Amyloid beta: functional protein or biological junk?

   
Koudinova N.V.1, Koudinov A.R.1 , Berezov T.T.2

1. Orekhovich Institute of Biomedical Chemistry of RAMS
2. Orekhovich Institute of Biomedical Chemistry of RAMS; Russian People`s Friendship University, Medical School, Department of Biochemistry
Section: Review
UDK: 612.82+616.001.31+577.112.115      PubMed Id: 17639713
Year: 2007  Volume: 53  Issue: 2  Pages: 119-127
During a decade there was a dogma that Alzheimer`s amyloid beta (Aβ) is produced only upon the disease, and that this protein is neurotoxic for neurons and brain tissue. Current scientific evidence demonstrate that Aβ is an essential molecule in synaptic plasticity that underlie learning and memory. Therefore, it was hypothesized that the change of Aβ biology in Alzheimer`s disease (as well as in a number of other human pathologies, including cardiovascular disease, Niemann-Pick type C disease and Down syndrome) represents a physiological mechanism serving to compensate the impaired brain structure or function. This review summarizes experimental evidence on Aβ as functional player in synaptic plasticity and neurochemical pathways.
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Koudinova N.V., Koudinov A.R., Berezov T.T. (2007) Biomeditsinskaya khimiya, 53(2), 119-127.
This paper is also available as the English translation:10.1134/S199075080703002X
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