How the element relates to neurodegeneration remains unclear.
Only 16 percent of seniors report being assessed for cognition during yearly checkups. Eighty-two percent think it should be routine.
Researchers publish 14 new AD variants. This includes one near WWOX, a gene that encodes a protein linked to tau and lipid metabolism.
Using a new optogenetic model for TDP-43 phase transitions, scientists see the protein aggregate outside, not inside stress granules. The model distinguishes physiological from abnormal phase transition.
A flavonoid reportedly spices up oxidative phosphorylation in microglial mitochondria, revving up phagocytosis of amyloid plaques in mouse models. The small study needs independent replication.
Aberrant gene-expression patterns found to be common to human neurodegenerative disease and animal models. MicroRNA and epigenetic modification may be to blame.
A score based on the combined burden of a person’s Alzheimer’s risk variants correlated with plaques, tangles, cognitive decline, and even non-AD pathology. Are polygenic hazard scores ready for direct-to-consumer marketing?
Human cells show more phenotypic variation than mouse microglia, but the two match up well overall.
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.
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.
A longitudinal study finds that middle-aged people with the highest levels of inflammation markers in their blood succumb to the greatest cognitive decline over the next 20 years.
In a tiny pilot trial, people with amyotrophic lateral sclerosis who took a “cellular health and optimization” supplement were reported to have improved on several clinical outcome measures.
In mouse models of Alzheimer’s, neutrophils stick to capillaries in the cerebral cortex, reducing blood flow. Keeping those cells moving or depleting them altogether improved memory.
New work implicates changes in chromatin structure and failed DNA repair in neurodegeneration.
In several animal models, stimulating mitophagy lowered amyloid deposits and tau phosphorylation while improving learning and memory.