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.
The FTD Prevention Initiative merges cohort studies from across the world with a common goal—to execute effective clinical trials for FTD.
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The Phase 2 trial provides the strongest evidence yet that removing most amyloid from the brain bolsters cognition, although the benefit is small.
Disturbed social and emotional cognition are among the most troubling features of FTD. They, too, can be quantified with new tools.
People with FTD wrestle with behavioral, cognitive, language, and motor impairments. Scientists are designing standardized tests that capture such symptoms.
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.
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.
As FTD consortia chase biomarkers, they see plasma NfL and neuronal pentraxin-2—which reflect neurodegeneration—change before symptoms. Trials nudge progranulin and poly-DP. Still needed: more markers of the pathophysiology that unfolds in the brain.
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.
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Simple addition of choline, a phospholipid building block, ameliorated ApoE4-related deficiencies.
Already implicated in dementia, this lysosomal receptor appears to play a role in the development of COVID-19.
The more a person’s gut microbiome becomes individualized with age, the longer that person's lifespan and the better his or her health, say scientists.
White matter-associated microglia express similar genes to plaque-associated DAMs. They seem to be triggered by the myelin breakdown associated with aging and disease.