The causal link between capillary amyloid‑β accumulation in the brain and cerebrovascular dysfunction, previously established in the Tg‑SwDI mouse model, is to be mitigated and remains to be fully uncovered.
Increased levels of brain Hebp1 starting from the presymptomatic stage of Alzheimer’s disease contributes to progressive neuronal loss by triggering mitochondrial-dependent apoptosis in neurons exposed to elevated heme.
Reducing Akt-mediated huntingtin phosphorylation decreases APP accumulation at the synapse by reducing its anterograde axonal transport and ameliorates learning and memory in a mouse model of familial Alzheimer disease.
An international collaboration between five independent research groups replicates findings confirming the importance of aquaporin-4 in glymphatic solute transport using five different mouse knockout lines.
The discovery of a unique brain lymphatic cell type in the zebrafish model will facilitate the study of embryonic development and physiology, an essential mission to understand how clearance of macromolecules impact neurological diseases.
APP mutations that either cause or prevent dementia alter APP metabolism in a complex and opposite fashion, suggesting a link between multiple APP processing events, dementia and ageing-dependent cognitive decline.