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Grappling with a rare disease whose variability is daunting, international cohort studies are charting the natural history of FTD. They have discovered biomarkers and honed physiological tests that underlie its behavioral symptoms.
The global platform trial for Alzheimer’s due to mutations in APP or presenilin will try to treat or prevent symptoms by deploying a therapeutic antibody that homes in on a piece of tau known to aggregate into neurofibrillary tangles.
International cohort studies reveal that the brain starts to shrink, and neural connections to crumble, many years before FTD symptoms arise. Where and when those changes occur depends on the offending mutation.
People with FTD wrestle with behavioral, cognitive, language, and motor impairments. Scientists are designing standardized tests that capture such symptoms.
Disturbed social and emotional cognition are among the most troubling features of FTD. They, too, can be quantified with new tools.
Donanemab Confirms: Clearing Plaques Slows Decline—By a Bit Astroglial Markers Poised for Stardom? Shuttle Unloads More Gantenerumab Into the Brain N-Terminal Tau Antibodies Fade, Mid-Domain Ones Push to the Fore Where to Now, Phospho-Tau? Clinicians from
The FTD Prevention Initiative merges cohort studies from across the world with a common goal—to execute effective clinical trials for FTD.
At this year’s ICFTD meeting, researchers reviewed the lay of the land of current and planned trials for FTD, with glimpses of how the newly formed FTD Prevention Initiative seeks to coordinate treatment and prevention trials in the future.
As life expectancy increases in countries such as Nigeria, Brazil, China, and others, so does the number of people with dementia. How to provide modern care for them?
At AD/PD 2021, clinicians discussed neurological symptoms and brain tissue damage in older people who died from COVID-19.
By shifting to home nursing and telemedicine, clinical researchers kept inching ahead during lockdowns.
In cell culture, neurons with the strongest expression of cell-cycle proteins survived best in the presence of Aβ oligomers.
Herpes infection upped risk in ApoE4 carriers, damaged brain tissue, and correlated with neurodegeneration markers in the CSF.
Sending low-intensity, gamma frequency electric current through the brain boosted short-term memory, perhaps by increasing cholinergic transmission.
A new trial will compare digital and blood-based biomarkers to amyloid PET scans in order to learn which ones best pick out early plaque accumulation.
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