Assessment of knowledge, attitude, and practices of Lebanese diabetic patients and their relation to medication adherence and doctor-patient communication: A cross-sectional study.

Alzheimer's disease (AD) is a multifactorial disorder in which vascular aging contributes to early neurodegenerative processes. Beyond traditional amyloid‐centric models, growing evidence suggests that vascular dysfunction contributes to tau pathology, neuroinflammation, and white matter damage before cognitive impairment emerges. These vascular contributions are particularly relevant for older African Americans, who experience a disproportionate burden of cerebrovascular disease, hypertension, and AD. Vascular stiffness is a hallmark of compromised vascular health and reflects cumulative damage to vascular structure and function. Reduced vascular compliance increases transmission of pulsatile forces to cerebral circulation, promoting neurovascular damage. Estimated pulse wave velocity (ePWV), derived from age and blood pressure, provides a validated and scalable index of vascular stiffness suitable for community and epidemiological studies, when carotid‐femoral pulse wave velocity (PWV) is not available., , Accelerated increases in vascular stiffness are common among older African Americans and may represent a key mechanism linking cardiovascular risk to neurodegeneration., However, the extent to which vascular stiffness contributes to early AD‐related biological changes in this population remains incompletely understood. In our prior work, we demonstrated that greater vascular stiffness, indexed by higher ePWV, was robustly associated with higher plasma concentrations of phosphorylated tau 217 (p‐tau217), but not the amyloid beta 42/40 ratio, among cognitively unimpaired older African Americans. Plasma p‐tau217 has emerged as one of the most sensitive and specific blood‐based biomarkers of AD, showing strong correspondence with tau positron emission tomography (PET), neurodegeneration, and longitudinal cognitive decline, even in preclinical stages. Taken together, these findings suggest that vascular stiffness may preferentially relate to tau‐linked neurodegenerative processes rather than early amyloid‐associated changes.