2022 年 39 巻 4 号 p. 439-443
Cerebral small vessel disease is a common disease that affects small vessels in the brain and is associated with stroke, cognitive impairment, and motor dysfunction. The blood–brain barrier and endothelial cell function have been the focus of attention as the etiology of the disease. Recently, the mechanisms of waste removal and neural activity–dependent redistribution of blood flow in the brain have been clarified, and the functions of pericytes, smooth muscle cells, and arterioles have been studied. However, the pathogenesis of the disease is still unknown. Since the prevalence of cerebral small vessel disease increases with age, aging is the most important risk factor. Hypertension is also one of the most important risk factor for cerebral small vessel disease, but even in modern times when antihypertensive therapy is widely available, the onset and progression of symptoms have not been adequately controlled. Recent genome–wide studies have revealed that many genes related to extracellular matrix are included in the risk genes for sporadic cerebral small vessel disease, and their involvement in the pathogenesis is suspected. In addition, HTRA1, the causative gene of hereditary cerebral small vessel disease, is included in the risk genes. This suggests that extracellular matrix changes may be a common pathogenesis of sporadic and hereditary cerebral small vessel disease.
