Objective Excessive cerebral microbleeds（CMB）are a critical risk factor for cognitive impairment in cerebral small vessel disease（CSVD），yet their neuroimaging mechanisms remain unclear. By using multivariate divergence among multi-contrast MRI features， this study constructs a morphometric inverse divergence （MIND） networks to reveal the pattern of CMB-related structural disruption at the network level and investigate the potential imaging mechanisms of cognitive impairment. Methods A total of 69 CSVD patients with CMB were enrolled as CSVD-c group， 61 patients without CMB were enrolled as CSVD-n group， and 66 healthy controls （HC） were enrolled as HC group. MIND network topology was compared between the three groups， and the correlation between network abnormalities and neuropsychological parameters was analyzed. Results At the cognitive domain level， CSVD patients showed global cognitive decline， significantly affecting multiple domains including memory，visuospatial ability， executive function， and language. Compared with the HCs， CSVD patients had reductions in MIND strength in the frontal lobe （left area 9a and right p32） and the right temporal lobe （Mβ and Pβ），as well as increases in the extent and severity of CMB. For global topology， the patients with CSVD showed significant reductions in global and local efficiency and a significant increase in shortest-path length， with significantly greater changes in the CSVD-c group； for regional topology， there was a significant reduction in nodal efficiency in right Mβ. The correlation analysis showed that global and local efficiency and shortest-path length were significantly correlated with the scores of global cognition and multiple cognitive domains. Network-based statistic further revealed diminished connectivity within the default-mode network （DMN） and between DMN and visual/sensorimotor networks in the CSVD-c group. Conclusion CMB not only exacerbate global cognitive decline in CSVD patients，but also significantly affect multiple cognitive domains including memory， visuospatial ability， executive function， and language.Characteristic network alterations， including reduced synchrony in fronto-temporal regions， impaired global network efficiency and local temporal lobe efficiency， and weakened DMN-related connectivity，may be the potential mechanisms by which CMB aggravate cognitive impairment in CSVD.

Objective White matter hyperintensity（WMH） is the core imaging marker for cerebral small vessel disease， and gait disturbance induced by WMH is a major cause of functional disability in middle-aged and elderly populations. Existing studies mostly focus on the static association between WMH and gait disturbance， while time-varying characteristics are observed in the functional connectivity of brain networks. The dynamic functional connectivity（dFC） technique can capture the real-time interaction characteristics of brain networks， providing a new perspective for analyzing the neural mechanism of WMH-related gait disturbance. This study aims to investigate the neuroimaging mechanism of patients with WMH and gait disturbance using the dFC technique and clarify the association of dynamic brain network imbalance with motor function and cognitive function. Methods Subjects were recruited in Nanjing Drum Tower Hospital from 2023 to 2025， and after screening based on inclusion and exclusion criteria， 93 subjects were enrolled in the group of WMH with gait disturbance （WMH-GD group）， 86 subjects were enrolled in the group of WMH without gait disturbance （WMH-nGD group）， and 92 subjects were enrolled in the normal control group （NC group）. Background data collection， neuropsychological assessment， gait testing， and cranial magnetic resonance imaging （MRI） scanning were performed for all subjects. The DynamicBC toolbox was used to perform the dFC analysis and extract the dynamic indicators including fractional windows（F）， mean dwell time （MDT）， number of transitions（NT）， and transition probability （TP）； network-based statistics（NBS） were used to identify differential connectivity between brain regions across groups； the correlation analysis was used to investigate the correlation between dynamic indicators and clinical parameters. Results The cluster analysis identified two brain functional connectivity states， i.e.， State Ⅰ （sparse and weak connectivity， accounting for 61.29%） and State Ⅱ （dense and strong connectivity， accounting for 38.71%）. Inter-group comparisons showed that compared with the WMH-nGD group， the WMH-GD group had significantly higher F value （72.48% vs 57.38%， P<0.05） and MDT （95.47 windows vs 54.46 windows， P<0.05） of State Ⅰ and a significantly lower value of NT （2.44 times vs 3.83 times）， as well as a significantly lower value of TP from State Ⅱ to State Ⅰ （TP Ⅱ→Ⅰ： 2.61% vs 5.84%， P<0.05） and a significantly higher value of TP from State Ⅱ to State Ⅱ （TP Ⅱ→Ⅱ：97.39% vs 94.16%， P<0.05）. The NBS analysis showed that compared with the WMH-nGD group， the WMH-GD group had a significant reduction in inter-regional connectivity between the occipital lobe， the parietal lobe， and the frontal lobe in State Ⅰ and a significant increase in connectivity within subcortical brain regions and between the limbic lobe and the subcortical region. The correlation analysis showed that in the WMH-GD group， Mini-Mental State Examination score was negatively correlated with MDT of State Ⅰ and TP Ⅱ→Ⅱ and was positively correlated with TP Ⅱ→Ⅰ and NT， and gait speed was positively correlated with NT. Conclusion Dynamic brain network imbalance is observed in patients with WMH and gait disturbance， which manifests as rigidity of the sparse and weak connectivity state， a reduction in transition flexibility， and reorganization of cortex-subcortex connectivity. These abnormalities are closely associated with cognitive and gait functions， suggesting that disruption of brain network metastability may be one of the core neural mechanisms underlying WMH-related gait disturbance.

Objective To investigate the change in morphometric similarity gradient in patients with white matter hyperintensity （WMH）-related cognitive impairment and its influence on cognitive function. Methods Baseline and neuroimaging data were collected from 141 healthy controls （HC group）， 66 patients with WMH and normal cognition （WMH-NC group）， and 134 patients with WMH and cognitive impairment （WMH-CI group）. The difference in gradient was compared between groups based on the morphometric similarity gradient analysis. The mediating effect model was used to investigate the association between WMH volume，plasma biomarkers for nerve injury， gradient， and cognitive function. Results The research findings showed significant aberrant alternations in morphometric similarity gradient， with a significant increase in variability in the second gradient （P=0.036， not surviving FDR correction）. There was a significant negative correlation between the second gradient and geodesic distance （P_spin<0.001）. In addition，visual cortex gradient played a key mediating role in the association between p-tau₁₈₁/WMH volume and visuospatial function. Conclusion Patients with WMH-related cognitive impairment have aberrant macroscopic connectivity patterns of the cortex. The aberrant pattern of regional cortex mediates the process in which p-tau₁₈₁ and WMH volume affect cognitive function， which provides a new perspective for understanding the potential structural mechanism of WMH-related cognitive impairment.

Cerebral small vessel disease （CSVD） has a high incidence rate， an insidious onset， a heterogeneous etiology， and serious damage. At present， there are still various critical issues in the clinical diagnosis and treatment of CSVD， including the difficulty in early warning， difficult etiological typing， and limited treatment methods. This article summarizes the clinical studies on the diagnosis and treatment of CSVD in recent years， in order to provide a reference for solving problems in diagnosis and treatment.

Obstructive sleep apnea-hypopnea syndrome（OSAHS） is a prevalent sleep-related breathing disorder characterized by recurrent pharyngeal collapse during sleep，and it is recognized as an important risk factor for cardiovascular and cerebrovascular events. Cerebral small vessel disease（CSVD） refers to a series of clinical， imaging， and pathological syndromes that arise from pathological alterations in the small arteries， arterioles， capillaries， venules， and small veins within the brain. There is a close association between OSAHS and CSVD，and OSAHS is significantly associated with various neuroimaging biomarkers for CSVD.This article reviews the current status of research on the association between the imaging features of OSAHS and CSVD and related mechanisms， in order to provide a reference for future research.

Cerebral small vessel disease （CSVD） is an important etiology of vascular cognitive impairment and stroke， and there are still many challenges in its early diagnosis and pathological mechanisms. As a type of extracellular vesicles that exist stably in body fluids and can cross the blood-brain barrier， exosomes have attracted wide attention in recent years. Studies have shown that various exosomal proteins have a potential value in the diagnosis and treatment of CSVD and related cognitive impairment， providing new research directions for the noninvasive management of these diseases. This article systematically reviews the latest advances in exosomal proteins for the diagnosis and treatment of CSVD and related cognitive impairment， in order to provide new perspectives for the application of exosomal proteins in the precise treatment of CSVD.