At AAIC, secondary endpoint data from the API Colombian study showed trends favoring crenezumab, while people taking gantenerumab in open-label extensions declined more slowly than matched controls.
With too few endothelial cells and too many fibroblasts in frontotemporal dementia due to insufficient progranulin, the blood-brain barrier and angiogenesis go haywire.
Advances in microscopy yield unprecedented views of Aβ plaques in vivo and ex vivo. The vistas offer new insights about how plaques form, grow, and clear.
High sST2, an IL-33 receptor fragment, raises the odds of Alzheimer’s in women who carry APOE4. A variant that lowers sST2 mobilizes microglia, protects against AD.
Other scientists found indications of potentially doctored western blots in multiple papers, including several on Aβ*56. Investigations are underway at journals, NIH, UMinnesota.
By consensus, leaders in the astrocyte and microglia fields recommend that investigators eschew names in favor of detailed descriptions of reactive glia, with a focus on functional changes.
Synuclein fibrils from Parkinson’s disease, PD dementia, and dementia with Lewy bodies share the same protofilament structure. MSA fibrils are different.
Phospho groups at key residues, such as threonine 181, promoted phosphorylation at multiple distant sites along the protein, suggesting a regulatory role.
Certain mutations in TDP-43, tau, and NfL add one hydrogen bond to their low-complexity domains. This warps phase transition and strengthens self-aggregation.
With its affinity for β-sheets, a probe called Capture Molecule for Amyloid Precipitation, aka CAP-1, pulls α-synuclein and other soluble amyloids out of solution.