FTD-GRN: A Disease of Angiogenesis and Vascular Fibrosis?
With too few endothelial cells and too many fibroblasts in frontotemporal dementia due to insufficient progranulin, the blood-brain barrier and angiogenesis go haywire.
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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.
In young adults with Down’s, plasma phospho-tau217 correlated with amyloid and tau PET positivity. With great accuracy.
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.
The agency accepted Eisai and Biogen’s application for priority review under the accelerated approval pathway, based on Phase 2 biomarker data.
In astrocytes, Aβ revs up urea metabolism, spitting out the intermediate putrescine. This gets turned into the neurotransmitter GABA, which blunts synaptic transmission and memory in mice.
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