Tag

Neuroinflammation

All articles tagged with #neuroinflammation

Unabsorbed fructose may fuel anxiety via gut-brain inflammation
science1 month ago

Unabsorbed fructose may fuel anxiety via gut-brain inflammation

New multi-part research links unabsorbed dietary fructose to increased anxiety indicators and brain inflammation. In a healthy male cohort, breath tests showed about 60% had fructose malabsorption; those individuals had higher inflammatory proteins, more bacterial toxins in blood, and distinct gut bacteria, with anxiety scores elevated though not clinically diagnostic. In a mouse model lacking the intestinal fructose transporter, a 5% fructose diet induced anxiety- and depression-like behaviors and strong microglial inflammatory responses, alongside significant gut microbiome shifts. Limitations include male-only participants and observational human data; the findings suggest fructose malabsorption could trigger gut-driven immune signals that affect the brain, warranting trials on fructose-free diets or anti-inflammatory approaches to mood disorders.

Nitrosylation Switch in STING Drives Alzheimer’s Brain Inflammation, Study Finds
health-and-medicine1 month ago

Nitrosylation Switch in STING Drives Alzheimer’s Brain Inflammation, Study Finds

Researchers at Scripps Research identified a chemical change known as S-nitrosylation of the STING protein at cysteine 148 that pushes brain immune cells into chronic inflammation in Alzheimer’s disease. Blocking this modification in a mouse model reduced neuroinflammation and protected synapses, and the same pathway was observed in human Alzheimer’s brain tissue and stem-cell models, suggesting a targeted therapy that quiets harmful inflammation without suppressing normal immunity. The team plans preclinical testing of small molecules to block cysteine 148.

Ozempic May Rewire the Brain, Changing Mood, Motivation and Cravings
science1 month ago

Ozempic May Rewire the Brain, Changing Mood, Motivation and Cravings

New research suggests GLP-1 drugs like Ozempic—used for obesity and diabetes—may reshape brain networks and influence appetite, mood, cognition and addiction. Early brain scans in teens and young women on GLP-1s showed increased connectivity in the salience network within months, hinting at direct neural effects or indirect changes via gut-brain pathways. Scientists are exploring roles beyond weight loss, including potential impacts on anxiety, compulsive thinking and addiction, while noting that long-term, developmental effects (especially in adolescents) remain unclear. Although some trials hint at neuroprotective signals, a major Alzheimer’s trial with a related drug failed to slow cognitive decline, underscoring that conclusions about brain health from GLP-1s are still uncertain and ongoing.

Two-dose nasal spray reverses brain aging markers in animal models
science1 month ago

Two-dose nasal spray reverses brain aging markers in animal models

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 Targets Hidden Alzheimer's Inflammation Trigger with Brain-Penetrant Inhibitor
health-and-medicine1 month ago

USC Targets Hidden Alzheimer's Inflammation Trigger with Brain-Penetrant Inhibitor

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.

Two Drugs Spark Remyelination in MS Models, Hinting at Nerve Repair
health2 months ago

Two Drugs Spark Remyelination in MS Models, Hinting at Nerve Repair

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.

Nitrosyl Switch in STING Fuels Alzheimer’s Brain Inflammation
science2 months ago

Nitrosyl Switch in STING Fuels Alzheimer’s Brain Inflammation

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.

Blocking a STING Switch Could Slow Alzheimer’s Brain Inflammation
science2 months ago

Blocking a STING Switch Could Slow Alzheimer’s Brain Inflammation

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.

Grey-matter microglia coordinate repair after focal white-matter demyelination
science2 months ago

Grey-matter microglia coordinate repair after focal white-matter demyelination

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.

Intranasal spray resets aging brain and sharpens memory
science2 months ago

Intranasal spray resets aging brain and sharpens memory

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.

Two-Dose Nasal Spray Reverses Brain Aging in Weeks, Texas A&M Finds
science2 months ago

Two-Dose Nasal Spray Reverses Brain Aging in Weeks, Texas A&M Finds

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 Reverses Brain Aging in Preclinical Study
science3 months ago

Two-Dose Intranasal Spray Reverses Brain Aging in Preclinical Study

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.