ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2015
Promoting autophagic clearance: viable therapeutic targets in Alzheimer's disease.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- Autophagy in Alzheimer's Disease: Mechanisms, Clinical Trials, and Horizons.Neuro-degenerative diseases · 2026Review
- Targeting the mTOR Pathway with Natural Products: A Potential Therapeutic Approach for Autism Spectrum Disorders.Current neuropharmacology · 2026Review
- The Use of Natural Products for Preventing Cognitive Decline/Providing Neuroprotection.Handbook of experimental pharmacology · 2025Review
- Inhibition of BET proteins modulates amyloid-beta accumulation and cognitive performance in middle-aged mice prenatally exposed to maternal immune activation.Frontiers in molecular neuroscience · 2025Article
- RPTOR Is an Alzheimer's Disease Susceptibility Gene Associated with the Risk Factors Body Mass Index and Infectious Encephalitis.Journal of Alzheimer's disease reports · 2024Article
- The potential role of human islet amyloid polypeptide in type 2 diabetes mellitus and Alzheimer's diseases.Diabetology & metabolic syndrome · 2023Review
- Immortalized Alzheimer's Disease Astrocytes: Characterization of Their Proteolytic Systems.Molecular neurobiology · 2023Article
- mTOR Signaling Disruption and Its Association with the Development of Autism Spectrum Disorder.Molecules (Basel, Switzerland) · 2023Review
- Current Naturopathy to Combat Alzheimer's Disease.Current neuropharmacology · 2023Review
- Tetrandrine ameliorates cognitive deficits and mitigates tau aggregation in cell and animal models of tauopathies.Journal of biomedical science · 2022Article
- History in Perspective: The prime pathological players and role of phytochemicals in Alzheimer's disease.IBRO neuroscience reports · 2022Review
- Deciphering therapeutic options for neurodegenerative diseases: insights from SIRT1.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Autophagy Regulation Influences β-Amyloid Toxicity in TransgenicFrontiers in aging neuroscience · 2022Article
- Neuroprotection by dipeptidyl-peptidase-4 inhibitors and glucagon-like peptide-1 analogsWorld journal of biological chemistry · 2021Review
- New therapeutics beyond amyloid-β and tau for the treatment of Alzheimer's disease.Acta pharmacologica Sinica · 2021Review
- Lysosome Depletion-Triggered Autophagy Impairment in Progressive Kidney Injury.Kidney diseases (Basel, Switzerland) · 2021Review
- Mitochondrially-Targeted Therapeutic Strategies for Alzheimer's Disease.Current Alzheimer research · 2021Review
- The biological pathways of Alzheimer disease: a review.AIMS neuroscience · 2021Review
- Therapeutic Potential of Phytoconstituents in Management of Alzheimer's Disease.Evidence-based complementary and alternative medicine : eCAM · 2021Review
- Plaque-Associated Oligomeric Amyloid-Beta Drives Early Synaptotoxicity in APP/PS1 Mice Hippocampus: Ultrastructural Pathology Analysis.Frontiers in neuroscience · 2021Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Many neurodegenerative disorders are characterized by the aberrant accumulation of aggregate-prone proteins. Alzheimer's disease (AD) is associated with the buildup of β-amyloid peptides and tau, which aggregate into extracellular plaques and neurofibrillary tangles, respectively. Multiple studies have linked dysfunctional intracellular degradation mechanisms with AD pathogenesis. One such pathway is the autophagy-lysosomal system, which involves the delivery of large protein aggregates/inclusions and organelles to lysosomes through the formation, trafficking, and degradation of double-membrane structures known as autophagosomes. Converging data suggest that promoting autophagic degradation, either by inducing autophagosome formation or enhancing lysosomal digestion, provides viable therapeutic strategies. In this review, we discuss compounds that can augment autophagic clearance and may ameliorate disease-related pathology in cell and mouse models of AD. Canonical autophagy induction is associated with multiple signaling cascades; on the one hand, the best characterized is mammalian target of rapamycin (mTOR). Accordingly, multiple mTOR-dependent and mTOR-independent drugs that stimulate autophagy have been tested in preclinical models. On the other hand, there is a growing list of drugs that can enhance the later stages of autophagic flux by stabilizing microtubule-mediated trafficking, promoting lysosomal fusion, or bolstering lysosomal enzyme function. Although altering the different stages of autophagy provides many potential targets for AD therapeutic interventions, it is important to consider how autophagy drugs might also disturb the delicate balance between autophagosome formation and lysosomal degradation.
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