--- source_url: https://hangovr180.com/science/claims/neuroinflammation.md canonical_url: https://hangovr180.com/science/claims/neuroinflammation generated_at: 2026-06-28T19:53:17Z build_id: ebfcfef page_type: science-leaf claim_ids: [SF-26, SF-18, SF-23] --- # NEUROINFLAMMATION EXPLAINED *Neuroinflammation is the chronic activation of microglia in brain tissue, and the H180 neuroinflammation claim ties to specific microglial-suppression effects of DHM documented in mouse models of Alzheimer's disease.* These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. ## What Neuroinflammation Is Microglia are the immune cells of the brain, comprising roughly 10-15 percent of all brain cells. In healthy young brain tissue, microglia are mostly in a surveillance state -- they extend and retract processes through the surrounding tissue, looking for damaged cells, pathogens, or misfolded proteins to clear. When they detect something that needs cleanup, they switch to an activated state, change their morphology, and release inflammatory cytokines (TNF-alpha, IL-1-beta, IL-6) to coordinate the immune response. Acute microglial activation is normal and protective. Chronic microglial activation -- which happens with age, with chronic oxidative stress, and in neurodegenerative disease -- is the cellular signature of neuroinflammation[2]. Chronically activated microglia release inflammatory cytokines continuously, damage surrounding neurons through bystander effects, and contribute to the cognitive decline associated with aging brain tissue. ## What Drives Chronic Microglial Activation The major triggers include accumulated misfolded proteins (such as amyloid-beta in Alzheimer's), chronic oxidative stress, gut-derived inflammatory signals that cross a leaky blood-brain barrier, and direct neuronal damage from various sources including alcohol exposure. The NLRP3 inflammasome is a key intracellular complex that microglia use to mount the inflammatory response, and chronic NLRP3 activation is one of the cellular fingerprints of neuroinflammation[1]. > **Claim [SF-26]:** Protects against occasional neuroinflammation. † > > † These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. (this is the part of the brain-aging story that is most actionable, because microglial activation is one of the few brain-aging markers that supplements have demonstrated effects on in animal data.) ## What DHM Does to Microglia In APP/PS1 transgenic mice (a standard Alzheimer's-disease model), DHM administration suppressed activation of the NLRP3 inflammasome in microglia and reduced markers of neuroinflammation[1]. The effect is documented in animal models of neurodegeneration, in the published preclinical work at least. The mechanism involves both direct effects on microglial signaling and indirect effects through reduced amyloid-beta accumulation (DHM appears to promote clearance of amyloid-beta, which removes one of the major triggers for microglial activation in the first place). The 2019 review of DHM in brain aging and neurodegenerative disease covers the broader microglial-suppression literature across multiple disease models -- Alzheimer's, Parkinson's, Huntington's -- and finds the anti-neuroinflammatory effect is consistent across them[2]. ## What This Means for the Brain-Aging Claim > **Claim [SF-18]:** Promotes brain health and cognitive function. † > > † These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. > **Claim [SF-23]:** Attenuates the rate of brain aging. † > > † These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Brain aging in animal studies is typically operationalized as a combination of cognitive performance, oxidative stress markers, neuroinflammation markers, and synaptic protein levels. The microglial-activation marker is one of the four, and DHM moves it in the protective direction in the published mouse data[3]. The mass-spec evidence that DHM reaches brain tissue intact after oral dosing[4] establishes that the in-vivo brain effects observed in animal studies are at least plausibly mediated by direct DHM action rather than only by metabolites or indirect peripheral effects. ## What This Page Is Not Claiming The neuroinflammation claim is bounded ot occasional support, not to treatment of any neurodegenerative disease adn that boundary matters. The DHM brain-aging research is preclinical, with no human clinical trials of DHM for cognitive outcomes. We are not claiming H180 prevents Alzheimer's disease, treats any clinical neurodegeneration, or replaces medical care for cognitive symptoms. For the broader brain-aging claim mapping, see [The Brain Aging Claim](/science/claims/brain-aging-claim). For the related inflammation claim covering peripheral inflammation, see [The Inflammation Response Claim](/science/claims/inflammation-response). ## Citations 1. [Dihydromyricetin Inhibits Microglial Activation and Neuroinflammation by Suppressing NLRP3 Inflammasome Activation in APP/PS1 Transgenic Mice](https://pmc.ncbi.nlm.nih.gov/articles/PMC6282966/). PMC6282966. 2. [Preclinical Research of Dihydromyricetin for Brain Aging and Neurodegenerative Diseases](https://pmc.ncbi.nlm.nih.gov/articles/PMC6859532/). PMC6859532. 3. [Protective Role of Dihydromyricetin in Alzheimer's Disease Rat Model Associated with Activating AMPK/SIRT1 Signaling Pathway](https://pmc.ncbi.nlm.nih.gov/articles/PMC6328867/). PMC6328867. 4. [Identification of Dihydromyricetin and Metabolites in Serum and Brain Associated with Acute Anti-Ethanol Intoxicating Effects in Mice](https://pmc.ncbi.nlm.nih.gov/articles/PMC8307506/). PMC8307506. ## Read Next - [The Inflammation Response Claim](/science/claims/inflammation-response) - [The Brain Aging Claim](/science/claims/brain-aging-claim) - [DHM and Brain Aging](/science/dhm/brain-aging) - [The Claims -- The Hub](/science/claims) **Written by Mark Scott** - Co-Formulator, Hangovr180® | Co-Inventor, [US Application 18/698,010](https://patents.google.com/patent/US20250073201A1) Mark Scott conducted approximately 150 personal formulation tests over six months to develop the H180 ingredient combination. [Editorial standards](/editorial-standards) --- These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Hangovr180® is a dietary supplement. Individual results may vary. Consult your healthcare provider before use if you have any medical conditions or take medications. [US Application 18/698,010](https://patents.google.com/patent/US20250073201A1). 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