ArticleFrontiers in neuroscience2018
Chronic Caffeine Treatment Protects Against α-Synucleinopathy by Reestablishing Autophagy Activity in the Mouse Striatum.
Article in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 84 citations in OpenAlex.
- Brain activity during a working memory task after daily caffeine intake and caffeine withdrawal: a randomized double-blind placebo-controlled trial.Scientific reports · 2023Trial
- Coffee and Parkinson's disease: associations by CYP1A2 genotype and sex in UK Biobank.NPJ Parkinson's disease · 2026Article
- Autophagy-Mitophagy Pathway-Linked Genetic Variants Associate with Systemic Inflammation and Interact with Dietary Factors in Asian and European Cohorts.International journal of molecular sciences · 2026Article
- The potential role of adenosinergic pathway and methylxanthines in Parkinson's disease: Blowing in the wind or not.Purinergic signalling · 2026Review
- Interactions Between Nutraceuticals and α-Synuclein Conformational States: Molecular Mechanisms and Neuroprotective Implications in Parkinson's Disease.International journal of molecular sciences · 2026Review
- Article
- Breaking the proteasome balance: α-synuclein and the ubiquitin-proteasome system.Frontiers in cell and developmental biology · 2026Review
- Caffeine mitigates ROS accumulation and attenuates motor neuron degeneration in the wobbler mouse model of amyotrophic lateral sclerosis.Cell communication and signaling : CCS · 2025Article
- Caffeine in Aging Brains: Cognitive Enhancement, Neurodegeneration, and Emerging Concerns About Addiction.International journal of environmental research and public health · 2025Review
- Investigating Plasma Metabolomics and Gut Microbiota Changes Associated With Parkinson Disease: A Focus on Caffeine Metabolism.Neurology · 2025Article
- A comprehensive review of natural compounds and their structure-activity relationship in Parkinson's disease: exploring potential mechanisms.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Selective protein degradation through chaperone‑mediated autophagy: Implications for cellular homeostasis and disease (Review).Molecular medicine reports · 2025Review
- A Review of the Protective Effects of Alkaloids against Alpha-synuclein Toxicity in Parkinson's Disease.Mini reviews in medicinal chemistry · 2025Review
- Caffeine and neonatal acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2024Review
- Targeting the adenosine AChinese journal of traumatology = Zhonghua chuang shang za zhi · 2024Review
- Review
- The potential of natural products to inhibit abnormal aggregation of α-Synuclein in the treatment of Parkinson's disease.Frontiers in pharmacology · 2024Review
- Chaperone-mediated autophagy in neurodegenerative diseases: mechanisms and therapy.Molecular and cellular biochemistry · 2023Review
- The Impact of Hormesis, Neuronal Stress Response, and Reproduction, upon Clinical Aging: A Narrative Review.Journal of clinical medicine · 2023Review
- Overview of Caffeine Effects on Human Health and Emerging Delivery Strategies.Pharmaceuticals (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite converging epidemiological evidence for the inverse relationship of regular caffeine consumption and risk of developing Parkinson's disease (PD) with animal studies demonstrating protective effect of caffeine in various neurotoxin models of PD, whether caffeine can protect against mutant α-synuclein (α-Syn) A53T-induced neurotoxicity in intact animals has not been examined. Here, we determined the effect of chronic caffeine treatment using the α-Syn fibril model of PD by intra-striatal injection of preformed A53T α-Syn fibrils. We demonstrated that chronic caffeine treatment blunted a cascade of pathological events leading to α-synucleinopathy, including pSer129α-Syn-rich aggregates, apoptotic neuronal cell death, microglia, and astroglia reactivation. Importantly, chronic caffeine treatment did not affect autophagy processes in the normal striatum, but selectively reversed α-Syn-induced defects in macroautophagy (by enhancing microtubule-associated protein 1 light chain 3, and reducing the receptor protein sequestosome 1, SQSTM1/p62) and chaperone-mediated autophagy (CMA, by enhancing LAMP2A). These findings support that caffeine-a strongly protective environment factor as suggested by epidemiological evidence-may represent a novel pharmacological therapy for PD by targeting autophagy pathway.
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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.