UNASSIGNED: The Montreal Cognitive Assessment (MoCA) is a valuable tool for detecting cognitive impairment, widely used in many countries. However, there is still a lack of large sample normative data and whose cut-off values for detecting cognitive impairment is considerable controversy.
UNASSIGNED: The assessment conducted in this study utilizes the MoCA scale, specifically employing the Mandarin-8.1 version. This study recruited a total of 3,097 healthy adults aged over 20 years. We performed multiple linear regression analysis, incorporating age, gender, and education level as predictor variables, to examine their associations with the MoCA total score and subdomain scores. Subsequently, we established normative values stratified by age and education level. Finally, we included 242 patients with vascular cognitive impairment (VCI) and 137 controls with normal cognition, and determined the optimal cut-off value of VCI through ROC curves.
UNASSIGNED: The participants in this study exhibit a balanced gender distribution, with an average age of 54.46 years (SD = 14.38) and an average education period of 9.49 years (SD = 4.61). The study population demonstrates an average MoCA score of 23.25 points (SD = 4.82). The multiple linear regression analysis indicates that MoCA total score is influenced by age and education level, collectively accounting for 46.8% of the total variance. Higher age and lower education level are correlated with lower MoCA total scores. A score of 22 is the optimal cut-off value for diagnosing vascular cognitive impairment (VCI).
UNASSIGNED: This study offered normative MoCA values specific to the Chinese adults. Furthermore, this study indicated that a score of 26 may not represent the most optimal cut-off value for VCI. And for detecting VCI, a score of 22 may be a better cut-off value.

Neurocognitive dysfunction is common in heart failure (HF), with 30% to 80% of patients experiencing some degree of deficits in one or more cognitive domains, including memory, attention, learning ability, executive function, and psychomotor speed. Although the mechanism is not fully understood, reduced cardiac output, comorbidities, chronic cerebral hypoperfusion, and cardioembolic brain injury leading to cerebral hypoxia and brain damage seem to trigger the neurocognitive dysfunction in HF. Cognitive impairment is independently associated with worse outcomes including mortality, rehospitalization, and reduced quality of life. Patients with poorer cognitive function are at an increased risk of severe disease as they tend to have greater difficulty complying with treatment requirements. Coronary revascularization in patients with ischemic HF has the potential to improve cardiovascular outcomes but risks worsening neurocognitive dysfunction even further. Revascularization by coronary artery bypass grafting carries inherent risks for delirium, cognitive impairment, neurologic injury, and stroke, which are known to exacerbate the risk of neurocognitive dysfunction. Alternatively, percutaneous coronary intervention, as a less-invasive approach, has the potential to minimize the risk of cognitive impairment but has not yet been evaluated as an alternative to coronary artery bypass grafting in patients with ischemic HF. Therefore, it is paramount to raise awareness of the neurocognitive consequences in ischemic HF and devise strategies for recognition and prevention as an important target of patient management and personalized decision making that contributes to patient outcomes.

UNASSIGNED: Effect of stenosis of vertebrobasilar artery (VBA) on cognitive function is elusive.
UNASSIGNED: To investigate association of cerebral hypoperfusion and poor collaterals with vascular cognitive impairment (VCI) in severe VBA stenosis patients.
UNASSIGNED: We consecutively enrolled patients with severe VBA stenosis confirmed by digital subtraction angiography who underwent computed tomographic perfusion (CTP) and cognitive assessments. Patients were divided into poor or good collaterals groups according to the collateral circulation status, and were grouped into different perfusion groups according to CTP. Cognitive function was measured by Montreal Cognitive Assessment (MoCA), Clock Drawing Test, Stroop Color Word Test, Trail Making Test, Digital Span Test, Auditory Verbal Learning Test, and Boston Naming Test scales. The association of cerebral perfusion and collaterals with VCI were explored.
UNASSIGNED: Among 88 eligible patients, VCI occurred in 51 (57.9%) patients experienced. Poor collateral was present in 73 (83.0%) patients, and hypoperfusion in 64 (72.7%). Compared with normal perfusion patients, the odds ratio with 95% confidence interval for VCI was 12.5 (3.7-42.4) for overall hypoperfusion, 31.0 (7.1-135.5) for multiple site hypoperfusion, 3.3 (1.0-10.5) for poor collaterals, and 0.1 (0-0.6) for presence of posterior communicating artery (PcoA) compensated for posterior cerebral artery (PCA) and basilar artery (BA). Additionally, decreased scores of cognitive function tests occurred in patients with decompensated perfusion or poor collaterals.
UNASSIGNED: Hypoperfusion and poor collaterals were positively associated with cognitive impairment in patients with severe VBA. However, PcoA compensated for the PCA and BA had a protective role in cognitive impairment development.

UNASSIGNED: Post-stroke cognitive impairment (PSCI) represents a serious post-stroke complication with poor cognitive consequences. A vascular consequence after a stroke is that the occurrence and progression of PSCI may be closely related to blood pressure (BP). Thus, we systematically reviewed and performed a meta-analysis of the literature to examine the correlations between BP and PSCI.
UNASSIGNED: We systematically queried databases, including PubMed, the Cochrane Library, Embase, and Scopus, and conducted meta-analyses on studies reporting odds ratios (ORs) related to the association between BP and PSCI. Two authors autonomously assessed all titles, abstracts, and full texts and extracted data following the Meta-Analysis of Observational Studies in Epidemiology guidelines. The quality of the studies was evaluated using the modified Newcastle-Ottawa scale.
UNASSIGNED: Meta-analyses incorporated 12 articles comprising a cumulative participant cohort of 21,732 individuals. The quality assessment indicated good in five studies, fair in one study, and poor in six. Through meta-analyses, we found that hypertension, systolic or diastolic BP (SBP or DBP) was significantly associated with PSCI (OR 1.53, 95% confidence interval (CI), 1.18-1.99; p = 0.001, I 2 = 66%; OR 1.13, 95% CI, 1.05-1.23; p = 0.002, I 2 = 52%; OR 1.38, 95% CI, 1.11-1.72; p = 0.004, I 2 = 90%, respectively). In the subgroup analysis, SBP < 120 mmHg, 120-139 mmHg, 140-159 mmHg, 160-179 mmHg, and DBP ≥ 100 mmHg highly predicted the occurrence of PSCI (OR 1.15, p = 0.0003; OR 1.26, p = 0.010; OR 1.15, p = 0.05; OR 1.02, p = 0.009; OR 1.96, p < 0.00001, respectively). However, the predictive effect of BP for PSCI declines when SBP ≥ 180 mmHg and DBP ≤ 99 mmHg (p > 0.05). Statistical heterogeneity was moderate to high, and publication bias was detected in SBP for PSCI.
UNASSIGNED: Considering the multifactorial etiology of PSCI, it is difficult to conclude that BP is an independent risk factor for PSCI. Given the restricted inclusion of studies, caution is advised when interpreting the findings from this meta-analysis. Subsequent investigations with substantial sample sizes are essential to exploring BP as a prospective target for addressing PSCI.
UNASSIGNED: CRD42023437783 from PROSPERO.

Vagus nerve stimulation (VNS) is acknowledged as a highly effective therapy for various neurological conditions, including refractory epilepsy, depression, Alzheimer\'s disease (AD), migraine, and stroke. Presently, there is an increasing focus on understanding the impact of VNS on cognitive aspects. Numerous studies suggest that VNS suppresses the body\'s inflammatory response, leading to enhanced cognitive function in patients. Vascular cognitive impairment (VCI) is a severe cognitive dysfunction syndrome resulting from prolonged chronic cerebral hypoperfusion (CCH), where the primary pathogenesis is CCH-induced neuroinflammation. In this paper, we present a comprehensive overview of the research advancements in using VNS for treating VCI and discuss that VNS improves cognitive function in VCI patients by suppressing neuroinflammation, offering insights into a potential novel approach for addressing this condition.

Cerebral small vessel disease (CSVD) is a prevalent vascular disorder that has been consistently associated with vascular cognitive impairment (VCI). The diagnosis of CSVD continues to rely on magnetic resonance imaging (MRI). Epidemiological data indicate that the characteristic MRI features of CSVD, including white matter hyperintensity (WMH) and lacunar infarction, are very common among individuals over 40 years of age in community studies. This prevalence poses a significant burden on many low- and middle-income families. The amygdala plays a crucial role in integrating sensory and associative information to regulate emotional cognition. Although many previous studies have linked alterations in the amygdala to various diseases, such as depression, there has been little research on CSVD-associated alterations in the amygdala due to the complexity of CSVD. In this paper, we summarize the various imaging features of CSVD and discuss the correlation between amygdala changes and VCI. We also explore how new neuroimaging methods can assess amygdala changes early, laying a foundation for future comprehensive exploration of the pathogenesis of CSVD.

OBJECTIVE: To explore the correlations between serum levels of brain-derived neurotrophic factor (BDNF), interleukin-18 (IL-18) and hypersensitivity C-reactive protein (hs-CRP) in patients with acute cerebral infarction and vascular cognitive impairment (VCI), and to provide some clinical bases for early prevention of VCI.
METHODS: A total of 160 patients with acute cerebral infarction admitted in Department of Neurology of Jincheng People\' s Hospital from May 2019 to April 2020 were enrolled in this study and were devided into three groups according to whether or not combined with cognitive impairment, including no cognitive impairment group (NCI, 57 cases), vascular cognitive impairment no dementia group (VCIND, 56 cases) and vascular dementia group (VaD, 47 cases). The cognitive function of all the patients were evaluated by Montreal cognitive assessment (MoCA). The National Institute of Health stroke scale (NIHSS) was used to assess the degree of neurological deficit (mild-, moderate-, severe-neurologic deficit group). The infarct size was calculated by Pullicino\' s method (small-, middle-, large-infarct group). The levels of serum BDNF and IL-18 were measured by enzyme-linked immunosorbent assay (ELISA), and serum levels of hs-CRP were measured by immunoturbidimetry during the acute phase (0-7 d), recovery period (15-30 d) and 6 months after cerebral infarction. The effects of varying degrees of neurological deficits and different size of infarction on BDNF, IL-18 and hs-CRP were observed. The levels of serum BDNF, IL-18 and hs-CRP in the patients of the three groups with acute, convalescent and six-month cerebral infarction were compared, and their correlations with VCI were analyzed.
RESULTS: Serum BDNF level and MoCA scores in mild-neurologic deficit group and small-infarct group were significantly higher than those in moderate- and severe-deficit group, middle- and large-infarct group, respectively (P < 0.05). Their levels of IL-18 and hs-CRP were significantly lower than those in moderate- and severe-deficit group, middle- and large-infarct group, respectively (P < 0.05). The levels of serum BDNF in NCI group, VCIND group and VaD group during the acute phase, convalescence and 6 months after cerebral infarction were in a significant decline, and the differences during the acute phase and recovery period were statistically significant (P < 0.05). The levels of IL-18 and hs-CRP during the acute phase, recovery period and 6 months after cerebral infarction showed a significant increasing trend with significance (P < 0.05). Correlation analysis revealed that the levels of BDNF was positively correlated with MoCA scores but negatively correlated with the severity of cognitive impairment while the expression levels of IL-18 and hs-CRP were negatively correlated with MoCA scores but positively correlated with the severity of cognitive impairment.
CONCLUSIONS: Serum BDNF, IL-18 and hs-CRP are involved in the pathological process of occurrence and development of VCI in the patients with acute cerebral infarction. BDNF has a protective effect on VCI while IL-18 and hs-CRP cause severe cognitive impairment. The levels of serum BDNF、IL-18 and hs-CRP in the patients with acute ischemic cerebral infarction are closely related to the severity of cognitive impairment and can be used as biomarkers of early diagnosis of VCI.

UNASSIGNED: Vascular cognitive impairment (VCI) manifests in memory impairment, mental slowness, executive dysfunction, behavioral changes, and visuospatial abnormalities, significantly compromising the quality of daily life for patients and causing inconvenience to caregivers. Neuroimaging serves as a crucial approach to evaluating the extent, location, and type of vascular lesions in patients suspected of VCI. Nevertheless, there is still a lack of comprehensive bibliometric analysis to discern the research status and emerging trends concerning VCI neuroimaging.
UNASSIGNED: This study endeavors to explore the collaboration relationships of authors, countries, and institutions, as well as the research hotspots and frontiers of VCI neuroimaging by conducting a bibliometric analysis.
UNASSIGNED: We performed a comprehensive retrieval within the Core Collection of Web of Science, spanning from 2000 to 2023. After screening the included literature, CiteSpace and VOSviewer were utilized for a visualized analysis aimed at identifying the most prolific author, institution, and journal, as well as extracting valuable information from the analysis of references.
UNASSIGNED: A total of 1,024 publications were included in this study, comprising 919 articles and 105 reviews. Through the analysis of keywords and references, the research hotspots involve the relationship between neuroimaging of cerebral small vessel disease (CSVD) and VCI, the diagnosis of VCI, and neuroimaging methods pertinent to VCI. Moreover, potential future research directions encompass CSVD, functional and structural connectivity, neuroimaging biomarkers, and lacunar stroke.
UNASSIGNED: The research in VCI neuroimaging is constantly developing, and we hope to provide insights and references for future studies by delving into the research hotspots and frontiers within this field.

UNASSIGNED: This study aims to examine the alterations in aberrant brain activity and network connectivity between individuals with mild and major vascular cognitive impairment (VCI).
UNASSIGNED: A total of 114 patients with cerebral small vessel disease (CSVD) were included in this study, comprising 61 individuals with mild VCI (mean age, 55.7 ± 6.9 years; male, 42.6%) and 53 cases with major VCI (mean age, 57.6 ± 5.5 years; male, 58.5%). Additionally, 53 age-, gender-, and education-matched healthy subjects were recruited as normal controls (NC) (mean age, 54.9 ± 7.9 years; male, 52.9%). All participants underwent neuropsychological assessments and magnetic resonance imaging scans. One-way analysis of variance was used to compare fractional amplitude of low-frequency fluctuation (fALFF) values among the three groups. Two-sample t-tests were conducted to assess functional connectivity matrices between different groups for each connection. Moreover, mediation analyses were performed to explore the mediating effect of aberrant brain activity on the relationship between cognitive impairment and CSVD total burden.
UNASSIGNED: VCI patients exhibited aberrant brain activity in regions such as the right thalamus (THA_R), right cuneus (CUN_R), left postcentral gyrus (PoCG_L), right postcentral gyrus (PoCG_R), right median cingulate, paracingulate gyri (PCG_R), and left precuneus (PCUN_L). Reduced positive functional connectivity was predominantly observed among nodes including PCUN_L, CUN_R, PoCG_L, PoCG_R, right posterior cingulate (PCG_R), and left occipital gyrus (IOG_L) in VCI patients. The aberrant baseline brain activity and disrupted brain network were more pronounced with worsening cognitive function. Increased fALFF values in THA_R, CUN_R, and PoCG_L mediated cognitive impairment in CSVD patients.
UNASSIGNED: Abnormal brain activities in THA_R, CUN_R, and PoCG_L, along with their associated abnormal functional connections, play a significant role in VCI. The study revealed a progressive increase in aberrant brain activity and network connectivity with advancing stages of VCI.

BACKGROUND: The purpose of this study was to investigate the relationship between blood-brain barrier (BBB) permeability and cognitive functioning in healthy older adults and individuals with neurodegenerative diseases.
RESULTS: A total of 124 participants with Alzheimer disease, cerebrovascular disease, or a mix Alzheimer\'s and cerebrovascular diseases and 55 controlparticipants underwent magnetic resonance imaging and neuropsychological testing. BBB permeability was measured with dynamic contrast-enhanced magnetic resonance imaging and white matter injury was measured using a quantitative diffusion-tensor imaging marker of white matter injury. Structural equation modeling was used to examine the relationships between BBB permeability, vascular risk burden, white matter injury, and cognitive functioning. Vascular risk burden predicted BBB permeability (r=0.24, P<0.05) and white matter injury (r=0.38, P<0.001). BBB permeability predicted increased white matter injury (r=0.34, P<0.001) and increased white matter injury predicted lower cognitive functioning (r=-0.51, P<0.001).
CONCLUSIONS: The study provides empirical support for a vascular contribution to white matter injury and cognitive impairment, directly or indirectly via BBB permeability. This highlights the importance of targeting modifiable vascular risk factors to help mitigate future cognitive decline.