Studying Diverse Populations May Require New Biomarkers
Amyloid and tau accumulation patterns differ in black, white, and Hispanic people.
Amyloid and tau accumulation patterns differ in black, white, and Hispanic people.
At HAI, scientists report that tangle accumulation in tracts from the locus coeruleus keeps neural systems from communicating with one another when neurons die.
In Puerto Rico, scientists agreed that jointly measuring multiple plasma tau markers could be a powerful readout of tau pathology in a person’s brain.
Scientists characterize early stage tau aggregates and develop a CSF test to track them.
In mice, this marker correlated better with amyloid protofibrils in the brain than with plaques. So did CSF markers of neurodegeneration, highlighting the toxicity of protofibrils.
Two studies tie repeated stretches of DNA to increased odds for AD. One encodes poly-GR peptides that aggregate.
Surveys of CSF proteins from the GENFI and ALLFTD genetic cohorts flag altered biological processes and point toward FTD fluid markers.
An endoplasmic reticulum protein helps lipids bud from this organelle. Knocking out the protein in microglia curtailed lipid droplets, and enhanced amyloid clearance.
After 14 years in Miami, HAI is on the move again. This January conference started in chilly Boston and moved around the north for some time, meeting in Chicago, Seattle, and Toronto, before settling in a warmer clime in 2011. For 2025, HAI pulled up stakes again and landed in San Juan, Puerto Rico. There, 419 attendees from 16 countries shared data about how to line up blood biomarkers with PET data, how locus coeruleus connectivity might influence tangle spread, and what the field is learning from its growing focus on studying non-white populations. Read Sara Reardon’s stories.
How do cerebrospinal fluid proteins change over the course of frontotemporal dementia? Hints come from proteomic analysis of CSF from the world’s two large genetic FTD cohorts, GENFI and ALLFTD. Synaptic proteins dropped in all forms of the disease, while extracellular matrix changes were mostly tied to MAPT mutations, and RNA-processing proteins to the TDP-43 proteopathy linked to C9ORF72 and GRN. The three genes had distinct proteomic profiles, implying that researchers could find biomarkers that distinguish each form.
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