Disrupting circadian clocks in astrocytes and microglia unleashed harmful responses in these glial cells, leading to neuronal damage.
By marrying iPSCs, human genomic data, and analysis of postmortem tissue, researchers tied loss of GABAergic signaling to tauopathies such as FTD and PSP, but not AD.
An ultrasensitive assay picked up elevated concentrations of N-terminal tau fragments in the blood of people with AD.
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?
At AAIC, scientists said that alterations in how the aging female brain uses energy and metabolizes fat may leave APOE4 carriers particularly susceptible to tau pathology.
New work implicates changes in chromatin structure and failed DNA repair in neurodegeneration.
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.
At a meeting in San Diego, researchers traded news about how TDP-43 gets trapped in the cytoplasm, finding both good and bad consequences of its exodus from the nucleus.
At an RNA metabolism meeting, scientists reported connections between C9ORF72 loss and gain of function. Their talks brimmed with new biology implicating autophagy, the cellular stress response, and RAN translation off introns.
Staufen1 may deplete certain mRNAs, precipitating the death of Purkinje and other neurons.