Skip to comments.Infection Defense May Spur Alzheimer’s
Posted on 03/09/2010 3:06:00 PM PST by neverdem
For years, a prevailing theory has been that one of the chief villains in Alzheimers disease has no real function other than as a waste product that the brain never properly disposed of.
The material, a protein called beta amyloid, or A-beta, piles up into tough plaques that destroy signals between nerves. When that happens, people lose their memory, their personality changes and they stop recognizing friends and family.
But now researchers at Harvard suggest that the protein has a real and unexpected function it may be part of the brains normal defenses against invading bacteria and other microbes.
Other Alzheimers researchers say the findings, reported in the current issue of the journal PLoS One, are intriguing, though it is not clear whether they will lead to new ways of preventing or treating the disease.
The new hypothesis got its start late one Friday evening in the summer of 2007 in a laboratory at Harvard Medical School. The lead researcher, Rudolph E. Tanzi, a neurology professor who is also director of the genetics and aging unit at Massachusetts General Hospital, said he had been looking at a list of genes that seemed to be associated with Alzheimers disease.
To his surprise, many looked just like genes associated with the so-called innate immune system, a set of proteins the body uses to fight infections. The system is particularly important in the brain, because antibodies cannot get through the blood-brain barrier, the membrane that protects the brain. When the brain is infected, it relies on the innate immune system to protect it...
(Excerpt) Read more at nytimes.com ...
Any pathogen recognized by the innate immune system might cause this reaction?
From the article:
In summary, our finding that Aβ is an antimicrobial peptide is the first evidence that the species responsible for amyloidosis may have a normal function. This stands in stark contrast to current models, which assume β-amyloid deposition to be an accidental process resulting from the abnormal behavior of an incidental product of catabolism. Our data suggest increased Aβ generation, and resulting AD pathology, may be a mediated by a response of the innate immune system to a perceived infection. This model has important implications for current and future AD treatment strategies. First, it raises the possibility of preventing amyloidosis from initiating by pre-emptive targeting of pathogens/insults that stimulate the brain's innate immune system. Second, our model identifies the inflammatory pathways of the innate immune system as targets for modulating Aβ generation/accumulation. The target pathways implicated here are downstream of the inflammatory trigger. Thus, this approach would likely be useful independently of the involvement of infectious agents in AD pathology.
I have no idea, but this reaction is limited to the central nervous system. Maybe that's why the rest of the immune system can't clean up the beta amyloid garbage left behind?
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So it’s the flip side of a coin? Makes sense...
Very interesting. Thanks for the ping; posts.
(an afterthought on seeing the author’s name...I’m usually down in the carribean this time of year having one of those blood-brain drinks)...just sayin’
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