In people who carry a repeat expansion in the C9ORF72 gene, gray and white matter are smaller and subtle impairments in cognition appear decades before symptom onset.
Clinical validation is showing automated Elecsys, Lumipulse assays to be reliable and predictive. The story on blood tests has turned from non-starter to intensely promising for broad-based screening.
Tau’s apparent lockstep with cognitive decline dominated the PET conversation. Piramal flaunted data, and Merck/Cerveau are close behind. A first stab at imaging synapses in the hippocampus drew notice, too.
Alzheimer’s science has undergone a paradigm shift toward the disease’s silent phase. For trials, this means change at every level: new participants, new screening tools, new outcome measurements. What’s the progress?
Slow vital capacity, a measure of respiratory function, predicted the rate of disease progression in ALS patients, suggesting the test could be used as a primary endpoint in clinical trials.
The neurodegeneration marker appears to track disease severity in AD and MS patients with great sensitivity.
A longitudinal study identified regions in the default mode network as among the first to accumulate Aβ.
Participants in the A4 prevention trial wanted to know the extent of their amyloid burdens and how that affected their risk for AD. Researchers need to carefully communicate the limitations of amyloid PET.
Researchers debut a statistical model that uses MRI, CSF, and demographic data to compute a cognitively impaired person’s risk for progressing to dementia.
Tau in the plasma rises after traumatic brain injury, with cognitive decline, and progression to mild cognitive impairment.
In a pilot study, a curcumin-based probe allowed researchers to detect retinal amyloid deposits in AD patients, but it remains to be seen if this can serve as an early biomarker.
Researchers at AAIC presented several imaging measures that may help explain the phenomenon of preserved cognition in the face of AD pathology.
AAIC presentations identified early imaging changes in aging and AD, and reinforced the idea that CSF markers change little over the short term.
Rather than changing one by one, many biomarkers—including cognition, tau PET, hippocampal atrophy, and CSF p-tau—shift together, around the time of symptom onset in young adults with familial AD.
Researchers at AAIC reinforced the idea that tau pathology drives cognitive decline, although amyloid plaques were implicated in semantic memory deficits.