Sequencing the protein-coding DNA regions of more than 60,000 people sheds light on disease-causing mutations.
As data pours in, DIAN leaders strive to share and publish it without accidentally disclosing mutation status. The more is learned about preclinical AD, the harder this may get.
Armed with what they consider comprehensive data sets from the DIAN initiative, researchers are beginning a quest to settle an old question that may become key to drug approvals for late-onset AD.
At AAIC, updated imaging data in autosomal-dominant AD shows that longitudinal MRI in large numbers of people confirms atrophy patterns. Tau PET is more variable in DIAN participants than in the Colombian families.
Serial measurements on hundreds of people in the Dominantly Inherited Alzheimer’s Network put proposed staging diagrams on an empirical footing. CSF markers sTREM2 and VILIP-1 track tau.
At AAIC, 28 scientific presentations and five attendant meetings of the Dominantly Inherited Alzheimer’s Network showed how data is rolling in while the platform expands to more countries and a second therapeutic trial.
People who skimp on seafood may be more likely to harbor amyloid deposits in their brains, according to a new amyloid PET imaging study.
Dementia incidence in intervention group was no different from control, though targeting hypertension may protect, researchers say.
Clinical trial centers are preparing to position themselves as standing networks, with standardized paperwork, clinical rater systems, and a central IRB, for trials anticipated to start late next year.
Alarmed by crushing screen failure rates of the first prodromal Alzheimer’s trials, EPAD and GAP are chasing new ways to reach people who don’t know they really should be in a secondary prevention trial.
This past year, the Global Alzheimer’s Platform and the European Prevention of Alzheimer’s Dementia have moved quickly, and jointly, to pave the way toward more, faster, cheaper trials. Will they be better, too?
At AAIC, researchers suggested splitting out the markers in a new staging scheme. Called ATN, it aims to clarify underlying causes of atypical dementias and suspected non-Alzheimer’s pathology (SNAP).
Antibodies that cling specifically to human APP revealed differences in expression patterns of the protein in mouse models of Alzheimer’s disease.
Scientists pool samples and creatively mine the genomes of thousands of patients to find coding and non-coding variants that associate with the disease.
Using PET tracers, researchers have linked the presence of tau tangles to neurodegeneration in preclinical and clinical AD, and fingered Aβ as the instigator of tau toxicity.