First Round of Awards from Chan Zuckerberg Initiative Announced
The awards total $52 million, divided among 17 early career investigators and nine collaborative science teams.
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The awards total $52 million, divided among 17 early career investigators and nine collaborative science teams.
Five years after its creation, the WDC met in London to reflect, articulate next steps, and announce more sharing of BACE trial data.
Many genes that increase risk for late-onset AD are expressed in microglia, and researchers are going cell by cell to unravel the pathways involved in the immune response to amyloid and tau.
At SfN, some scientists described how circulating immune cells deliver aging to the mouse hippocampus; others held off parkinsonism by blocking the effects of eotaxin’s rise in blood. Human trials are starting.
At SfN and in new papers, scientists describe how synapses crater under the combined onslaught of Aβ and tau. They also link gene-expression signatures to the selective vulnerability of excitatory neurons to tau pathology.
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.
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.
CryoEM 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.