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

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. © Pleiades Publishing, Ltd., 2012.

Авторы
Koudinov A.R. 1, 2 , Koudinova N.V. 2 , Kezlya E.V.3 , Kozirev K.M.4 , Medvedev A.E.1 , Berezov T.T. 1, 2
Редакторы
-
Издательство
-
Номер выпуска
1
Язык
Английский
Страницы
1-10
Статус
Опубликовано
Подразделение
-
Номер
-
Том
6
Год
2012
Организации
  • 1 Institute of Biomedical Chemistry, Russian Academy of Medical Sciences, ul. Pogodinskaya 10, Moscow, 119121, Russian Federation
  • 2 Department of Biochemistry, School of Medicine, Russian Peoples' Friendship University, Moscow, Russian Federation
  • 3 Interhospital Medical Center Intermedcenter, Moscow, Russian Federation
  • 4 Department of Pathological Anatomy, North Osetia State Medical Academy, Vladikavkaz Republic of North Ossetia Alania, Russian Federation
Ключевые слова
Alzheimer's disease; amyloid beta; amyloid plaque; cholesterol; hippocampus; lipoproteins; phospholipids; synaptic plasticity
Дата создания
19.10.2018
Дата изменения
19.10.2018
Постоянная ссылка
https://repository.rudn.ru/ru/records/article/record/2351/