Two mouse models presented at AD/PD may hand scientists more translationally relevant tools to explore LOAD pathophysiology and treatment. The tricks: targeted replacement and knocking in multiple GWAS variants.
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?
Researchers envision p-tau-based blood tests for Alzheimer’s disease within a few years, but maybe not a stand-alone test.
The field is shifting from targeting tau’s tips to its mid-region, especially where tau binds microtubules. Several new candidates are in the clinic; whether the strategy will work remains to be seen.
New data presented at the AD/PD conference offer the first evidence that a brain-shuttle strategy can work in people; the lecanemab and aducanumab antibody programs offer small updates.
A new PET tracer. Plasma glial fibrillary acidic protein. Two new, promising surrogates for astrogliosis are filling in the Alzheimer’s biomarker toolbox. Both reflect Aβ amyloid better than they do tau tangles.
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.