ArticleJournal of Alzheimer's disease : JAD2015
Caffeine, Through Adenosine A3 Receptor-Mediated Actions, Suppresses Amyloid-β Protein Precursor Internalization and Amyloid-β Generation.
Article in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- A3 Adenosine Receptor Agonists as Multisystem Disease Modifiers: From Molecular Signaling to Clinical Translation.Biomolecules · 2026Review
- Review
- Psychoactive substances: novel molecular insights and therapeutic potential for Alzheimer's disease.Translational neurodegeneration · 2025Review
- An Expanded Narrative Review of Neurotransmitters on Alzheimer's Disease: The Role of Therapeutic Interventions on Neurotransmission.Molecular neurobiology · 2025Review
- Caffeine: A Multifunctional Efficacious Molecule with Diverse Health Implications and Emerging Delivery Systems.International journal of molecular sciences · 2024Review
- Evaluating the Neuroprotective Potential of Caffeinated Coffee in the Context of Aluminum-Induced Neurotoxicity: Insights from a PC12 Cell Culture Model.Antioxidants (Basel, Switzerland) · 2024Article
- Association of Caffeine Consumption and Brain Amyloid Positivity in Cognitively Normal Older Adults.Journal of Alzheimer's disease : JAD · 2023Article
- Gene Expression Profiling of Peripheral Blood Mononuclear Cells in Type 2 Diabetes: An Exploratory Study.Medicina (Kaunas, Lithuania) · 2022Article
- Neuroprotective Effect of Caffeine in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2022Review
- Review
- Two-pore channels regulate Tat endolysosome escape and Tat-mediated HIV-1 LTR transactivation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Article
- Coffee intake and decreased amyloid pathology in human brain.Translational psychiatry · 2019Article
- Methylxanthines: Potential Therapeutic Agents for Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2019Article
- Research progress on adenosine in central nervous system diseases.CNS neuroscience & therapeutics · 2019Review
- Combined Effect Of Coffee Consumption And Cigarette Smoking On Serum Levels Of Vitamin B12, Folic Acid, And Lipid Profile In Young Male: A Cross-Sectional Study.International journal of general medicine · 2019Article
- Apolipoprotein E isoform dependently affects Tat-mediated HIV-1 LTR transactivation.Journal of neuroinflammation · 2018Article
- The Adenosinergic Signaling: A Complex but Promising Therapeutic Target for Alzheimer's Disease.Frontiers in neuroscience · 2018Review
- Effect of Paullinia cupana Mart. Commercial Extract During the Aging of Middle Age Wistar Rats: Differential Effects on the Hippocampus and Striatum.Neurochemical research · 2017Article
- Caffeine Blocks HIV-1 Tat-Induced Amyloid Beta Production and Tau Phosphorylation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Intraneuronal accumulation and extracellular deposition of amyloid-β (Aβ) protein continues to be implicated in the pathogenesis of Alzheimer's disease (AD), be it familial in origin or sporadic in nature. Aβ is generated intracellularly following endocytosis of amyloid-β protein precursor (AβPP), and, consequently, factors that suppress AβPP internalization may decrease amyloidogenic processing of AβPP. Here we tested the hypothesis that caffeine decreases Aβ generation by suppressing AβPP internalization in primary cultured neurons. Caffeine concentration-dependently blocked low-density lipoprotein (LDL) cholesterol internalization and a specific adenosine A3 receptor (A3R) antagonist as well as siRNA knockdown of A3Rs mimicked the effects of caffeine on neuronal internalization of LDL cholesterol. Further implicating A3Rs were findings that a specific A3R agonist increased neuronal internalization of LDL cholesterol. In addition, caffeine as well as siRNA knockdown of A3Rs blocked the ability of LDL cholesterol to increase Aβ levels. Furthermore, caffeine blocked LDL cholesterol-induced decreases in AβPP protein levels in neuronal plasma membranes, increased surface expression of AβPP on neurons, and the A3R antagonist as well as siRNA knockdown of A3Rs mimicked the effects of caffeine on AβPP surface expression. Moreover, the A3R agonist decreased neuronal surface expression of AβPP. Our findings suggest that caffeine exerts protective effects against amyloidogenic processing of AβPP at least in part by suppressing A3R-mediated internalization of AβPP.
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Registered trials
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 Socratic graph.