At a workshop on engaging more black Americans in ADRD research, new CSF findings stood out against a general dearth of data on Alzheimer’s disease in underrepresented minorities.
Despite having a higher incidence of Alzheimer’s or a related dementia, relatively few black people participate in research studies or drug trials. How to achieve full representation?
In AD brain, scientists see a genome-wide histone acetylation pattern replete with peaks near familiar AD genes such as APP, presenilin, tau, complement receptor, and more.
Clusters of neurons harboring somatic mutations in 56 genes linked to neurodegenerative diseases may be commonplace in the human brain.
X-ray crystallography yields high-resolution structure.
An antibody that binds fibrin blocks neuro-inflammatory signaling while allowing normal clotting.
Analysis of MRI brain volume data identifies multiple AD and FTD/ALS disease subtypes with distinct patterns of degeneration over time.
The most detailed look yet at hippocampal wiring may guide future functional studies and disease research.
Neuromuscular junctions between human stem cell-derived motor neurons and skeletal muscle fibers faltered when cells came from an ALS patient.
A small molecule that protects neurons fends off a short region of Aβ from a specific pocket on the LilrB2 receptor.
A large-scale expression study finds mis-splicing of a specific set of genes in AD brain that includes several known risk genes.
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.