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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.
Recent conferences revealed that tau is most toxic in oligomeric form, that tau oligomers propagate throughout the brain, and that tau oligomers might harm synapses from within or via astrocytes.
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.
The material, previously used to treat children with growth deficiencies, triggered amyloid deposition in transgenic mice.
Case study in early onset AD finds PET ligand tracks regional tau burden.
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.
Five years after its creation, the WDC met in London to reflect, articulate next steps, and announce more sharing of BACE trial data.
In several model systems, α-synuclein boosts oleic acid production and the fatty acid worsens α-synuclein pathology.
The awards total $52 million, divided among 17 early career investigators and nine collaborative science teams.
In patients across a range of neurodegenerative diseases, NfL ramps up in the cerebrospinal fluid. Levels are higher in those with worse disease.
Proteomics and protein-protein interaction research may yield clues to etiology, tracking, and treatment of granulin-related and other forms of FTD/ALS.
New scales debuted at ICFTD could help clinical trials.
At ICFTD in Sydney, researchers update the community on ARTFL/LEFFTDS.
11th ICFTD Meeting in Sydney Sorts Out Clinical Subtypes Natural History Studies Provide Foundation for FTD Research Tracking Onset and Progression of Frontotemporal Dementia A Proteomics Dive into Cause of Frontotemporal Dementia Encompassing more than h
Can genetics please parse the confusing spectrum of frontotemporal dementias? Whole genome sequences make a start.
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