Titel
Autophagy and Alzheimer’s Disease: From Molecular Mechanisms to Therapeutic Implications
Autor*in
Md. Sahab Uddin
Department of Pharmacy, Southeast University, Bangladesh
Autor*in
Anna Stachowiak
Department of Experimental Embryology, Institute of Genetics and Animal Breeding, Polish Academy of Sciences
Autor*in
Abdullah Al Mamun
Department of Pharmacy, Southeast University, Bangladesh
... show all
Abstract
Alzheimer’s disease (AD) is the most common cause of progressive dementia in the elderly. It is characterized by a progressive and irreversible loss of cognitive abilities and formation of senile plaques, composed mainly of amyloid β (Aβ), and neurofibrillary tangles (NFTs), composed of tau protein, in the hippocampus and cortex of afflicted humans. In brains of AD patients the metabolism of Aβ is dysregulated, which leads to the accumulation and aggregation of Aβ. Metabolism of Aβ and tau proteins is crucially influenced by autophagy. Autophagy is a lysosome-dependent, homeostatic process, in which organelles and proteins are degraded and recycled into energy. Thus, dysfunction of autophagy is suggested to lead to the accretion of noxious proteins in the AD brain. In the present review, we describe the process of autophagy and its importance in AD. Additionally, we discuss mechanisms and genes linking autophagy and AD, i.e., the mTOR pathway, neuroinflammation, endocannabinoid system, ATG7, BCL2, BECN1, CDK5, CLU, CTSD, FOXO1, GFAP, ITPR1, MAPT, PSEN1, SNCA, UBQLN1, and UCHL1. We also present pharmacological agents acting via modulation of autophagy that may show promise in AD therapy. This review updates our knowledge on autophagy mechanisms proposing novel therapeutic targets for the treatment of AD.
Stichwort
autophagyAlzheimer’s diseaseamyloid betatau
Objekt-Typ
Sprache
Englisch [eng]
Persistent identifier
https://phaidra.univie.ac.at/o:1032912
Erschienen in
Titel
Frontiers in Aging Neuroscience
Band
10
Verlag
Frontiers Media SA
Erscheinungsdatum
2018
Zugänglichkeit
Rechteangabe
© 2018 Uddin, Stachowiak, Mamun, Tzvetkov, Takeda, Atanasov, Bergantin, Abdel-Daim and Stankiewicz

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