Year: 2021
Type: review
Abstract: Autophagy is a lysosomal degradation pathway and the main clearance route of many toxic protein aggregates. The molecular pathology of Alzheimer's disease (AD) manifests in the form of protein aggregates-extracellular amyloid-β depositions and intracellular tau neurofibrillary tangles. Perturbations at different steps of the autophagy pathway observed in cellular and animal models of AD might contribute to amyloid-β and tau accumulation. Increased levels of autophagosomes detected in patients' brains suggest an alteration of autophagy in human disease. Autophagy is also involved in the fine-tuning of inflammation, which increases in the early stages of AD and possibly drives its pathogenesis. Mounting evidence of a causal link between impaired autophagy and AD pathology uncovers an exciting opportunity for the development of autophagy-based therapeutics.
Source: Current Opinion in Pharmacology
Institutions: University of Cambridge, UK Dementia Research Institute
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: hybrid
Estimated APC paid: $3,210
Funders: Alzheimer's Society, National Institute for Health and Care Research, European Commission, Alzheimer’s Research UK, Fondation Roger de Spoelberch, UK Dementia Research Institute, Merck Sharp and Dohme, Tau Consortium, Medical Research Council, Horizon 2020, NIHR Cambridge Biomedical Research Centre
OpenAlex ID: W3194364132