Longitudinal and genetic studies reveal that intelligence underlies cognitive reserve.
Mutations that destabilize α-synuclein tetramers leave young mice with severe and progressive motor problems resembling those of PD.
Using TNEs—snippets of RNA transcribed from noncoding regions—as a gauge of enhancer activity, researchers tied Parkinson’s risk variants to gene regulation.
In a fly model, C9ORF72 pathology pulls TDP-43 from the nucleus, which leads to disrupted nuclear import and neurodegeneration.
A Wnt pathway inhibitor rescued dendritic spines in cultured neurons and cleared plaques in an AD mouse model.
Families of ALS and FTD patients with C9ORF72 expansions have more mental illness, suggesting the gene affects brain function throughout life.
VX-765 could be a therapeutic candidate for Alzheimer’s disease.
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.