Tau2020: Meeting for Tauopathies Debuts Genetic Variants Behold the First Human α-Synuclein CryoEM Fibril Structure New at Tau2020: PET Detects First Traces of Tangles in Rhinal Cortex Primary Tauopathies Get New PET Ligands Tau Receptor Identified on ...
New Assay, New Cohorts—Plasma p-Tau181 Looks Even Better 217—The Best Phospho-Tau Marker for Alzheimer’s? In DIAN-TU, Gantenerumab Brings Down Tau. By a Lot. Open Extension Planned Confused About the DIAN-TU Trial Data? Experts Discuss Active Tau Vaccine: ...
Plasma p-Tau217 Set to Transform Alzheimer’s Diagnostics Could Common Vaccines Protect Against Alzheimer’s Disease? Doubling Down on Sequencing Serves up More Alzheimer’s Genes IDEAS Finds Small Drop in Hospitalizations, Missing Goal Lancet Commission’s ...
BANish Aβ? BAN2401 Antibody Makes Its Move in Phase 3 Program BAN2401 Forges AHEAD into Phase 3, Preclinical AD TRC-PAD Funnel Finally Touches Down Learning Troubles Spied by Smartphone Track with Biomarkers In Phase 2 Trial, Neflamapimod Aids Cognition ...
Amyloid and tau PET are helping scientists pinpoint the underlying cause of specific AD symptoms. Perhaps imaging of certain brain regions will help predict an individual’s progression.
At HAI 2020, scientists more precisely quantified the relationship between plaques, tangles, and cognitive decline.
By engaging scientists studying every tau-based disorder, a new conference aimed to foster collaborations and research directions.
Centenarians who scored high on the MMSE stayed cognitively and physically active over the next two years, even if they carried genetic risk factors for Alzheimer’s. What protects these lucky few?
Two epigenetic proteins accelerated age-related behavioral decline in worms and in mice, at least partly by dampening mitochondrial function. Orthologs in the human brain ramped up with aging and with AD progression.
The monoclonal antibody activated TREM2 signaling on mouse microglia. It supported their survival and stimulated their clearance of amyloid plaques.
In the human brain, alpha waves fell out of sync, while delta-theta waves swelled in concert with amyloid plaques, neurofibrillary tangles. Alpha modulation correlated with cognitive decline.
Under diabetic conditions, SERP1 binds secretase subunit, cranking up cleavage of APP but not Notch. The finding offers a mechanistic link between diabetes and Alzheimer’s.
Not sure where that is? You are not alone. It is a tiny spot deep behind the nose, newly defined by the PET signal of early neurofibrillary tangle deposition. It also prompted a tau-staging scheme.
In motor neurons of TMEM106b knockout mice, swollen vacuoles piled up in axons near the soma, rendering the mice wobbly and slow to react. The finding contradicts prior reports.
Different forms of p-tau in cerebrospinal fluid reflect worsening plaque load, metabolism, and atrophy in the brain. They could help stage Alzheimer’s disease.