Can BACE Inhibitors Stage a Comeback?
At AAIC, and a separate BACE symposium, scientists argued the case for resuming evaluation of these drugs in clinical trials.
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At AAIC, and a separate BACE symposium, scientists argued the case for resuming evaluation of these drugs in clinical trials.
Stalwart of dementia neuropathology was best known for his work on tau pathology.
Crenezumab Secondaries Negative; Gantenerumab OLE Hints at Efficacy Can BACE Inhibitors Stage a Comeback? High-Res Spatial Transcriptomics Offers New Views of Mouse Brain Alzheimer's Blood Tests Have Arrived; Road to Broad Use Still Stretches On Bloo
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.
In old mice, and young mice with amyloid, astrocytes in the hippocampus swell with autophagosomes, which sequester protein and derail cell functions.
With too few endothelial cells and too many fibroblasts in frontotemporal dementia due to insufficient progranulin, the blood-brain barrier and angiogenesis go haywire.
Correlating PET imaging with spatial transcriptomics revealed paths for the progression of tau pathology throughout the brain.
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.
New data show the pia is a permeable mesh that filters CSF and harbors macrophages. It thins with age but thickens in a mouse model of amyloidosis.
Phospho groups at key residues, such as threonine 181, promoted phosphorylation at multiple distant sites along the protein, suggesting a regulatory role.
Obesity, hypertension, and physical inactivity account for one in five cases.
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