Endocannabinoid Hydrolysis Generates Brain Prostaglandins That Promote Neuroinflammation
Open accessAbstract
A new tissue-specific pathway for the synthesis of proinflammatory prostaglandins is described.
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MAGL is the main enzyme in the brain responsible for the hydrolysis of >85% 2-AG into AA, a precursor of bioactive oxylipins.
“MAGL is the main enzyme in the brain responsible for the hydrolysis of >85% 2-AG into AA, a precursor of bioactive oxylipins63,75.”
From Foamy microglia link oxylipins to disease progression in multiple sclerosis (2026) · cites this paper as [63]
The indexed passage labeled Abstract (page unavailable) identifies MAGL as hydrolyzing brain 2-AG and reports that disrupting it raises 2-AG while lowering AA and downstream eicosanoids. This supports the pathway and MAGL’s major role, but our copy does not give the claimed >85% share of 2-AG hydrolysis. (LLM, conf=0.88)
Experimental — accuracy not yet measuredOxidized signaling lipids act as chemoattractants for adaptive immune cells, potentially driving T cell and B cell infiltration, enhancing TH17 cell and plasma cell differentiation, and increasing immunoglobulin production, collectively contributing to neuroinflammation and a sustained demyelinating milieu.
“These oxidized signaling lipids act as chemoattractants for adaptive immune cells, potentially driving T cell and B cell infiltration33, enhancing TH17 cell76 and plasma cell differentiation, and increasing immunoglobulin production, collectively contributing to neuroinflammation and a sustained demyelinating milieu63,77–81.”
From Foamy microglia link oxylipins to disease progression in multiple sclerosis (2026) · cites this paper as [63]
Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredMAGL catalyzes the conversion of 2-arachidonoylglycerol into arachidonic acid in the brain, which is a precursor for oxylipins.
“MAGL catalyzes the conversion of the endocannabinoid (eCB) 2-arachidonoylglycerol (2-AG) into arachidonic acid (AA) in the brain, which is a precursor for oxylipins33,63”
From Foamy microglia link oxylipins to disease progression in multiple sclerosis (2026) · cites this paper as [63]
MAGL is the primary hydrolytic enzyme for 2-AG and a rate-limiting enzyme in the production of free arachidonic acid in brain, liver, and lung, but not in the gastrointestinal tract or other organs.
“In addition to being the primary hydrolytic enzyme for 2-AG (Dinh et al, 2002), MAGL is a rate-limiting enzyme in the production of free arachidonic acid in brain, liver, and lung, but not in the gastrointestinal tract or other organs (Nomura et al, 2011).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Nomura et al, 2011
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- Authors
- Nomura, D. K., Morrison, B. E., Blankman, J. L., Long, J. Z., Kinsey, S. G., Marcondes, M. C. G., Ward, A. M., Hahn, Y. K., Lichtman, A. H., Conti, B., & Cravatt, B. F.
- Affiliations
- Scripps Research Institute (US)
- Molecular and Integrative Neurosciences Department, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
- West Virginia University (US)
- Virginia Commonwealth University (US)
- Corresponding author
- Nomura, Daniel K.
- Cravatt, Benjamin F.
- ORCID
- Venue
- Science
- Published
- 2011-11-11
- Volume
- 334
- Issue
- 6057
- Pages
- 809-813
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3249428
- OpenAlex
- W2029471635
- Cited by
- 727
- References
- 39
- Citations by year
- 2026: 29 · 2025: 42 · 2024: 33 · 2023: 51 · 2022: 45 · 2021: 60 · 2020: 43 · 2019: 40 · 2018: 59 · 2017: 46 · 2016: 50 · 2015: 67 · 2014: 63 · 2013: 50 · 2012: 43
- FWCI
- 38.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (AG028040, R01AG028040)
- National Institute on Drug Abuse (K99DA030908, P01DA009789, DA-017259, P01DA01725, R00DA030908, R03DA027936, F31DA026261, P01DA017259, DA026261, T32DA007027)
- Topics
- Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Keywords
- monoacylglycerol lipase, 2-arachidonoylglycerol, prostaglandins, neuroinflammation, arachidonic acid, cyclooxygenase, phospholipase A2, parkinsonism, neuroprotection, cyclooxygenase inhibitors, neurodegenerative diseases, brain
- MeSH terms
- Animals, Arachidonic Acids, Brain, Enzyme Inhibitors, Glycerides, Hydrolysis, Inflammation, Lipopolysaccharides, Liver, Lung, Mice, Inbred C57BL, Monoacylglycerol Lipases, Piperidines, Prostaglandins, Signal Transduction, Eicosanoids, Cytokines, Arachidonic Acid, Neuroprotective Agents, Inflammation Mediators, Parkinsonian Disorders, Mice, Cyclooxygenase 1, Benzodioxoles, Phospholipases A2, Metabolomics, Cannabinoid Receptor Modulators, Endocannabinoids
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