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.
Researchers at AAIC described different correlates of CSF and PET measures of Aβ and tau.
The aging brain winds down rapid glucose metabolism in regions that will go on to accumulate amyloid, perhaps raising the risk of neurodegeneration.
Interim data from IDEAS study find that amyloid PET has a greater effect in real-world practice than in research settings. Nearly half of people diagnosed with AD did not have the disease.
At AAIC, researchers debuted a method that detects changes in plasma Aβ42 in people with brain amyloid. If confirmed, a widely available screening test for presymptomatic AD could follow.
Gaps surrounding blood vessels in the brain may predict cognitive decline and vascular dementia.
Analysis of brain tissue from Alzheimer’s patients offers a glimpse of proteomic changes in the disease.
New diagnostic guidelines on dementia with Lewy bodies fold in science about sleep and the heart, two aspects that distinguish this disorder from Alzheimer’s and Parkinson’s.
Longitudinal ADNI data revealed that people with elevated Aβ declined toward AD, while those with normal levels maintained their cognitive abilities.
People with ALS—especially those who progress fast—express myriad inflammatory genes in their blood monocytes.