ReviewNeuron2022
The different autophagy degradation pathways and neurodegeneration.
Open access · greenAbstract readReview
In one paragraph
Review in Neuron, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 262 papers, 1 of them a synthesis that pooled it.
0numbers the graph read from it
0cells of the map it votes in
262citing papers in PubMed, 1 pooled it
68.7field-weighted citation impact, top 1% of its field
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
262 citing papers in PubMed, 1 synthesis or guideline pooled it, 455 citations in OpenAlex.
- Meta-analysis fails to show any correlation between protein abundance and ubiquitination changes.FEBS open bio · 2026Pooled it
- Chaperone-mediated autophagy in physiological homeostasis, disease and ageing.Nature reviews. Molecular cell biology · 2026Review
- mTORC1 Activation Links Chronic Stress to Meso-Circuit Desynchronization and Accelerated Amyloid Pathology via Autophagic Dysfunction.CNS neuroscience & therapeutics · 2026Article
- Targeting Fgr-STAT3 Mediated Autophagy Inhibition in the Spinal Cord Alleviates Neuropathic Pain in Rats.Neuroscience bulletin · 2026Article
- Nanotechnology-Enabled Targeted Protein Degradation: Strategies, Opportunities, and Challenges.Small methods · 2026Review
- Engineered autophagy receptors administered with extracellular vesicles eliminate pathological Tau and TDP-43.Nature biomedical engineering · 2026Article
- Therapeutic Advances in Major NBIA Disorders: Current Strategies and Translational Challenges.Neurology international · 2026Review
- Retrograde axonal transport of autophagic vesicles and dynein-dynactin protein interaction are attenuated during aging in the rat optic nerve in vivo.Neural regeneration research · 2026Article
- The SQSTM1 L341V Variant Associated With Sporadic ALS Promotes the Accumulation of Enlarged Ubiquitin-Positive SQSTM1 Bodies.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- Article
- An ROS-responsive, RGC-targeted nanotherapeutic strategy with a TRPV4 antagonist restores autophagic flux and protects RGCs in a rat model of chronic ocular hypertension.Journal of nanobiotechnology · 2026Article
- The Dual Roles of Autophagy in Important Picornaviruses Infecting Livestock and Poultry.Veterinary sciences · 2026Review
- Non-coding RNAs in neurodegeneration: an axis-based, evidence-tiered mechanistic synthesis.Metabolism open · 2026Review
- Where and how do mammalian cells shape autophagosomes?The Journal of biological chemistry · 2026Review
- EGR2 affects mixed stroke repair through BNIP3L-mediated microglial mitophagy.IBRO neuroscience reports · 2026Article
- Regulated Cell Death in Fungi, the Role of Metacaspases and Assay Techniques.Methods and protocols · 2026Review
- Mitochondrial dynamics in depression: friend or foe?Metabolic brain disease · 2026Review
- Cell death pathways and targeting therapeutics in cancer therapy.Acta pharmacologica Sinica · 2026Review
- The emerging role and therapeutic targeting of autophagy-lysosome pathway in the pathogenesis of Parkinson's disease.Translational neurodegeneration · 2026Review
- Study on the improvement effect and mechanism of resveratrol on cognitive impairment in tau mutant adenovirus-induced alzheimer's disease model mice.Psychopharmacology · 2026Article
202 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 3 countries.
Angeleen FlemingDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK.
Mathieu BourdenxUniversité de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France.
Motoki FujimakiDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Cansu KarabiyikDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Gregory J KrauseDepartment of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY, USA; Institute for Aging Studies, Albert Einstein College of Medicine, Bronx, NY, USA.
Ana LopezDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK.
Adrián Martín-SeguraDepartment of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY, USA; Institute for Aging Studies, Albert Einstein College of Medicine, Bronx, NY, USA.
Claudia PuriDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Aurora ScrivoDepartment of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY, USA; Institute for Aging Studies, Albert Einstein College of Medicine, Bronx, NY, USA.
John SkidmoreThe ALBORADA Drug Discovery Institute, University of Cambridge, Island Research Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0AH, UK.
Sung Min SonDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Eleanna StamatakouDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Lidia WrobelDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Ye ZhuDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Ana Maria CuervoDepartment of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY, USA; Institute for Aging Studies, Albert Einstein College of Medicine, Bronx, NY, USA. Electronic address: ana-maria.cuervo@einsteinmed.org.
David C RubinszteinDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, University of Cambridge, Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK. Electronic address: dcr1000@cam.ac.uk.
University of Cambridge · GBAlbert Einstein College of Medicine · USCentre National de la Recherche Scientifique · FR
Funding
Uncovering Alzheimer's disease risk mechanisms through neuron-specific analysis of autophagy and endosomal-lysosomal functionP01AG017617 · NIA · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI NIXON, RALPH A. · 2000 to 2021
$40.0MRole of Autophagy in T Cell Function and Immunosenescence (Project 3)P01AG031782 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CUERVO, ANA MARIA · 2009 to 2024
$36.2MMEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6MTRAINING PROGRAM IN CELLULAR &MOLEC. BIOLOGY &GENETICST32GM007491 · NIGMS · YESHIVA UNIVERSITY · PI QUERY, CHARLES C · 1985 to 2021
$17.0MProject 3: Autophagy dysfunction and neuronal activity in FTDU54NS100717 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI KOSIK, KENNETH STEPHEN · 2016 to 2020
$10.8MDecreased Protein Degradation in AgingR37AG021904 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CUERVO, ANA MARIA · 2013 to 2022
$4.4MDECREASED PROTEIN DEGRADATION IN AGINGR01AG021904 · NIA · YESHIVA UNIVERSITY · PI CUERVO, ANA MARIA · 2003 to 2012
$3.7MUnderstanding Alzheimer's Disease in the Context of the Aging BrainRF1AG054108 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CUERVO, ANA MARIA · 2016 to 2016
$2.1MMedical Research Council UKDRI-2002NIA NIH HHS P01 AG017617NIA NIH HHS P01 AG031782NIA NIH HHS R01 AG021904NIA NIH HHS R37 AG021904NIA NIH HHS RF1 AG054108NIGMS NIH HHS T32 GM007288NIGMS NIH HHS T32 GM007491NINDS NIH HHS U54 NS100717
Abstract
The term autophagy encompasses different pathways that route cytoplasmic material to lysosomes for degradation and includes macroautophagy, chaperone-mediated autophagy, and microautophagy. Since these pathways are crucial for degradation of aggregate-prone proteins and dysfunctional organelles such as mitochondria, they help to maintain cellular homeostasis. As post-mitotic neurons cannot dilute unwanted protein and organelle accumulation by cell division, the nervous system is particularly dependent on autophagic pathways. This dependence may be a vulnerability as people age and these processes become less effective in the brain. Here, we will review how the different autophagic pathways may protect against neurodegeneration, giving examples of both polygenic and monogenic diseases. We have considered how autophagy may have roles in normal CNS functions and the relationships between these degradative pathways and different types of programmed cell death. Finally, we will provide an overview of recently described strategies for upregulating autophagic pathways for therapeutic purposes.
Indexed as
AutophagyLysosomesApoptosisBrainHumansNeurons
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.