ArticleMolecular neurobiology2021
Inhibition of 2-Arachidonoylglycerol Metabolism Alleviates Neuropathology and Improves Cognitive Function in a Tau Mouse Model of Alzheimer's Disease.
Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 50 citations in OpenAlex.
- Radical Revelations: The Interplay of Nitrosative Stress, the Endocannabinoid System, and Treatment of Age-Related Disorders.International journal of molecular sciences · 2026Review
- Selective Inactivation of Astrocytic Monoacylglycerol Lipase for Alzheimer's Disease Therapy.bioRxiv : the preprint server for biology · 2025Article
- Psychoactive substances: novel molecular insights and therapeutic potential for Alzheimer's disease.Translational neurodegeneration · 2025Review
- Flavonoid carbamate hybrids: design, synthesis, and evaluation as multi-target enzyme inhibitors for Alzheimer's disease.RSC advances · 2025Article
- Augmentation of Endogenous 2-Arachidonoylglycerol Mitigates Autistic Behaviors of BTBR Mice.Molecular neurobiology · 2025Article
- Alterations of endocannabinoid signaling and microglia reactivity in the retinas of AD-like mice precede the onset of hippocampal β-amyloid plaques.Journal of neurochemistry · 2025Article
- Overabundant endocannabinoids in neurons are detrimental to cognitive function.bioRxiv : the preprint server for biology · 2024Article
- Interactions Between the Ubiquitin-Proteasome System, Nrf2, and the Cannabinoidome as Protective Strategies to Combat Neurodegeneration: Review on Experimental Evidence.Neurotoxicity research · 2024Review
- Inhibition of cannabinoid degradation enhances hippocampal contextual fear memory and exhibits anxiolytic effects.iScience · 2024Article
- Investigating the Effects of Exogenous and Endogenous 2-Arachidonoylglycerol on Retinal CB1 Cannabinoid Receptors and Reactive Microglia in Naive and Diseased Retina.International journal of molecular sciences · 2023Article
- Lamivudine (3TC), a Nucleoside Reverse Transcriptase Inhibitor, Prevents the Neuropathological Alterations Present in Mutant Tau Transgenic Mice.International journal of molecular sciences · 2023Article
- Endocannabinoid control of neuroinflammation in traumatic brain injury by monoacylglycerol lipase in astrocytes.Neural regeneration research · 2023Article
- Inhibiting degradation of 2-arachidonoylglycerol as a therapeutic strategy for neurodegenerative diseases.Pharmacology & therapeutics · 2023Review
- Augmentation of 2-arachidonoylglycerol signaling in astrocytes maintains synaptic functionality by regulation of miRNA-30b.Experimental neurology · 2023Article
- Inhibition of 2-arachidonoylglycerol degradation enhances glial immunity by single-cell transcriptomic analysis.Journal of neuroinflammation · 2023Article
- Review
- Article
- Endocannabinoid levels in peripheral blood mononuclear cells of multiple sclerosis patients treated with dimethyl fumarate.Scientific reports · 2022Article
- Endocannabinoid metabolism and Alzheimer's disease.Neural regeneration research · 2022Article
- TDP-43 drives synaptic and cognitive deterioration following traumatic brain injury.Acta neuropathologica · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most common cause of dementia, which affects more than 5 million individuals in the USA. Unfortunately, no effective therapies are currently available to prevent development of AD or to halt progression of the disease. It has been proposed that monoacylglycerol lipase (MAGL), the key enzyme degrading the endocannabinoid 2-arachidonoylglycerol (2-AG) in the brain, is a therapeutic target for AD based on the studies using the APP transgenic models of AD. While inhibition of 2-AG metabolism mitigates β-amyloid (Aβ) neuropathology, it is still not clear whether inactivation of MAGL alleviates tauopathies as accumulation and deposition of intracellular hyperphosphorylated tau protein are the neuropathological hallmark of AD. Here we show that JZL184, a potent MAGL inhibitor, significantly reduced proinflammatory cytokines, astrogliosis, phosphorylated GSK3β and tau, cleaved caspase-3, and phosphorylated NF-kB while it elevated PPARγ in P301S/PS19 mice, a tau mouse model of AD. Importantly, tau transgenic mice treated with JZL184 displayed improvements in spatial learning and memory retention. In addition, inactivation of MAGL ameliorates deteriorations in expression of synaptic proteins in P301S/PS19 mice. Our results provide further evidence that MAGL is a promising therapeutic target for AD.
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