Beta-casein in human milk is associated with infant stool frequency: A pilot proteomics study.

Cerebral amyloid angiopathy (CAA) is a common cause of cognitive impairment and lobar intracerebral hemorrhage in older adults. It is defined by progressive amyloid beta (Aβ) deposition within cortical and leptomeningeal vessels and is diagnosed in vivo using the Boston v2.0 criteria. CAA frequently co‐occurs with Alzheimer's disease (AD), characterized by parenchymal Aβ plaques and hyperphosphorylated tau tangles. This overlap generates a biological continuum of mixed vascular and neurodegenerative pathology,, which influences clinical presentation, prognosis, and therapeutic vulnerability, including the risk of amyloid‐related imaging abnormalities (ARIAs) during anti‐amyloid therapy., Concomitant AD pathology is associated with greater cognitive burden compared to pure CAA, and recognizing this co‐pathology helps clarify the relative contribution of vascular versus neurodegenerative mechanisms to symptoms. Identifying AD co‐pathology in patients with CAA is therefore clinically relevant, particularly in those presenting with cognitive impairment, in whom overlapping mechanisms may lead to heterogeneous clinical trajectories and complicate both diagnosis and prognostic interpretation. Cerebrospinal fluid (CSF) biomarkers enable reliable detection of AD‐related amyloid and tau pathology, but their invasiveness limits use in patients with vascular or hemorrhagic phenotypes. Blood‐based biomarkers have emerged as accessible alternatives. Among them, plasma phosphorylated tau at threonine 217 (p‐tau217) shows high diagnostic accuracy for AD pathology, a strong concordance with CSF biomarkers, particularly CSF p‐tau181 and the CSF Aβ42/p‐tau181 ratio, as well as amyloid positron emission tomography, and has recently been validated on fully automated clinical platforms., , Although patients with CAA exhibit reduced CSF Aβ40 compared to AD,, , , no fluid biomarker has been validated for diagnosing CAA itself. Recent studies have reported altered plasma p‐tau isoforms in CAA,, but their diagnostic meaning remains unclear. Performance against CSF‐defined AD status using automated assays is lacking. Additionally, the potential correlations between plasma p‐tau217 concentrations and magnetic resonance imaging (MRI) markers of vascular burden–such as cerebral microbleeds (CMBs), cortical superficial siderosis (cSS), and the total CAA–small vessel disease (CAA–SVD) score—remain unexplored.