التفاصيل البيبلوغرافية
العنوان: |
Amyloid beta: Functional protein or biological junk? |
المؤلفون: |
Koudinova N.V., Koudinov A.R., Beerzov T.T. |
المصدر: |
Biomeditsinskaya Khimiya |
بيانات النشر: |
Russian Academy of Medical Sciences |
سنة النشر: |
2020 |
المجموعة: |
NORA (National aggregator of open repositories of Russian universities) / Национальный агрегатор открытых репозиториев российских университетов |
مصطلحات موضوعية: |
Alzheimer's disease, Amyloid beta, Amyloid cascade hypothesis, Cholesterol, Long term potentiation, Neuronal function, Synaptic plasticity |
الوصف: |
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. |
نوع الوثيقة: |
article in journal/newspaper |
اللغة: |
Russian |
العلاقة: |
https://openrepository.ru/article?id=253732Test |
الإتاحة: |
https://openrepository.ru/article?id=253732Test |
حقوق: |
open access |
رقم الانضمام: |
edsbas.718CF1B2 |
قاعدة البيانات: |
BASE |