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 ...
Can genetics please parse the confusing spectrum of frontotemporal dementias? Whole genome sequences make a start.
Scientists say chaperones keep FUS from joining up with aggregating proteins as FUS makes its way down axons to deliver RNAs for local translation. ALS/FTD mutations bungle the process.
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.
It’s ‘And,’ Not ‘Either-Or’: C9ORF72 Mechanisms of Action are Linked Beyond the Nucleus: TDP-43 Sticks Together, For Better or Worse Going the Distance: FUS Travels to Terminals, Drops Off RNA When RNA transcripts aren’t processed properly or don’t make ...
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.
Swine that express mutated human SOD1 exhibit the hallmarks of ALS pathology, including aggregates and degeneration in motor neurons, preceded by a lengthy preclinical phase.