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.
FDG PET revealed the formation of a new functional brain network. It explains clinical improvements noted previously.
In mice, a daily low dose restored regulatory T cells and held off symptoms of a demyelinating disease. Could an old, over-the-counter drug help with ALS, in which similar cells decline?
The Food and Drug Administration has said it will accept cognition alone as the basis for approval in preclinical AD. Now what? Industry is confronting the challenge to show robust and meaningful change.
In sporadic and familial forms of AD, progranulin climbs in the cerebrospinal fluid as disease progresses, perhaps reflecting microglial activation.
In a new take on mosaicism and Alzheimer’s, scientists claim that APP mRNAs convert into DNA and reinsert into the genome. Full of mutations, these “genomic cDNAs” crop up in aging and sporadic AD.
At CTAD, researchers discussed baseline data from the first 500 participants in the EPAD cohort and, finally, the start of recruitment for TRC-PAD.