A large multicenter study confirms the tau PET ligand identifies AD at the dementia stage, but not so well at prodromal stages.
In cognitively normal people, a set of blood proteins may predict whether or not amyloid plaques have deposited in a person’s brain.
The approach provides an in vitro system that more closely resembles the brain milieu than do cell cultures, and can be used to model other proteinopathies as well.
Knocking down or blocking the CCR5 receptor with an HIV drug improved motor symptoms and learning and memory in a mouse model of stroke. Recently, researchers in China knocked out this gene in babies using CRISPR.
Only 16 percent of seniors report being assessed for cognition during yearly checkups. Eighty-two percent think it should be routine.
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.