Injury to the brain, even what might be considered mild, can have devastating consequences on brain physiology...
Advances in therapy saw little sprigs of news pop up in talks that otherwise took stock of the current status of immunotherapy as one of the major new approaches...
In addition to immunotherapy, a meeting in Uppsala, Sweden, focused on recent progress in the development of novel disease biomarkers...
This is part 3 of a 5-part series. See also <a href="/news/conference-coverage/translational-biomarkers-alzheimer-disease-research-part-1">part 1</a> and <a href="/news/conference-coverage/translational-biomarkers-alzheimer-disease-research-part-2">part 2</a>...
Among 20 focus areas, 47 research recommendations cover the gamut from basic science to health disparities.
A majority of amyloid PET scans led physicians to change how they managed a patient’s disease. The effect on later outcomes is yet to be come.
Diagnostics Accelerator to fund projects that develop dementia biomarkers from patient data.
At AAIC, competitors vied for advantage, and discussion moved swiftly to the issue of assay standardization.
Using different techniques, contestants vied for the best way to tell which ADNI participants would develop clinical, cognitive, or imaging signs of Alzheimer’s disease.
The field is searching for a combination of clinical features and biomarkers that will identify the disease in people with mild cognitive impairment.
At AAIC, researchers presented baseline data from an ongoing, five-year study asking whether the anti-Aβ antibody crenezumab can forestall cognitive decline in autosomal-dominant Alzheimer’s disease.
What’s with all those head-to-head comparison studies of academic and commercial biomarker tests? Could we not just pick one that works, and be done?
Clinical trial design could benefit from new estimates of how slowly amyloid accumulates and how best to detect it at various disease stages.
ALS patients eliminate more p75 neurotrophin receptor than do healthy controls. P75 urine levels rise as disease worsens.
At AAIC, researchers touted phospho-tau species, especially p217 and p181. They tick up in CSF as an early response to amyloid accumulation.