Aβ and other pathogenic proteins may cause neurodegenerative disease by spreading throughout the brain like infectious diseases spread through populations, according to a new mathematical model.
Whether by themselves or in the company of mutations that cause frontotemporal dementia, microRNAs may play a hand in driving disease.
At ICFTD, researchers proposed new genes and explored genetic differences that contribute to the vast diversity of FTD clinical presentations.
In debating how C9ORF72 causes neurodegeneration, researchers struggle to connect cell-culture results with divergent patterns of human disease.
Variants in the genome that increase the risk for Alzheimer’s also lower the age of onset.
In a two-year study, a heaping dose of vitamin B did nothing to sharpen cognition in people over 65, casting further doubt on the supplement’s ability to stave off dementia.
FORUM Pharmaceuticals announced that its histone deacetylase inhibitor has passed a Phase 1 trial, and will advance to Phase 2 immediately. It was one of two trials presenting data on active investigational drugs at ICFTD.
Using physiological measurements, researchers are tracing behavior changes in frontotemporal dementia back to crumbling neural circuitry.
Not to be outdone by ongoing FTLD cohort studies underway mostly in Europe, U.S.-Canadian studies are now forging structured networks to track presymptomatic and symptomatic cases and to engage a panoply of funders and advocacy groups in a clinical trials initiative.
You might not think it possible to assemble large, longitudinal cohorts of loyal study subjects for rare dementias marked by apathy and emotional blunting. Think again—at the International Conference for Frontotemporal Dementia, researchers showed that they just did it.
Confirming hints from case reports, the Genetic FTD Initiative, a European-Canadian frontotemporal dementia network, shows which brain areas change long before tau, progranulin, and C9ORF72 mutation carriers become symptomatic.
Researchers detect aberrant methylation in genome regions that associate with late-onset AD.
Trophic factor may rejuvenate aging cells and protect neurons.
Term covers tauopathy in the absence of Aβ, regardless of cognitive state.
Researchers claim basic conclusions still sound.