Cryo-EM helps explain how the inhibitory receptors open and close their ion channels.
Absent the receptor, microglia ignore Aβ seeds and new plaques, which then absorb little ApoE and stay diffuse.
Stakeholders have until February 11 to comment on draft FDA guidance for biomarker qualification.
In neurons derived from FTD patients, microtubules distort the nucleus, warping its normally rounded membrane and disrupting communication with the cytoplasm.
In familial Alzheimer’s disease, rise in NfL in the blood precedes disease onset by 16 years.
Frail people may be more likely to have Aβ plaques and neurofibrillary tangles; when they do, they are more likely to have dementia. Physical activity correlated with better global cognition, regardless of brain pathology.
Reducing systolic blood pressure staves off cognitive decline, but what about dementia?
The FDA has prioritized review of C2N’s blood test for amyloid-β. A pivotal clinical trial will correlate the test with amyloid PET scans.
New work implicates changes in chromatin structure and failed DNA repair in neurodegeneration.
This past year, therapeutic antibodies massively reduced brain amyloid, blood tests came into their own, and systems-based approaches transformed the study of gene expression, glial cells, and selective vulnerability.
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.
Human cells show more phenotypic variation than mouse microglia, but the two match up well overall.
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.
Deleting BACE1 with CRISPR nanocomplexes tempered Aβ pathology and boosted memory.