Introduction: Vascular aging influences both cerebrovascular reserve and neurodegeneration, yet the role of the choroid plexus (CHP)—a critical vascular interface for cerebrospinal fluid production, immune signaling, and waste clearance—remains poorly defined. The hippocampus, highly sensitive to perfusion and metabolic compromise, is a key structure affected in vascular cognitive impairment. We examined how distinct CHP hemodynamic parameters relate to hippocampal integrity in older adults. Objective: To interrogate the associations between CHP perfusion, total blood flow, and volume with hippocampal volume in community dwelling older adults. Methods: We studied 278 community dwelling healthy adults (52–83 years; 130 men, 148 women) using arterial spin labeling MRI to quantify CHP perfusion and structural MRI for CHP and hippocampal volumetrics. Multiple linear regression models tested independent associations of CHP perfusion, CHP blood flow, and CHP volume with hippocampal volume, controlling for age, sex, and intracranial volume. Results: The model explained 24.3% of variance in hippocampal volume (R-square=0.243, p<0.0001). Higher CHP perfusion was significantly associated with larger hippocampal volume (p<0.001), independent of blood flow, CHP volume, and demographics. By contrast, greater total CHP blood flow was inversely associated with hippocampal volume (p<0.001). Larger normalized CHP volume also correlated positively with hippocampal volume (p<0.001). As expected, advancing age predicted smaller hippocampal volumes (p<0.001). Conclusions: Choroid plexus hemodynamics exhibit divergent associations with hippocampal integrity: higher perfusion relates to hippocampal preservation, whereas greater bulk blood flow associates with atrophy. These findings suggest that specific microvascular versus macrovascular remodeling processes in the CHP may differentially influence hippocampal vulnerability. Such vascular signatures could represent novel biomarkers of brain aging and vascular cognitive impairment. Longitudinal studies and mechanistic exploration are warranted to establish whether CHP perfusion patterns reflect compensatory responses or maladaptive remodeling relevant to cerebrovascular disease.
Jamshidi et al. (2026) studied this question.