Journal
DNA AND CELL BIOLOGY
Volume 34, Issue 4, Pages 261-273Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/dna.2014.2757
Keywords
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Funding
- Fundacao para a Ciencia e a Tecnologia [SFRH/BPD/84163/2012, SFRH/BPD/34712/2007]
- Alzheimer's Association [NIRG-13-282387]
- Fundação para a Ciência e a Tecnologia [SFRH/BPD/34712/2007, SFRH/BPD/84163/2012] Funding Source: FCT
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Autophagy is a housekeeping process responsible for the bulk degradation of misfolded protein aggregates and damaged organelles through the lysosomal machinery. Given its key role as a cellular quality control mechanism, autophagy is now a focus of intense scrutiny in Alzheimer's disease (AD). The hallmarks of this devastating neurodegenerative disease are the accumulation of misfolded amyloid-beta (A beta) peptide and hyperphosphorylated tau protein and neuronal loss, which are accompanied by mitochondrial dysfunction and endoplasmic reticulum (ER) stress, suggesting that faulty autophagy is a contributing factor to AD pathology. Indeed, the AD brain is characterized by a massive accumulation of autophagic vacuoles within large swellings along dystrophic neurites and defects at different steps of the autophagic-lysosomal pathway. In this sense, this review provides an overview on the role of autophagy on A beta metabolism, tau processing and clearance, and the contribution of ER-phagy and mitophagy to AD pathology. From a therapeutic perspective, this review also intends to clarify whether, when, and how autophagy can be targeted to efficaciously counteract AD-related symptomatic and neuropathological features.
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