J Alzheimers Dis. 2012;29(3):487-92. doi: 10.3233/JAD-2011-111928.
Hormesis and amyloid-β protein: physiology or pathology?
Morley JE, Farr SA.
This article reviews available data suggesting that the physiological role of amyloid-beta is memory enhancement
I think this a very interesting question. Would you explain here something more about it or share the paper?
Our data and that by others has shown that at low doses amyloid-beta improves memory in normal animals and long term potentiation. Antibodies to AB or antisense to Amyloid Precursor Protein decreases memory in young animals. There is a variety of biochemical pieces scattered throughout the literature suggesting that low dose amyloid beta has the opposite effect to high doses.
These data would be supplemented if a biological role for each species of beta amyloid was found. For example, it is known that Abeta42 is ready to form rings that might be involved in calcium uptake (Truncated β-amyloid peptide channels provide an alternative mechanism for Alzheimer’s Disease and Down syndrome; doi/10.1073/pnas.0914251107), or what is the role of AICD in the nucleus.
Many years ago we showed in PNAS that amyloid-beta 18-22 is the component involved in memory; oxidative damage is caused by 34 to 40. Thanks for the thoughts john
Dear John, based in your research we can say that elder people with good memory would have some amyloid-beta protein deposits in their brains?
Dear John, One approach could be to examine if Abeta-lowering APP-mutations (http://www.ncbi.nlm.nih.gov/pubmed/22801501) impacts memory in non-demented. Another could be to explore concentrations of different CSF Abeta isoforms in relation to memory, also in non-demented. Cheers, Niklas
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