Vascular cognitive impairment (VCI) is a syndrome defined as cognitive decline caused by vascular disease, which is associated with Alzheimer's disease (AD) and vascular dementia (VaD). Chronic cerebral hypoperfusion (CCH), which is elicited by aging, metabolic syndromes, atherosclerosis, hypertension, obesity, and hypotension, is commonly present in various types of dementia, and CCH-associated small vessels disease is the major contributor to VCI. Growing evidence suggests that CCH is the cause of white matter lesions, which are a key character of VCI. White matter lesions that precede neuronal dysfunction have been observed in a CCH-induced VCI mouse model. Furthermore, patients with AD and VaD show white matter lesions. Thus, although the importance of CCH-induced white matter lesions in VCI has received widespread attention, effective therapeutic targets for VCI are still under development, because the precise molecular mechanisms that detect and regulate pathological changes in VCI remain to be elucidated. Here, we employed bilateral carotid artery stenosis (BCAS) mice as a CCH-induced VCI model, and found that minor disruption of the blood-brain barrier and generation of reactive oxygen species (ROS) were observed, leading to brain inflammation and white matter damage, which in turn led to cognitive impairment. In the pathogenesis of BCAS-induced cognitive impairment, we investigated the involvement of TRPM2, a ROS-sensitive Ca²⁺-permeable cation channel, and found that TRPM2 mediates microglial activation and contribute to the exacerbation of the symtoms. Furthermore, we have recently found that TRPA1, another ROS-sensitive TRP channel expressed in astrocytes, may be involved in the pathogenesis of BCAS, and we will also introduce our recent findings on TRPA1 in astrocytes. These findings suggest there are two-sidedness to the ROS-sensitive TRP channel and that TRPM2 and TRPA1 could be a therapeutic target for CCH-related CNS diseases.