Amyloid beta: Functional protein or biological junk?

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.

Авторы
Редакторы
-
Издательство
Russian Academy of Medical Sciences
Номер выпуска
2
Язык
Русский
Страницы
119-127
Статус
Опубликовано
Подразделение
-
DOI
-
Номер
-
Том
53
Год
2007
Организации
  • 1 Orekhovich Institute of Biomedical Chemistry of RAMS, Pogodinskaya str. 10, Moscow 119121, Russian Federation
  • 2 Russian People's Friendship University, Medical School, Department of Biochemistry, Mikluho-Maklay str. 8, Moscow 117198, Russian Federation
Ключевые слова
Alzheimer's disease; Amyloid beta; Amyloid cascade hypothesis; Cholesterol; Long term potentiation; Neuronal function; Synaptic plasticity
Дата создания
19.10.2018
Дата изменения
19.10.2018
Постоянная ссылка
https://repository.rudn.ru/ru/records/article/record/3284/