期刊
AGEING RESEARCH REVIEWS
卷 58, 期 -, 页码 -出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2019.101006
关键词
Neurodegenerative diseases; Neurodegeneration; Biomarker; Apoptosis; Exosomes
资金
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) 1D Researcher Productivity Grant [307980/2018-9]
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
Alzheimer's Disease (AD) is characterized by progressive loss of cognitive abilities; senile plaques represent the major histopathological findings. Amyloid precursor protein (APP) processing machinery, and its product amyloid-beta (AP) peptide, have been found in extracellular vesicles (EVs), specifically exosomes, which allows for A beta peptide aggregation and subsequent senile plaques deposition. We review the APP processing imbalance in EVs, autophagic and endosomal pathways in AD. Increased intraluminal vesicle (ILV) production and exosome release appear to counteract the endosomal dysfunction of APP processing; however, this process results in elevated amyloidogenic processing of APP and augmented senile plaque deposition. Several players related to APP processing and dysfunctional endosomal-lysosomal-exosomal (and other EVs) pathway are described, and the interconnected systems are discussed. The components Arc, p75, Rab11 and retromer complex emerge as candidates for key convergent mechanisms that lead to increased EVs loaded with APP machinery and Aj3 levels, in atrophy and damage of basal forebrain cholinergic neurons in AD.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据