Lifelong Active Brains Have Fewer Deposits Of Alzheimer's Protein
Featured ArticleAcademic Journal
Main Category: Alzheimer's / Dementia
Also Included In: Neurology / Neuroscience
Article Date: 24 Jan 2012 - 2:00 PST
A new study using PET scans to to examine the brains of healthy older people finds those who have been mentally stimulated all their lives, doing things like reading, writing, and playing games and puzzles, have fewer deposits of beta-amyloid, a destructive protein that is a hallmark of Alzheimer's Disease. The researchers suggest their findings will encourage scientists to think differently about how mental stimulation affects the biology of the brain.
A team from the University of California, Berkeley led the study, and with their colleagues, write about their findings in a report published online in the Archives of Neurology on Monday. Funds for their work came partly from the National Institutes of Health and partly from the Alzheimer's Association.
Beta-amyloid deposits are fibrils of proteins that have misfolded into fibrous sheet structures that accumulate in the brain and clog up the spaces between brain cells. They are the prime suspect in the pathology of Alzheimer's Disease and a much pursued goal by researchers in this field is to find a way to reduce them.
Previous studies have already suggested that keeping the brain active by pursuing activities that challenge thinking skills, such as reading, writing and playing games, may help put off Alzheimer's Disease later in life. But none has yet pointed to a link with the underlying suspected biology.
Lead author Susan Landau, a research scientist at the Helen Wills Neuroscience Institute and the Berkeley Lab, said in a statement:
"This is the first time cognitive activity level has been related to amyloid buildup in the brain."
Dr. William Jagust, a professor with appointments at UC Berkeley's Helen Wills Neuroscience Institute, the School of Public Health and Lawrence Berkeley National Laboratory, led the research. He said the results point us in a new direction about how lifelong mental stimulation affects the brain:
"Rather than simply providing resistance to Alzheimer's, brain-stimulating activities may affect a primary pathological process in the disease. This suggests that cognitive therapies could have significant disease-modifying treatment benefits if applied early enough, before symptoms appear."
Amyloid build up is also affected by genes and age (a third of the over-60s have some amyloid build up in their brains), and while we can't do anything about those, something we can change is cognitive stimulation, such as doing more reading and writing, said the researchers.
But it seems the message about this has to go out early, before the disease sets in.
Landau said:
"Amyloid probably starts accumulating many years before symptoms appear. So it's possible that by the time you have symptoms of Alzheimer's, like memory problems, there is little that can be done to stop disease progression."
The study participants were 65 healthy older adults (mean age 76), 10 patients with Alzheimer's Disease (mean age 75) and 11 young people (the controls, mean age 25). The setting was Berkeley, California, and the period of study was from October 2005 to February 2011.
The researchers used two sources of data: one came from PET scans of the participants' brains and the other from questionnaires where the 65 healthy older participants rated their lifelong participation (since age of 6) in mentally stimulating activities such as reading, writing, and playing games. It also asked them about exercise.
The PET scan method they used employs an imaging agent called carbon 11-labeled Pittsburgh Compound B or [11C]PiB. This compound sticks to amyloid deposits so they can then be "seen" in the PET scan. A reduced "uptake" of [11C]PiB correlates with fewer deposits.
When they analyzed the results of the PET scans with the lifelong mental activity response ratings in the questionnaires, the researchers found:
- Greater participation in mentally stimulating activities across the lifespan (but particularly in early and middle life), was linked to reduced [11C]PiB uptake.
- The link was found to be independent of other factors such as memory function, physical activity, self-rated memory ability, level of education and gender.
- Ranking the older participants by amount of participation in mentally stimulating activities, the top one third had [11C]PiB uptake that was comparable to the younger controls.
- In contrast, the [11C]PiB uptake of those in the lowest third was similar to that of the patients with Alzheimer's Disease.
- Although greater mentally stimulating activity was linked to more physical exercise, exercise itself was not linked to [11C] PiB uptake.
"We report a direct association between cognitive activity and [11C]PiB uptake, suggesting that lifestyle factors found in individuals with high cognitive engagement may prevent or slow deposition of [beta]-amyloid, perhaps influencing the onset and progression of AD [Alzheimer's Disease]."
They also point out they did not find a strong link between signs of amyloid deposit and levels of current cognitive activity.
Landau said this suggests that a "whole lifetime of engaging in these activities has a bigger effect than being cognitively active just in older age".
However, the researchers don't wish to downplay the importance of increasing brain activity later in life.
Jagust said "there is no downside to cognitive activity". It can only do good, even if for reasons other than reducing amyloid deposits in the brain:
"And actually, cognitive activity late in life may well turn out to be beneficial for reducing amyloid. We just haven't found that connection yet," he added.
The number of Americans living with Alzheimer's disease is rising as the baby boomer generation ages. There are around 5.4 million Americans living with Alzheimer's, the sixth-leading killer in the US, where deaths from the disease went up by 66% between 2000 and 2008.
There is no cure for Alzheimer's, but last week the US Health Authorities set 2025 as the deadline for coming up with an effective treatment.
Written by Catharine Paddock PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today
Additional source: UC Berkeley Newscenter
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Alzheimer's is transmissible, infectious prion disease
posted by Helane Shields, Alton, NH on 24 Jan 2012 at 5:45 pmAlzheimer's Disease (AD) and sporadic Creutzfeldt Jakob Disease (sCJD)
are sister prion diseases, transmissible, infectious by medical
equipment, (scopes, etc.) dental and eye equipment, blood, urine, feces,
saliva, mucous (aerosols: possibly by coughs & sneezes) Doctors
frequently misdiagnose AD and sCJD one for the other. The symptoms and
neuropathology are almost identifical.
Right now the US is in the middle of a raging, always fatal, prion
disease epidemic: There are over 6 million victims of AD and 1 million
Parkinson's Disease victims, with a new AD case every 69 seconds !
Recent research (October 2011) by Dr. Claudio Soto, et al, University of
Texas Medical School, has confirmed earlier research which found
injecting Alzheimer's brain material into mice brains caused infectious
prion disease.
http://www.sciencedaily.com/releases/2011/10/111004113757.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily+%28ScienceDaily%3A+Latest+Science+News%29
AD and sCJD victims shed prions in their urine and feces. Sewage
treatment does not inactivate prions - it concentrates them in the
sewage sludge. The US EPA acknowledges that the landspreading of sewage
sludge is also a pathway of prion risk for humans and animals (Mad Cow,
CWD, etc.)
alzheimers-prions.com
EPA NATIONAL WATER RESEARCH COMPENDIUM 2009-2014 lists PRIONS eight times
as an EMERGING CONTAMINANT of concern in sewage sludge "biosolids" ,
water and manure:
sludgevictims.com/prions/PRIONS-EPA-EMERGINGCONTAMINANTSINSLUDGEBIO.
pdf
"Could Alzheimer's be infectious? "
neurophilosophy.wordpress.com/2006/11/24/could-alzheimers-be-infectious/
SEE reply posted by:
Dr. Murray Waldman, coroner for the city of Toronto, Canada:
"In answer to the question how would Alzheimer’s (AD) be transmitted, I
have written a book “Dying For A Hamburger” that hypothesizes that AD is
spread by how we in North America and Europe feed and process meat,
mainly beef.
If you study the rates of AD and its geographical distribution, you will
find that rates start to soar when a country becomes meat eating (i.e.
Japan and Korea in the 1960s) and rises even faster when it adopts a
fast food culture (the US and Western Europe in the 50s and 60s) and
remains low in vegetarian countries (India) and those without a
processed meat industry or fast foods (equatorial Africa)…Murray "
hshields (at) tds.net
Scientists agree variant Creutzfeldt Jakob Disease (vCJD) is caused by eating prion tainted beef.
Many believe sporadic CJD/aka Alzheimer's Disease (AD) is also caused by eating prion contaminate4d meat e.g. BSE -Mad cow and CWD - Chronic Wasting Disease
(deer, elk, moose, etc.)
Inadequate/non-existent mad cow testing, and control and influence over USDA by the cattle industry guarantees the Alzheimer's Disease epidemic will continue to spread through US, Canada and UK.
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