ArticleAlzheimer's research & therapy2024
N, N-Dimethyltryptamine, a natural hallucinogen, ameliorates Alzheimer's disease by restoring neuronal Sigma-1 receptor-mediated endoplasmic reticulum-mitochondria crosstalk.
Article in Alzheimer's research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Mitochondrial quality control in neurodegenerative diseases: from molecular mechanisms to natural product therapies.Frontiers in physiology · 2025Pooled it
- A programmable spatiotemporal bioelectrical conduit promotes peripheral nerve regeneration by suppressing ferroptosis through modulation of ER-mitochondria coupling in Schwann cells.Bioactive materials · 2027Article
- Moving beyond 5-HTPsychopharmacology · 2026Article
- Toxicokinetics and analytical toxicology of four N, N-dimethyltryptamine derivatives studied in human in vitro systems and in vivo by means of zebrafish embryos.Archives of toxicology · 2026Article
- Single ayahuasca administration mitigates long-term behavioral and neurochemical effects of early-life stress in rats.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Mitochondria‑endoplasmic reticulum contact site nexus: Molecular integration, disease pathogenesis and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- N,N-Dimethyltryptamine (DMT) Acutely Exposed to Mouse Ventral Tegmental Area IJournal of neurochemistry · 2026Article
- Alzheimer's disease: disrupted communication between the endoplasmic reticulum and mitochondria.Journal of neurology · 2026Review
- Design, synthesis, and characterization of F-18 sigma-1 receptor radiotracers for Alzheimer disease.European journal of medicinal chemistry · 2026Article
- Pretreatment with the psychedelic DOI mitigates LPS-induced hippocampal inflammation and behavioral impairments in mice.BMC neuroscience · 2026Article
- The spatiotemporal dynamics of MAMs: mechanisms, pathologies, and therapeutic rewiring.Cellular & molecular biology letters · 2026Review
- Psychedelics in the Treatment of Neurologic and Psychiatric Disorders: Coincidence or a New Point of View.Molecular neurobiology · 2025Review
- Hypoxia, Psychedelics, and Terminal Lucidity: A Perspective on Neuroplasticity and Neuropsychiatric Disorders.ACS pharmacology & translational science · 2025Review
- Sigma-1 receptor activation by PRE-084 attenuates sepsis-associated encephalopathy by targeting microglial p38 MAPK-mediated neuroinflammation and neuronal endoplasmic reticulum stress.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Implications of Indolethylamine N-Methyltransferase (INMT) in Health and Disease: Biological Functions, Disease Associations, Inhibitors, and Analytical Approaches.Brain sciences · 2025Review
- Psychedelics and the Serotonin Hypothesis of Eating Disorders.Brain sciences · 2025Review
- The complex web of membrane contact sites in brain aging and neurodegeneration.Cellular and molecular life sciences : CMLS · 2025Review
- Choline-An Essential Nutrient with Health Benefits and a Signaling Molecule.International journal of molecular sciences · 2025Review
- Modulation of neuronal α1-adrenergic receptor reduces tauopathy and neuroinflammation by inhibiting the STING/NF-κB/NLRP3 signaling pathway in Alzheimer's disease mice.Journal of neuroinflammation · 2025Article
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Corrections and comments
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Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAberrant neuronal Sigma-1 receptor (Sig-1r)-mediated endoplasmic reticulum (ER)- mitochondria signaling plays a key role in the neuronal cytopathology of Alzheimer's disease (AD). The natural psychedelic N, N-dimethyltryptamine (DMT) is a Sig-1r agonist that may have the anti-AD potential through protecting neuronal ER-mitochondrial interplay.
methods3×TG-AD transgenic mice were administered with chronic DMT (2 mg/kg) for 3 weeks and then performed water maze test. The Aβ accumulation in the mice brain were determined. The Sig-1r level upon DMT treatment was tested. The effect of DMT on the ER-mitochondrial contacts site and multiple mitochondria-associated membrane (MAM)-associated proteins were examined. The effect of DMT on calcium transport between ER and mitochondria and the mitochondrial function were also evaluated.
resultschronic DMT (2 mg/kg) markedly alleviated cognitive impairment of 3×TG-AD mice. In parallel, it largely diminished Aβ accumulation in the hippocampus and prefrontal cortex. DMT restored the decreased Sig-1r levels of 3×TG-AD transgenic mice. The hallucinogen reinstated the expression of multiple MAM-associated proteins in the brain of 3×TG-AD mice. DMT also prevented physical contact and calcium dynamic between the two organelles in in vitro and in vivo pathological circumstances. DMT modulated oxidative phosphorylation (OXPHOS) and ATP synthase in the in vitro model of AD.
conclusionThe anti-AD effects of DMT are associated with its protection of neuronal ER-mitochondria crosstalk via the activation of Sig-1r. DMT has the potential to serve as a novel preventive and therapeutic agent against AD.
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