alzheimer's.
The answer may lie in the two types of beta-amyloid that did not cause symptoms.
Now, the question is why one has the damaging effect and not others.
"A lot of work needs to be done," Morrison-Bogorad said. "Nature keeps sending us down paths that look straight at the beginning, but there are a lot of curves before we get to the end."
Dr. Richard J. Hodes, director of the National Institute on Aging, said that "while more research is needed to replicate and extend these findings, this study has put yet one more piece into place in the puzzle that is Alzheimer's."
In addition to the Institute on Aging, the research was funded by Science Foundation Ireland, Wellcome Trust, the McKnight and Ellison foundations and the Lefler Small Grant Fund.
__
Copyright 2008 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
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