All articles tagged with #tau
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.
An international study shows boosting NAD+ levels can protect and reverse Alzheimer's-related brain damage by activating an EVA1C-regulated RNA-splicing pathway, correcting mis-splicing, improving hundreds of genes tied to brain health, and restoring memory in worm and mouse models with supporting human brain data—hinting at a new therapeutic approach beyond targeting plaques or tangles.
At UFC 325 weigh-ins, Alexander Volkanovski (144.5 lb) and Diego Lopes (145 lb) made the featherweight limit for their title rematch, with Dan Hooker vs. Benoit Saint Denis also hitting the non-title limit (155.75). Aaron Tau missed weight in a late, box-referenced weigh-in, initially showing 122.5 before re-weighing at 129, which led to the cancellation of his Road to UFC Flyweight Final against Namsrai Batbayar. The rest of the card remained on schedule.
Researchers show the enzyme OTULIN acts as a master regulator of tau production in neurons: blocking OTULIN reduced tau levels and removing its gene even halted tau synthesis, while RNA analysis revealed widespread changes in gene activity, notably in inflammatory pathways; the findings open a potential new route to slow brain aging and Alzheimer's, but safety concerns remain since OTULIN and tau have essential functions and much more research is needed.
A study identifies OTULIN as a high-level regulator in neurons that controls gene expression and RNA metabolism, shaping tau biology in brain aging and Alzheimer's disease. Partial inhibition of OTULIN reduced pathogenic tau, while CRISPR deletion nearly abolished tau by silencing MAPT mRNA, but also caused widespread transcriptome changes. The work suggests therapies could recalibrate neuronal regulatory networks to counter aging and neurodegeneration, though complete loss of OTULIN would be harmful and requires precise tuning.
Researchers at the University of New Mexico found that OTULIN, an enzyme known for immune regulation, also controls tau production in neurons. By inhibiting OTULIN with a small molecule or knocking out the OTULIN gene, they stopped new tau formation and cleared existing tau in human neuron models, suggesting a novel target for treating Alzheimer’s disease and related tauopathies. The findings also linked OTULIN to RNA metabolism and inflammatory pathways, and researchers note the need to study effects across different brain cell types before pursuing therapies.
Warframe will receive a new narrative chapter 'The Old Peace' in 2025, exploring Tau's past and the war between the Orokin and Dax Anarch Warriors, followed by the Tau-focused chapter in 2026. The update will include new storylines, character models, a new ultimate ability, and other improvements, with additional updates and a closed beta arriving later this year.
Warframe announced its upcoming year of updates including a major quest called The Old Peace, a cinematic tutorial on Mods, new characters, enemy factions, graphical remasters, collaborations, and a planned narrative chapter Tau for 2026, with various seasonal and special content releases throughout 2023 and 2024.
Certain microbes in the gut microbiome are more common in those with very early signs of Alzheimer's disease, pointing to a potential new method of diagnosis for a disease that affects millions worldwide. The researchers found distinct differences in the gut microbiome profiles of older people with and without signs of preclinical Alzheimer's. Analyzing a person's gut microbiome to assess their risk of developing the disease would offer a non-invasive, more accessible way of identifying those at risk of developing Alzheimer's at an earlier stage, allowing them more time to plan and prepare for the future.
Researchers have identified several blood biomarkers that can aid in the diagnosis and monitoring of Alzheimer's disease, including CSF biomarkers such as Aβ42/Aβ40 and p-tau217, as well as plasma biomarkers such as β-amyloid 42/40 and phospho-tau217. These biomarkers have been shown to correlate with amyloid and tau pathology in the brain, and can be used in clinical practice and trials to track disease progression and response to treatment.