In people at intermediate risk for cardiovascular disease, the meds had no effect on cognitive decline over six years.
Among British civil servants, the quality of their diet did not correlate with their risk of developing dementia cognitive decline over 25 years.
A prospective progeria drug revs up cellular autophagy and clears tau in neurons derived from patients with frontotemporal dementia. In mouse models, the drug rescues abnormal behavior.
A large-scale expression study finds mis-splicing of a specific set of genes in AD brain that includes several known risk genes.
Using TNEs—snippets of RNA transcribed from noncoding regions—as a gauge of enhancer activity, researchers tied Parkinson’s risk variants to gene regulation.
Senolytic drugs kill these cells, temper Aβ, and improve cognition in transgenic mice.
In people carrying two mutated copies of the trophic receptor, important brain structures, such as the corpus callosum, never developed.
Inhibiting the receptor activates microglia to mop up debris, making CD33 an attractive therapeutic target.
Scientists are probing saliva and skin secretions for telltale signs of Parkinson’s disease. Their prize? A diagnostic test at the pre-motor stage.
In the largest study yet to track tau via repeated PET scans, researchers found that tau pathology increased over baseline only in people with Aβ deposition. The more tau a person had at baseline, the more tau increased later on, and the more they slipped on cognitive tests.
An FDA-approved insomnia drug lengthened total sleep time in patients with mild to moderate Alzheimer’s, suggesting it might be able to lessen a troublesome symptom of the disease.
More mouse data add to the argument that a flashing light sequence could potentially fight cognitive decline.
Lanabecestat, elenbecestat, and umibecestat all showed data at the AD/PD conference in Lisbon. Learn what definitely doesn’t work and what might yet.
Thousands of stretches of the genome go undetected by standard short-read sequencing techniques. Unmasking these “dark regions” revealed a potential AD risk variant in the CR1 gene.
Scientists link this mysterious form of dementia to higher plasma LDL-cholesterol, and to genetic variants in APOB, which encodes the major component of low-density lipoprotein.