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Issue:
Volume 53, issue 2

Title: AMYLOID BETA: FUNCTIONAL PROTEIN OR BIOLOGICAL JUNK?

Authors: N.V. Koudinova¹, A.R. Koudinov¹, T.T. Berezov^1,2

Address:

1.Orekhovich Institute of Biomedical Chemistry of RAMS, Pogodinskaya str. 10, Moscow 119121, Russia, tel./fax: (495)245-08-57

2.Russian People’s Friendship University, Medical School, Department of Biochemistry,

Mikluho-Maklay str. 8, Moscow 117198, Russia, tel./fax: (495)434-0412, e-mail: tberezov@alzclub.org

Abstract:

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.

Key words: Alzheimer’s disease, amyloid beta, amyloid cascade hypothesis, synaptic plasticity, long term potentiation, cholesterol, neuronal function.

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