Compensatory mechanisms to heal neuroplasticity impairment under Alzheiemer's disease neurodegeneration. I: The role of amyloid beta and its' precursor protein

Koudinova N.V.1, Koudinov A.R.1 , Kezlya E.V.2, Kozirev K.M.3, Medvedev A.E.4, Berezov T.T.5

1. Orekhovich Institute of Biomedical Chemistry of RAMS
2. Interhospital Medical Center "Intermedcenter"
3. Department of Pathological Anatomy, North Osetia State Medical Academy
4. Institute of Biomedical Chemistry, Russian Academy of Medical Sciences
5. Orekhovich Institute of Biomedical Chemistry of RAMS Russian People`s Friendship University, Medical School, Department of Biochemistry
Section: Review
DOI: 10.18097/pbmc20125804385      UDK: 612.82; 616.00.1; 577.112.115      PubMed Id: 23413683
Year: 2012  Volume: 58  Issue: 4  Pages: 385-399
In-depth scholar literature analysis of Alzheimer's disease neurodegenerative features of amyloid beta protein neurochemistry modification and excessive phosphorylation of tau protein (and associated neuronal cytoskeleton rearrangements) are secondary phenomena. At early disease stage these neurobiochemical mechanisms are reversible and serve to heal an impairment of biophysical properties of neuronal membranes, neurotransmission, basic neuronal function and neuroplasticity, while preserving anatomical and functional brain fields. Aβ and tau could well serve to biochemically restore physico-chemical properties of neual membranes due to a role these proteins play in lipid metabolism. Under such scenario therapeutic block of aggregation and plaque formation of Aβ and inhibition of tau phosphorylation, as well as pharmaceutical modification of other secondary neurodegenerative features (such as a cascade of oxidative stress reactions) are unable to provide an effective cure of Alzheimer's disease and related pathologies of the Central and peripheral nervous systems, because they are not arraying primary pathagenetic cause. We review the role of Aβ in compensatory mechanisms of neuroplasticity restoration under normal physiological condition and Alzheimer's disease.
Download PDF:

Koudinova N.V., Koudinov A.R., Kezlya E.V., Kozirev K.M., Medvedev A.E., Berezov T.T. (2012) Biomeditsinskaya khimiya, 58(4), 385-399.
This paper is also available as the English translation:10.1134/S1990750812010076
 2019 (vol 65)
 2018 (vol 64)
 2017 (vol 63)
 2016 (vol 62)
 2015 (vol 61)
 2014 (vol 60)
 2013 (vol 59)
 2012 (vol 58)
 2011 (vol 57)
 2010 (vol 56)
 2009 (vol 55)
 2008 (vol 54)
 2007 (vol 53)
 2006 (vol 52)
 2005 (vol 51)
 2004 (vol 50)
 2003 (vol 49)

© Institute of Biomedical Chemistry, Moscow, Russia