AI Networking Cookbook: Practical recipes for AI-assisted network automation and development
This scientific commentary refers to ‘Modelling the temporal evolution of plasma p-tau217, amyloid PET, tau PET and cognition’ by Cogswell et al. (https://doi.org/10.1093/brain/awag075).
This scientific commentary refers to ‘Data-driven modelling of tau pathology reveals distinct progressive supranuclear palsy subtypes’ by Cullinane et al. (https://doi.org/10.1093/brain/awag131).
This scientific commentary refers to ‘White matter lesions disrupt cholinergic pathways important for cognition in Parkinson’s disease’ by Carli et al. (https://doi.org/10.1093/brain/awag172).
Plasma phosphorylated tau 217 (p‐tau217) is a promising biomarker for monitoring treatment response in Alzheimer's disease (AD), but its longitudinal dynamics and clinical relevance remain unclear.
Functional brain network alterations associated with Alzheimer's disease (AD) pathology, including amyloid beta (Aβ) and phosphorylated tau (p‐tau), are difficult to interpret due to overlapping aging‐associated and non‐amyloid biological processes.
[This corrects the article DOI: 10.3389/fmed.2026.1826377.].
Blood–brain barrier (BBB) dysfunction is an early feature of Alzheimer's disease (AD). Fibrinogen represents a sensitive marker of BBB leakage, but whether it modifies longitudinal tau progression in cognitively unimpaired (CU) individuals remains unknown.
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