629 RESULTS
Sort By:
Neuronal markers in the cerebrospinal fluid suggest the degree of white-matter damage correlates with time needed for recovery, and that repetitive brain injury spurs amyloid deposition.
Researchers at AAIC proposed several different measures of brain connectivity that may predict progression to AD.
Clinical trial design could benefit from new estimates of how slowly amyloid accumulates and how best to detect it at various disease stages.
In a validation study, three common software packages produced excessive false positives, but initial stories about previous suspect data might have been overblown.
Researchers at AAIC discussed technical limitations of current tracers and ways to improve the signal. A new ligand debuted that may be more specific for tangles.
Researchers at AAIC presented congruent data on the place tau tangles take in AD progression, and their close correlation with cognitive decline.
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.
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).
Researchers may soon add another imaging agent to their tool kit—one that tracks synapse loss.
A PET study comparing amyloid, tau, and volumetric imaging in preclinical AD identifies a region where local tangles correlate with brain-wide amyloid.
Assessed in toto, thousands of gene alterations portend changes in cognition, brain structure, and amyloid deposition in people without dementia. A step on the way to a gene chip for AD?
