ArticleNPJ aging and mechanisms of disease2016
Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids.
Article in NPJ aging and mechanisms of disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.
- Analysis of genetically determined gene expression suggests role of inflammatory processes in exfoliation syndrome.BMC genomics · 2023Pooled it
- The Heart of the Alzheimer's: A Mindful View of Heart Disease.Frontiers in physiology · 2020Pooled it
- Novel Small-Molecule Analogues of IU1 Ameliorate Amyloid-β Mediated Toxicity in Alzheimer's Disease Cell and Worm Models.International journal of molecular sciences · 2026Article
- Delta-9-tetrahydrocannabinol delineates D-galactose and aluminium chloride-induced cognitive dysfunction and neurodegeneration in the hippocampus of the Wistar rat model.Journal of biosciences · 2026Article
- Translating Alzheimer's Disease Mechanisms into Therapeutic Opportunities.Biomolecules · 2025Review
- Ergolide Regulates Microglial Activation and Inflammatory-Mediated Dysfunction: A Role for the Cysteinyl Leukotriene Pathway.International journal of molecular sciences · 2025Article
- Recreational drugs repurposed for medicinal use-cannabis.CNS spectrums · 2025Review
- Ellagic acid improves the symptoms of early-onset Alzheimer's disease: Behavioral and physiological correlates.Heliyon · 2024Article
- Circadian and sleep phenotypes in a mouse model of Alzheimer's disease characterized by intracellular accumulation of amyloid β oligomers.Experimental animals · 2024Article
- Effects and mechanisms of APP and its cleavage product Aβ in the comorbidity of sarcopenia and Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Review
- Pleiotropic loci for cannabis use disorder severity in multi-ancestry high-risk populations.Molecular and cellular neurosciences · 2023Article
- Chronic pain in Alzheimer's disease: Endocannabinoid system.Experimental neurology · 2023Review
- Multi-Targeting Intranasal Nanoformulation as a Therapeutic for Alzheimer's Disease.Biomolecules · 2023Article
- Impact of the Cannabinoid System in Alzheimer's Disease.Current neuropharmacology · 2023Review
- β-carotene genetically-enriched lyophilized orange juice increases antioxidant capacity and reduces β-amyloid proteotoxicity and fat accumulation inFood chemistry. Molecular sciences · 2022Article
- Senegenin Rescues PC12 Cells with Oxidative Damage Through Inhibition of Ferroptosis.Molecular neurobiology · 2022Article
- Cannabinoid extract in microdoses ameliorates mnemonic and nonmnemonic Alzheimer's disease symptoms: a case report.Journal of medical case reports · 2022Article
- Role of Intracellular Amyloid β as Pathway Modulator, Biomarker, and Therapy Target.International journal of molecular sciences · 2022Review
- Chronic edible dosing of Δ9-tetrahydrocannabinol (THC) in nonhuman primates reduces systemic platelet activity and function.American journal of physiology. Cell physiology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The beta amyloid (Aβ) and other aggregating proteins in the brain increase with age and are frequently found within neurons. The mechanistic relationship between intracellular amyloid, aging and neurodegeneration is not, however, well understood. We use a proteotoxicity model based upon the inducible expression of Aβ in a human central nervous system nerve cell line to characterize a distinct form of nerve cell death caused by intracellular Aβ. It is shown that intracellular Aβ initiates a toxic inflammatory response leading to the cell's demise. Aβ induces the expression of multiple proinflammatory genes and an increase in both arachidonic acid and eicosanoids, including prostaglandins that are neuroprotective and leukotrienes that potentiate death. Cannabinoids such as tetrahydrocannabinol stimulate the removal of intraneuronal Aβ, block the inflammatory response, and are protective. Altogether these data show that there is a complex and likely autocatalytic inflammatory response within nerve cells caused by the accumulation of intracellular Aβ, and that this early form of proteotoxicity can be blocked by the activation of cannabinoid receptors.
Identifiers
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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 OpenQuestion graph.