Removing senescent cells from mouse brain ameliorates the effects of mutant human tau.
Believed to be an amyloid-lowering agent, the blood pressure drug did not help people at the dementia stage of disease.
The bill tops last year’s budget for the disease by $425 million.
Staufen1 may deplete certain mRNAs, precipitating the death of Purkinje and other neurons.
In DIAN, participants who are more physically active may also have slower disease progression.
Serial data establishes different trajectories for CSF t-tau and p-tau.
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.