For several neurodegenerative diseases, scientists identified which cell types exert a person’s inherited risk. In Alzheimer’s, it’s microglia; in Parkinson’s, it’s dopaminergic and enteric neurons—and oligodendrocytes.
Avid’s postmortem validation data indicate Alzheimer’s can be diagnosed by visual examination of flortaucipir PET scans.
Award recognizes discoveries of genetic variants that perturb liquid-liquid phase separation and increase risk for ALS-FTD and other neurodegenerative diseases.
Two studies reveal new aspects of the neurovascular physiology that regulate the flow of oxygenated blood into the brain’s arterioles and capillaries in response to neuronal stimulation.
Trialists are shooting new arrows at the disease, including compounds that tweak autophagy, neuroinflammation, and glycolipid recycling.
Loss-of-function variants in the demethylase TET2 raise a person’s risk for early and late-onset Alzheimer’s, as well as FTD and ALS, suggesting a common mechanism.
Hippocampal imaging and fluid markers of BBB damage found in ApoE4 carriers.
This update of the Allen Brain Institute atlas reveals detailed anatomical structures and provides a common framework for comparing brain datasets.
A large, cross-sectional study finds that RO-948 PET discriminates AD dementia from other disorders more accurately than do CSF biomarkers or MRI.
Harvard or MIT? The microbiomes of mice raised in different facilities dictated their response to C9 deficiency, including whether they died young. Do gut microbes influence ALS?
Separately, cerebrovascular disease drove an uptick in neurofilament light in the brain, indicating neurodegeneration.
Chemicals and particulates may slip across the blood-brain barrier or travel up olfactory nerves to directly affect brain cells. What are the consequences for cognition?
Growing evidence suggests exposure to air pollution increases risk of brain damage and dementia. More definitive research is needed.
The plasma biomarker neurofilament light was able to distinguish individual mutation carriers from noncarriers three years prior to onset.
Umbilical cord stem cells from presenilin 1 E280A carriers, once differentiated into cholinergic-like neurons, pumped out Aβ42 and accumulated phosphorylated tau and apoptotic markers.