All articles tagged with #tau
Among 69 women aged 65+ with high genetic risk for Alzheimer’s, poorer sleep quality correlated with worse visual memory and greater tau buildup in brain regions tied to the disease, strongest in the highest-risk group. The finding is observational, not causal, and researchers will collect more data to see if improving sleep could mitigate risk.
Biogen reported that the Phase 2 CELIA trial of diranersen achieved robust reductions in CSF tau and tau pathology and showed slowing of cognitive decline across doses—most notably at 60 mg every 24 weeks—despite not meeting the primary dose-response endpoint (CDR-SB at Week 76). Safety was generally consistent with prior data, with more serious adverse events at the highest dose. Biogen plans to advance diranersen to registrational development and will present further data at AAIC 2026.
A study, largely in mice, suggests long-term EPA from fish oil can destabilize brain blood vessel walls and block repair signals after repeated mild head injuries, while promoting tau buildup. Researchers caution that the findings may not directly translate to humans and that fish oil’s effects are context-dependent, underscoring the need for more research on its risks and benefits especially for those at risk of brain trauma.
A Mayo Clinic study of 2,082 participants found two broad windows where dementia-related changes begin long before diagnosis: cognition and amyloid changes start in the 50s–60s, followed by tau changes and blood biomarkers (GFAP, NfL, p-tau) in the late 60s to early 70s, along with brain atrophy. This could enable earlier detection and screening approaches, even though no single test currently exists.
Alzheimer's blood tests that detect amyloid or tau are being considered for early risk assessment, but doctors say their predictive value for asymptomatic people is uncertain, with potential false positives/negatives and no clear benefit from early intervention; FDA has cleared two tests for symptomatic patients, not for screening; patient interest is high, with surveys showing many would take a test if advised, though distress is common.
A systematic review of 30 preclinical studies finds GLP-1 receptor agonists (liraglutide, semaglutide, exenatide, dulaglutide) consistently reduce Alzheimer's hallmarks amyloid-beta plaques and tau tangles in animal and cell models, with liraglutide showing the strongest and most consistent effects; human data are limited and mixed so far, though some trials show preserved brain glucose metabolism and inflammatory marker changes, suggesting these drugs may help prevent dementia if used earlier rather than cure established disease.
Researchers report a 40-gene pattern that distinguishes normal aging, symptomatic Alzheimer's, and a resilient state, and identify Chromogranin A (CgA) as a stress-related protein that links cellular stress to Tau tangles. In mice, removing CgA reduced Tau buildup and preserved memory, especially in females, suggesting resilience pathways can sustain cognition despite brain damage. While promising, these findings are in animals and must be validated in humans, with resilience markers potentially guiding early prevention.
A Baylor College of Medicine study suggests increasing cellular tubulin can steer Tau and alpha-synuclein away from harmful aggregates toward healthy microtubule activity, offering a potential therapeutic strategy for Alzheimer’s and Parkinson’s by boosting tubulin rather than blocking condensate formation.
UC Riverside researchers propose that Alzheimer’s disease may arise from a competition inside neurons where amyloid beta and tau vie for the same microtubule binding sites, disrupting intracellular transport; this could mean plaques are a downstream effect rather than the root cause and shift therapy toward preventing this intracellular interference or boosting protein clearance.
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.
A new study suggests Alzheimer's may start when amyloid beta competes with tau for binding to microtubules in neurons, displacing tau and destabilizing the cell’s transport system. This microtubule nexus could unify amyloid- and tau-centered theories and open pathways for therapies that target tau displacement from microtubules.
A large USC-led study from the HABS-HD cohort finds early Alzheimer’s biomarkers differ by race/ethnicity: Black and Hispanic participants showed higher tau in memory-related brain regions even when amyloid levels were similar to White participants, and the amyloid–cognition link varied by group. Scanner limitations and social determinants of health may also influence readings, underscoring the need for population-tailored diagnostics and more inclusive research.
A Mayo Clinic study finds misfolded alpha-synuclein linked to tau buildup that progresses up to 20 times faster in women with Alzheimer's brain changes, suggesting a sex-specific mechanism behind women's higher Alzheimer's risk and guiding targeted trials and diagnostics.
A Mayo Clinic study finds that women with coexisting alpha-synuclein (Parkinson’s) and tau (Alzheimer’s) abnormalities experience tau accumulation and brain degeneration up to 20 times faster than those without the co-pathology, a sex-specific effect not seen in men, suggesting the need for gender-tailored screening and treatments.
A CRISPR-based screen in human neurons with disease-causing tau mutations identified the CRL5SOCS4 protein complex as a key driver of tau protein degradation, helping some brain cells resist toxic tau clumps and dementia. Findings align with brain atlas data showing higher CRL5SOCS4 expression correlates with cell survival, and researchers note mitochondrial dysfunction can increase pathogenic tau fragments. Potential therapies include boosting CRL5SOCS4 activity or protecting proteasomes to enhance tau clearance.