Cerebral small vessel disease (CSVD) gives rise to one in five strokes worldwide,which affect the small arteries,arterioles,capillaries and small veins of the brain.CSVD is associated with recent small subcortical infarct,lacuna of presumed vascular origin,white matter hyperintensity of presumed vascular origin,perivascular space,cerebral microbleeds,and brain atrophy.CSVD constitutes a major source of cognitive decline,affective disorder,urinary disorders,gait disturbances,impaired activities of daily living particularly in the elderly.The review will focus on recent progress on the clinical features of cognition,the neuroimaging,treatment and the prospective in the future study.

Cerebral small-vessel disease(CSVD)is a major cause of cognitive decline, dementia, affective disorders, urinary dysfunction and functional disability in the elderly.This review will focus and elaborates on the pathogenic classification, pathogenesis, clinical features and treatment and propose the prospect in the future study, in order to raise the importance of CSVD and provide a certain theoretical basis for clinical diagnosis and treatment.

Cerebral microbleeds (CMBs),as an important imaging marker of cerebral small vessel disease (CSVD),is a subclinical damage caused by small hemosiderin deposits indicative of prior cerebral microscopic hemorrhage.In recent years,CMBs have become an important research issue in the field of neuroimaging with the development of newer magnetic resonance imaging (MRI) methods for the higher detection rate of the CMBs.It must to be mentioned that CMBs plays a crucial role in the formatting process of vascular cognitive impairment (VCI),which caused researcher's attention.This review focuses on the research progress in epidemiological status,pathological mechanisms,risk factors,imaging manifestations,clinical features and treatment therapies of CMBs,in order to provide theoretical references for the early detection,prevention and treatment of CSVD and VCI.

Fear memory contextualization is critical for selecting adaptive behavior to survive. Contextual fear conditioning (CFC) is a classical model for elucidating related underlying neuronal circuits. The primary visual cortex (V1) is the primary cortical region for contextual visual inputs, but its role in CFC is poorly understood. Here, our experiments demonstrated that bilateral inactivation of V1 in mice impaired CFC retrieval, and both CFC learning and extinction increased the turnover rate of axonal boutons in V1. The frequency of neuronal Ca²⁺ activity decreased after CFC learning, while CFC extinction reversed the decrease and raised it to the naïve level. Contrary to control mice, the frequency of neuronal Ca²⁺ activity increased after CFC learning in microglia-depleted mice and was maintained after CFC extinction, indicating that microglial depletion alters CFC learning and the frequency response pattern of extinction-induced Ca²⁺ activity. These findings reveal a critical role of microglia in neocortical information processing in V1, and suggest potential approaches for cellular-based manipulation of acquired fear memory.
Mice ; Animals ; Primary Visual Cortex ; Extinction, Psychological/physiology* ; Learning/physiology* ; Fear/physiology* ; Hippocampus/physiology*