SNCA and cerebral small vessel disease: From a pathophysiological perspective, OH may accelerate cognitive decline through dual pathways: (1) direct hypoperfusion injury: Blood pressure fluctuations cause intermittent hypoperfusion in regions such as the entorhinal cortex and anterior cingulate cortex (ACC), disrupting neuronal functions related to reward processing, attentional control, and motivation regulation (45); (2) synergistic cerebral small vessel disease injury: α-synuclein-mediated autonomic dysfunction compounds OH-induced hypoperfusion, selectively damaging white matter watershed zones (46).