All articles tagged with #neuroinflammation
Texas A&M researchers report that a two-dose intranasal spray delivering extracellular vesicles loaded with microRNAs reduced brain inflammation, restored mitochondrial function, and improved memory in animal models—hinting at a potential, noninvasive therapy for age-related cognitive decline and dementia, though human trials are not yet underway and findings are preclinical.
USC researchers identified selective inhibitors of the brain inflammation enzyme cPLA2 that may lower Alzheimer’s risk, especially for APOE4 carriers; the compounds cross the blood-brain barrier, showed activity in brain cells and mouse models, and represent a promising but early-stage drug discovery path with safety and feasibility in humans to be determined.
Finnish researchers identified two drug molecules that promote remyelination in MS models, suggesting a potential path to repairing nerve damage rather than only reducing inflammation. One drug targets the unfolded protein response in brain cells, while the other alters scar tissue around damaged areas. Both produced strong remyelination and lower neuroinflammation in animal and cell models, but human trials and brain-delivery challenges remain before clinical use.
A Nature News & Views piece summarizes Lee et al.'s finding that loss of male sex hormones triggers neuroinflammation and disrupts hormonal and immune signaling via the HPA axis, potentially accelerating brain tumor growth, contrasting with androgen-blockade benefits seen in many other cancers.
A Kindai University study shows that the inexpensive amino acid arginine can reduce amyloid-β buildup and brain inflammation in Alzheimer’s models (flies and mice), improving behavior; given its safety and low cost, arginine could be a rapid candidate for repurposing, but human trials and optimal dosing are still needed.
Researchers identify S-nitrosylation of the immune protein STING at cysteine 148 as a driver of brain inflammation in Alzheimer's; blocking this switch in mice reduced inflammation and protected synapses, with the same pathway active in human Alzheimer’s samples and stem-cell models, suggesting a new therapeutic target that dampens harmful inflammation without shutting down normal immunity.
Researchers pinpoint S-nitrosylation of the STING protein at cysteine 148 as a driver of chronic brain inflammation and synapse loss in Alzheimer’s. In mouse models, preventing this modification reduced inflammation and protected synapses, a result mirrored in human Alzheimer’s tissue and stem-cell models. The findings suggest a targeted therapy that dampens harmful inflammation without suppressing overall immunity, with small molecules designed to block the cysteine-148 site in development.
A targeted white‑matter lesion in a defined neural circuit triggers a transient grey‑matter microglial response, synapse loss, and reduced neuronal activity upstream of the lesion; these changes resolve as remyelination proceeds. Blocking microglia impairs remyelination, while aging diminishes this regenerative grey‑matter response, leading to chronic inflammation. The study reveals a circuit‑level regenerative plasticity that couples white‑matter integrity to grey‑matter function and suggests myelin‑regenerative therapies could mitigate chronic neuroinflammation in MS and related diseases.
Texas A&M researchers report that a two-dose intranasal spray delivering extracellular vesicles with microRNAs reduced brain inflammation, recharged neuronal mitochondria, and noticeably improved memory in preclinical aging models, suggesting a noninvasive therapy for brain aging and dementia that bypasses the blood-brain barrier; the team has filed a US patent with backing from the National Institute on Aging.
A two-dose intranasal spray of extracellular vesicles from human stem cells reduced brain inflammation and restored memory in aged mice, suggesting a noninvasive approach to age-related cognitive decline, though human trials are needed to assess applicability to dementia.
Texas A&M researchers report a two-dose nasal spray that uses microRNA-loaded extracellular vesicles to bypass the blood-brain barrier, reduce neuroinflammation, and restore cognitive function in aging animal models within weeks — with effects lasting months and observed in both sexes. Human trials are years away; the team has filed a patent and has backing from the National Institute on Aging, though safety details remain undisclosed.
Two-dose intranasal spray delivering extracellular vesicle microRNA cargo reduced brain inflammation, recharged mitochondrial function, and significantly improved memory in aging brain models within weeks—effects lasting months—which could reshape neurodegenerative therapies and offer a noninvasive alternative to invasive procedures or long-term meds, with a U.S. patent filed.
New research shows harmful sugars produced by gut bacteria trigger immune responses that damage brain cells in ALS and frontotemporal dementia; elevated levels were found in a majority of patients studied, and experiments reducing these sugars improved brain health and lifespan, pointing to gut-targeted therapies and biomarkers to slow disease progression—especially in carriers of the C9orf72 mutation.
A new study suggests brain immune cells (microglia) can actively initiate amyloid plaques by reshaping amyloid-beta into fibers and promoting tau tangles, challenging the view that microglia only clear plaques and implying that early inflammatory responses may set the stage for Alzheimer’s progression; this could influence timing and targets of future therapies.
Preclinical study in a mouse model of Alzheimer's found inhaled cannabidiol (CBD) reduced key inflammatory pathways (IDO and cGAS), lowered proinflammatory cytokines, and improved recognition memory, suggesting CBD may exert a multitarget anti-inflammatory effect that could complement other approaches. However, results are early and in animals, and human studies are needed to assess safety and efficacy.