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).
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?
Seeking strength in numbers, families gathered to swap stories and to learn about an upcoming DIAN-TU therapy trial geared specifically to their particular form of early onset AD.
Scientists match up PET scans of neurofibrillary tangles against Aβ imaging, CSF measures, and cognitive tests to see how biomarkers change relative to function.
Citing “fantastic opportunity,” FDA and EMA call for rigorous science. Agency scientists tell FTD Treatment Study Group: Explore individualized outcomes, and connect biomarkers to meaningful improvement.
Hoping for better luck in clinical trials than their Alzheimer’s colleagues had in the past decade, FTD researchers are now chasing biomarkers. It’s slim pickings so far, but neurofilament, tau PET, and MRI are showing promise.
At a workshop of the Frontotemporal Dementia Treatment Study Group, advocates and regulatory scientists urged leaders from industry and academia to forge a collaborative approach while the field is still young.
Alois was right: Among cognitively normal middle-aged people followed for more than a decade, memory worsened only in those in whom markers for both amyloid and tau were abnormal.