Even at below threshold levels, cortical amyloid can drive cognitive decline, tau accumulation.
A large retrospective study in veterans finds that even brain injuries that cause no loss of consciousness come with a twofold higher risk of developing all-cause dementia.
Better tissue extraction and Aβ assays could help identify the most toxic Aβ species and most promising immunotherapies.
The findings offer one way this RNA-binding protein gets into cytoplasm, where it sets the stage for pathological aggregation.
UCB-J hints at early synaptic loss in the hippocampus, but not the cortex. Researchers puzzle over the pattern.
The hippocampus trickles out new neurons throughout life, a process that falters without BACE1 or in the presence of ApoE4.
Vascular microchannels linking the skull bone marrow to the dura mater supply the brain with neutrophils in response to stroke and inflammation.
Males are inflammatory, females are neuroprotective: Profiling of microglia from adult mice suggests sex-specific phenotypes, likely set at birth.
Computational models predict that ALS mutations tax the flexibility of profilin-1, weaken binding with key partners including actin, and boost the protein’s propensity to aggregate.
By promoting the exocytosis of cellular debris, the kinase may facilitate spread of α-synuclein aggregates.
What goes up can come down—rising tides of VILIP-1, neurogranin, and SNAP-25 ebb after onset of AD symptoms.
Ablating BACE1 in adult mice spares them from most problems found in germline knockouts. However, axons extending from newborn hippocampal neurons still lose their way.
Treatments that promote neurogenesis and elevate BDNF act as exercise does to improve memory in mouse models of Alzheimer’s disease.
An 856-patient, proof-of-concept trial of the anti-protofibril Aβ antibody suggests the highest dose slowed cognitive decline and cleared plaques.
The largest study so far to compare brain scans and CSF among African-Americans and Caucasians finds differences, but participant numbers remain small.