ArticleScience advances2022
Mutant glucocerebrosidase impairs α-synuclein degradation by blockade of chaperone-mediated autophagy.
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Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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98citing papers in PubMed
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Who cites it
98 citing papers in PubMed.
- Chaperone-mediated autophagy in physiological homeostasis, disease and ageing.Nature reviews. Molecular cell biology · 2026Review
- Interplay of GBA1 with lysosomal dysfunction and inflammation in Parkinson's disease.Neural regeneration research · 2026Article
- Article
- Roles of autophagy in brain homeostasis and disease.Nature neuroscience · 2026Review
- Lipid Metabolism Reprogramming in the Aging Brain: Glial-Mediated Pathogenic Mechanisms and Translational Strategies in Neurodegeneration.International journal of molecular sciences · 2026Review
- Time vortex: the circadian-dopaminergic dialogue in Parkinson's disease.NPJ Parkinson's disease · 2026Review
- Lysine acetyltransferase 8-mediated histone acetylation, regulated by GBA1, is associated with lysosomal function related to α-Synuclein pathology.Cell death & disease · 2026Article
- The emerging role and therapeutic targeting of autophagy-lysosome pathway in the pathogenesis of Parkinson's disease.Translational neurodegeneration · 2026Review
- Parkin regulates NLRP3 degradation through chaperone-mediated autophagy to suppress PANoptosis and protect dopaminergic neurons in Parkinson's disease.Journal of neuroinflammation · 2026Article
- WDR44 drives de novo α-synuclein aggregation at the lysosomal membrane and promotes neuronal dysfunction in Parkinson's Disease.bioRxiv : the preprint server for biology · 2026Article
- GBA1 F213I mutation increases the expression of LCN2 promoting neurodegeneration.Cell death and differentiation · 2026Article
- The dual impact of GBA1 in disease: from germline mutations in neurological disorders to alterations in cancer.Cell death discovery · 2026Review
- Polymeric nanoparticle-mediated GBA1 gene therapy is neuroprotective in a preclinical model of Parkinson's disease.Drug delivery and translational research · 2026Article
- α-Synuclein expression is required for somatodendritic dopamine release and immediate early gene induction.Science advances · 2026Article
- Multi-omics insights into GBA1-associated Parkinson's disease: interplay of genomics, transcriptomics, proteomics, and lipidomics.Molecular neurodegeneration · 2026Review
- Unraveling the intersection of aging and Parkinson's disease: a collaborative roadmap for advancing research models.NPJ Parkinson's disease · 2026Review
- Oxidative Stress and Lysosomal Dysfunction in Neurodegenerative Diseases: Underlying Mechanisms and Nanotherapeutic Targeting Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Research progress on the α-synuclein-lysosome axis in Parkinson's disease: molecular mechanisms of protein aggregation, autophagy dysfunction, and therapeutic targeting.Frontiers in neuroscience · 2026Review
- Inhibition or genetic reduction of ASAH1/acid ceramidase restore α-synuclein clearance in mutant GBA1 dopamine neurons from Parkinson's patients.Human molecular genetics · 2025Article
- Parkinson's Disease: The Epidemiology, Risk Factors, Molecular Pathogenesis, Prevention, and Therapy.MedComm · 2025Review
38 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors.
Sheng-Han KuoDepartment of Neurology, Columbia University , New York, NY 10032, USA.ORCID 0000-0002-9412-931X
Inmaculada TassetDepartment of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.ORCID 0000-0003-0730-6750
Melody M ChengDepartment of Neurology, Columbia University , New York, NY 10032, USA.
Antonio DiazDepartment of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.ORCID 0000-0001-7871-0828
Ming-Kai PanDepartment of Neurology, Columbia University , New York, NY 10032, USA.ORCID 0000-0001-5535-2714
Ori J LiebermanDepartment of Neurology, Columbia University , New York, NY 10032, USA.ORCID 0000-0002-0467-0875
Samantha J HuttenDepartment of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.ORCID 0000-0002-8435-744X
Roy N AlcalayDepartment of Neurology, Columbia University , New York, NY 10032, USA.ORCID 0000-0002-5717-4875
Sangjun KimDepartment of Neurology, Johns Hopkins University, Baltimore, MD 21205, USA.ORCID 0000-0003-3052-3163
Pilar Ximénez-EmbúnProteomics Unit, Spanish National Cancer Research Centre (CNIO), ProteoRed-ISCIII, Madrid, Spain.ORCID 0000-0002-2582-9443
Li FanHelen and Robert Appel Alzheimer's Disease Research Institute, Weill Cornell Medicine, New York, NY 10065, USA.ORCID 0000-0003-1780-6919
Donghoon KimDepartment of Neurology, Johns Hopkins University, Baltimore, MD 21205, USA.
Han Seok KoDepartment of Neurology, Johns Hopkins University, Baltimore, MD 21205, USA.ORCID 0000-0002-0864-5239
Talene YacoubianDepartment of Neurology, University of Alabama at Birmingham, Birmingham, AL 35233, USA.ORCID 0000-0003-2227-7310
Ellen KanterDepartments of Psychiatry and Pharmacology, Columbia University , New York, NY 10032, USA.
Ling LiuDepartment of Neurology, Columbia University , New York, NY 10032, USA.
Guomei TangDepartment of Neurology, Columbia University , New York, NY 10032, USA.
Javier MuñozProteomics Unit, Spanish National Cancer Research Centre (CNIO), ProteoRed-ISCIII, Madrid, Spain.ORCID 0000-0003-3288-3496
Sergio Pablo SardiSanofi Genzyme, Boston, MA 02134, USA.
Aiqun LiDepartment of Neurology, Johns Hopkins University, Baltimore, MD 21205, USA.ORCID 0000-0003-1485-5352
Li GanHelen and Robert Appel Alzheimer's Disease Research Institute, Weill Cornell Medicine, New York, NY 10065, USA.ORCID 0000-0003-4600-275X
Ana Maria CuervoDepartment of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.ORCID 0000-0002-0771-700X
David SulzerDepartment of Neurology, Columbia University , New York, NY 10032, USA.
Funding
Role of Autophagy in T Cell Function and Immunosenescence (Project 3)P01AG031782 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI SINGH, RAJAT · 2009 to 2024
$36.2MMEDICAL SCIENTIST TRAINING PROGRAMT32GM007367 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI REINER, STEVEN L · 1985 to 2021
$25.1MEinstein's Nathan Shock Center of Excellence in Basic Biology of AgingP30AG038072 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI HUFFMAN, DEREK MAJOR · 2010 to 2024
$10.8MThe Dopamine Synapse and Associative LearningR01DA007418 · NIDA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI David Sulzer · 1999 to 2026
$9.4MAutoimmune Features of Neurodegenerative DisordersR01NS095435 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SETTE, ALESSANDRO, SULZER, DAVID · 2018 to 2022
$4.2MTargeting Cerebellar Endoplasmic Reticulum Calcium Handling in Essential TremorR01NS124854 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PHYLLIS L FAUST, Sheng-Han Kuo · 2022 to 2026
$2.9MTargeting Cerebellar Excitatory Synapses for Tremor ProgressionR01NS118179 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KUO, SHENG-HAN · 2020 to 2024
$2.2MCerebellar Circuitry in the Pathophysiology of TremorR01NS104423 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KUO, SHENG-HAN · 2018 to 2022
$2.0MCellular and Molecular Basis for Cognitive Impairment Associated with Glucocerebrosidase (GBA1) MutationR01NS104390 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TANG, GUOMEI · 2018 to 2022
$1.8MThe role of glucocerebrosidase and chaperone_mediated autophagy in Parkinsons disK08NS083738 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KUO, SHENG-HAN · 2013 to 2017
$940kMitochondrial dysfunction due to aberrant mTOR-regulated mitophagy in autismK01MH096956 · NIMH · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TANG, GUOMEI · 2013 to 2016
$734kNIA NIH HHS P01 AG031782NIA NIH HHS P30 AG038072NIDA NIH HHS R01 DA007418NIGMS NIH HHS T32 GM007367NIMH NIH HHS K01 MH096956NINDS NIH HHS K08 NS083738NINDS NIH HHS R01 NS095435NINDS NIH HHS R01 NS104390NINDS NIH HHS R01 NS104423NINDS NIH HHS R01 NS118179NINDS NIH HHS R01 NS124854
Abstract
The most common genetic risk factors for Parkinson's disease (PD) are a set of heterozygous mutant (MT) alleles of the
Indexed as
Chaperone-Mediated AutophagyParkinson Diseasealpha-SynucleinAnimalsGlucosylceramidaseHumansMiceMutationalpha-SynucleinGlucosylceramidase
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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.