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.
At AAIC 2017, scientists offered new clues on sleep and AD neuropathology. They identified parts of the brain that may be involved and highlighted the benefits of treating sleep disorders.
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.
Report details ways to improve care of people who have dementia, argues for societies to implement ambitious prevention strategies, but offers only reduction of hypertension as a plausible intervention.
Scientists at AAIC described a large, multidomain intervention trial in the United States to test if lifestyle changes can stave off cognitive decline. YMCAs nationwide are in on the project; similar trials are in the works in other countries.
Researchers will enroll young adults who carry familial AD mutations in the first trial of a mechanism-based, investigational drug to try to prevent amyloid from depositing in the brain.
In London, researchers claimed that a monomer is the minimal structure required for tau strains. On the other hand, the sky seems the limit for the number of Aβ strains that form in an individual brain.
At AAIC 2017, researchers presented new approaches to find genetic variants linked to AD risk and to understand their contributions to disease.
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.
An astrocytic Aβ protease, destabilization of γ-secretase by FAD mutations, and an sAPP receptor all made their debuts at Heidelberg conference.
Analysis of brain tissue from Alzheimer’s patients offers a glimpse of proteomic changes in the disease.
At a conference in Heidelberg, researchers proposed that Aβ oligomers trigger local translation of tau in cytosol and dendrites, and that targeting this aberrant tau may preserve synapses.