A large multicenter study confirms the tau PET ligand identifies AD at the dementia stage, but not so well at prodromal stages.
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.
By promoting the exocytosis of cellular debris, the kinase may facilitate spread of α-synuclein aggregates.
Neuropsychological impairments are common in amyotrophic lateral sclerosis, even more so for people at late stages of disease.
A behavioral intervention slowed memory slippage and functional decline over two years.
In large cohorts, older people tested in summer and autumn scored higher on cognitive tests than people tested in winter and spring. Is a seasonal clock ticking in the background?
A new finding questions the usefulness of some mouse models.
Treatments that promote neurogenesis and elevate BDNF act as exercise does to improve memory in mouse models of Alzheimer’s disease.
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 yanking a nuclear protein out of its pore, phosphorylated tau makes nuclei leaky, disrupting the strictly controlled passage of proteins and setting tau up for aggregation.
PET tracer predicts tau pathology and AD, according to company press release.
Study links changes in the retina’s microvasculature to brain amyloid in cognitively normal adults.
Loss-of-function mutations in TBK1 combined with age-related dearth of an analog spell trouble for motor neurons and the central nervous system.
A molecular-level view of tau filaments from a person with Pick’s disease reveals that the protein folds up differently than it does in Alzheimer’s disease.
Vascular microchannels linking the skull bone marrow to the dura mater supply the brain with neutrophils in response to stroke and inflammation.
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