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.

Modelling beta-amyloid deposition in bioengineered human vessels represents a notable advance to further investigate the role of the vasculature in Alzheimer's disease.

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.

The first non-invasive technique to assess the action of brain clearance mechanisms, driven by the perivascular inflow of cerebrospinal fluid, has been developed using magnetic resonance imaging.

The number of inflows and outflows at the occluded capillary governs the local flow reduction, and the different topological configurations are probably designed for distinct functional tasks.

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.

A critical review of the limitations posed by current preclinical animal models of Alzheimer's disease and of the oversimplistic assumptions proposed by the amyloid cascade hypothesis (ACH).

A neural precursor cell defect precedes widespread inflammation, amyloid plaque pathology, and cognitive deficit in Alzheimer's disease, which can be reversed by inhibiting USP16.

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.