Exploring the therapeutic potential of Qi Teng Mai Ning recipe in ischemic stroke and vascular cognitive impairment

Background:This study aims to explore the therapeutic effects of the Qi Teng Mai Ning recipe on ischemic stroke and vascular cognitive impairment through its potential to modulate cellular autophagy,with a focus on identifying its active ingredients and their target proteins.Methods:The study began with the identification of active ingredients in the Qi Teng Mai Ning recipe.It proceeded to screen the gene expression omnibus database for ischemic stroke and vascular cognitive impairment-associated differentially expressed mRNAs and to identify cellular autophagy-related proteins via the Human Autophagy Database.These proteins were annotated with Gene Ontology and Kyoto Encyclopedia of Genes and Genomes functions and subjected to molecular docking with the recipe’s core active ingredients.In vitro cell experiments were conducted on hypoxic HT22 cells,involving CCK8 assay,lentiviral transfection to silence autophagy related 9B(ATG9B),immunofluorescence staining,and qPCR validation to investigate the effects of the recipe on autophagy.Results:The analysis identified 104 active ingredients targeting 408 proteins and forming a complex ingredient-target network.Intersecting 55 ischemic stroke-related and 909 vascular cognitive impairment-related differentially expressed mRNAs revealed 14 co-expressed mRNAs.Molecular docking showed quercetin,kaempferol,myrcene,and conferone as key ingredients targeting autophagy-related proteins.Cellular experiments indicated that the recipe significantly enhanced cell viability under hypoxic conditions,reduced apoptosis,and modulated the expression of autophagy-related factors,thereby decreasing apoptosis rates in HT22 cells.Conclusion:The Qi Teng Mai Ning recipe offers protective effects against ischemic stroke and vascular cognitive impairment by modulating autophagy-related proteins.Its efficacy highlights the potential of traditional Chinese medicine in treating these conditions,though further research is needed to fully understand its mechanisms and clinical applications.

Comparative efficacy and safety of cognitive enhancers for treating vascular cognitive impairment: systematic review and Bayesian network meta-analysis

Objective: To assess and compare the clinical efficacy and safety of cognitive enhancers(donepezil, galantamine, rivastigmine, and memantine) on cognition, behavior, function, and global status in patients with vascular cognitive impairment.Data sources: The initial literature search was performed with PubMed, EMBASE, the Cochrane Methodology Register, the Cochrane Central Register of Controlled Trials, and Cumulative Index to Nursing & Allied Health(CINAHL) from inception to January 2018 for studies regarding donepezil, galantamine, rivastigmine, and memantine for treatment of vascular cognitive impairment.Data selection: Randomized controlled trials on donepezil, galantamine, rivastigmine, and memantine as monotherapy in the treatment of vascular cognitive impairment were included. A Bayesian network meta-analysis was conducted. Outcome measures: Efficacy was assessed by changes in scores of the Alzheimer's Disease Assessment Scale, cognitive subscale, Mini-Mental State Examination, Neuropsychiatric Inventory scores and Clinician's Interview-Based Impression of Change Scale Plus Caregiver's Input, Activities of Daily Living, the Clinical Dementia Rating scale. Safety was evaluated by mortality, total adverse events(TAEs), serious adverse events(SAEs), nausea, vomiting. diarrhea, or cerebrovascular accidents(CVAs). Results: After screening 1717 citations, 12 randomized controlled trials were included. Donepezil and rivastigmine(mean difference(e) = –0.77, 95% confidence interval(CI): 0.25–1.32; MD = 1.05, 95% CI: 0.18–1.79) were significantly more effective than placebo in reducing Mini-Mental State Examination scores. Donepezil, galantamine, and memantine(MD = –1.30, 95% CI: –2.27 to –0.42; MD = –1.67, 95% CI: –3.36 to –0.06; MD = –2.27, 95% CI: –3.91 to –0.53) showed superior benefits on the Alzheimer's Disease Assessment Scale–cognitive scores compared with placebo. Memantine(MD = 2.71, 95% CI: 1.05–7.29) improved global status(Clinician's Interview-Based Impression of Change Scale Plus Caregiver's Input) more than the placebo. Safety results revealed that donepezil 10 mg(odds ratio(OR) = 3.04, 95% CI: 1.86–5.41) contributed to higer risk of adverse events than placebo. Galantamine(OR = 5.64, 95% CI: 1.31–26.71) increased the risk of nausea. Rivastigmine(OR = 16.80, 95% CI: 1.78–319.26) increased the risk of vomiting. No agents displayed a significant risk of serious adverse events, mortality, cerebrovascular accidents, or diarrhea.Conclusion: We found significant efficacy of donepezil, galantamine, and memantine on cognition. Memantine can provide significant efficacy in global status. They are all safe and well tolerated.

Microbleeds in fronto-subcortical circuits are predictive of dementia conversion in patients with vascular cognitive impairment but no dementia

Cerebral small vessel disease（CSVD） is a common etiology of vascular cognitive impairment with no dementia（V-CIND）. Studies have revealed that cerebral microbleeds（CMBs）, a feature of CSVD, contribute to cognitive impairment. However, the association between CMBs and dementia conversion in individuals with V-CIND is still unclear. Here, we analyzed the predictive role of CMBs in the conversion from V-CIND to dementia in CSVD patients. We recruited and prospectively assessed 85 patients with CSVD and V-CIND. V-CIND was evaluated using a series of comprehensive neuropsychological scales, including the Chinese version of the Montreal Cognitive Assessment and the Clinical Dementia Rating. MRI assessments were used to quantify lacunar infarcts, white matter hyperintensities, CMBs, and medial temporal lobe atrophy. Eighty-two of the 85 patients completed the assessment for dementia conversion at a 1-year follow-up assessment. Multivariate logistic regression analyses were conducted to examine independent clinical and MRI variables associated with dementia conversion. Twenty-four patients（29.3%） had converted to dementia at the 1-year follow-up, and these individuals had significantly more CMBs in the fronto-subcortical circuits. Multivariate logistic regression analyses revealed that the patients with CMBs in the fronto-subcortical circuits（odds ratio = 4.4; 95% confidence interval： 1.602-12.081, P = 0.004） and 5 or more CMBs overall（odds ratio = 17.6, 95% confidence interval： 3.23-95.84, P = 0.001） had a significantly increased risk of dementia at the 1-year follow-up. These findings indicate that CMBs in the fronto-subcortical circuits may be predictive of dementia conversion in CSVD patients with V-CIND, and thus extend the clinical significance of CMBs.

Microstructural damage pattern of vascular cognitive impairment: a comparison between moyamoya disease and cerebrovascular atherosclerotic disease

Moyamoya disease and cerebrovascular atherosclerotic disease are both chronic ischemic diseases with similar presentations of vascular cognitive impairment. The aim of the present study was to investigate the patterns of microstructural damage associated with vascular cognitive impairment in the two diseases. The study recruited 34 patients with moyamoya disease(age 43.9 ± 9.2 years; 20 men and 14 women, 27 patients with cerebrovascular atherosclerotic disease(age: 44.6 ± 7.6 years; 17 men and 10 women), and 31 normal controls(age 43.6 ± 7.3 years; 18 men and 13 women) from Huashan Hospital of Fudan University in China. Cognitive function was assessed using the Mini-Mental State Examination, long-term delayed recall of Auditory Verbal Learning Test, Trail Making Test Part B, and the Symbol Digit Modalities Test. Single-photon emission-computed tomography was used to examine cerebral perfusion. Voxel-based morphometry and tract-based spatial statistics were performed to identify regions of gray matter atrophy and white matter deterioration in patients and normal controls. The results demonstrated that the severity of cognitive impairment was similar between the two diseases in all tested domains. Patients with moyamoya disease and those with cerebrovascular atherosclerotic disease suffered from disturbed supratentorial hemodynamics. Gray matter atrophy in bilateral middle cingulate cortex and parts of the frontal gyrus was prominent in both diseases, but in general, was more severe and more diffuse in those with moyamoya disease. White matter deterioration was significant for both diseases in the genu and body of corpus callosum, in the anterior and superior corona radiation, and in the posterior thalamic radiation, but in moyamoya disease, it was more diffuse and more severe. Vascular cognitive impairment was associated with regional microstructural damage, with a potential link between, gray and white matter damage. Overall, these results provide insight into the pathophysiological nature of vascular cognitive impairment. This study was approved by the Institutional Review Board in Huashan Hospital, China(approval No. 2014-278). This study was registered with ClinicalTrials.gov on December 2, 2014 with the identifier NCT02305407.

Diagnosis advances in vascular cognitive impairment

Vascular cognitive impairment（VCI） encompasses the entire range of cognitive deficits associated with cerebrovascular disease（CVD）, from mild deficits with little or no functional impairment, such as vascular cognitive impairment-no dementia（VCIND）, to full-blown vascular dementia（VaD）. Accurate diagnosis of vascular cognitive impairment is important but may be difficult. In this review we report advances in VCI in the following areas： etiology, subtypes, neuropsychology, biomarkers, neuroimaging, and diagnostic criteria.

Vascular endothelial growth factor B improves impaired glucose tolerance through insulin-mediated inhibition of glucagon secretion

BACKGROUND Impaired glucose tolerance(IGT)is a homeostatic state between euglycemia and hyperglycemia and is considered an early high-risk state of diabetes.When IGT occurs,insulin sensitivity decreases,causing a reduction in insulin secretion and an increase in glucagon secretion.Recently,vascular endothelial growth factor B(VEGFB)has been demonstrated to play a positive role in improving glucose metabolism and insulin sensitivity.Therefore,we constructed a mouse model of IGT through high-fat diet feeding and speculated that VEGFB can regulate hyperglycemia in IGT by influencing insulin-mediated glucagon secretion,thus contributing to the prevention and cure of prediabetes.AIM To explore the potential molecular mechanism and regulatory effects of VEGFB on insulin-mediated glucagon in mice with IGT.METHODS We conducted in vivo experiments through systematic VEGFB knockout and pancreatic-specific VEGFB overexpression.Insulin and glucagon secretions were detected via enzyme-linked immunosorbent assay,and the protein expression of phosphoinositide 3-kinase(PI3K)/protein kinase B(AKT)was determined using western blot.Further,mRNA expression of forkhead box protein O1,phosphoenolpyruvate carboxykinase,and glucose-6 phosphatase was detected via quantitative polymerase chain reaction,and the correlation between the expression of proteins was analyzed via bioinformatics.RESULTS In mice with IGT and VEGFB knockout,glucagon secretion increased,and the protein expression of PI3K/AKT decreased dramatically.Further,in mice with VEGFB overexpression,glucagon levels declined,with the activation of the PI3K/AKT signaling pathway.CONCLUSION VEGFB/vascular endothelial growth factor receptor 1 can promote insulin-mediated glucagon secretion by activating the PI3K/AKT signaling pathway to regulate glucose metabolism disorders in mice with IGT.

Depressive Symptom Endorsement among Alzheimer’s Disease, Vascular Dementia and Mild Cognitive Impairment

Background: The Geriatric Depression Scale (GDS) is widely used to assess depressive symptoms in clinical and research settings. This study utilized a 4 factor solution for the 30-item GDS to explore differences in the presentation of depressive symptoms in various types of cognitive impairment. Method: Retrospective chart review was conducted on 254 consecutive cases of community dwelling elderly newly diagnosed with mild Alzheimer’s Dementia (AD) n = 122, mild Vascular Dementia (VaD) n = 71 or Amnestic Mild Cognitive Impairment (aMCI) n = 32 and Non-Amnestic MCI (nMCI) n = 29. Results: Analysis revealed no significant differences (p 05). No statistically significant differences were found between VaD and nMCI or between the MCI groups. Conclusions: Support is provided for the use of GDS subscales in a wide range of cognitively impaired elderly. This study suggests in mild dementia the number and type of depressive symptoms vary significantly between AD and VaD. There are indications that aMCI patients are similar in their symptom endorsement to AD and nMCI are similar to VaD which is consistent with some of the notions regarding likely trajectories of the respective MCI groups.

Research Progress on the Relationship Between White Matter Lesions and Vascular Cognitive Impairment

As the incidence of cerebrovascular disease increases,the incidence of white matter lesions (WMLs) and vascular cognitive impairment (VCI) also increases.Ischemic WMLs is directly related to VCI,especially non-dementia VCI.Early symptoms of non-dementia VCI are hidden and difficult to identify.About 50% of patients develop dementia.This article reviews the correlation between WMLs and VCI in terms of etiology,risk factors,pathogenesis and imaging manifestations.It provides scientific basis or ideas for clinical diagnosis and treatment for WMLs and VCI.

Characterization of cerebrovascular changes in Alzheimer's disease mice by photoacoustic imaging

The cerebral vasculature plays a significant role in the development of Alzheimer's disease(AD),however,the specific association between them remains unclear.In this paper,based on the benefits of photoacoustic imaging(PAI),including label-free,high-resolution,in vivo imaging of vessels,we investigated the structural changes of cerebral vascular in wild-type(WT)mice and AD mice at different ages,analyzed the characteristics of the vascular in different brain regions,and correlated vascular characteristics with cognitive behaviors.The results showed that vascular density and vascular branching index in the cortical and frontal regions of both WT and AD mice decreased with age.Meanwhile,vascular lacunarity increased with age,and the changes in vascular structure were more pronounced in AD mice.The trend of vascular dysfunction aligns with the worsening cognitive dysfunction as the disease progresses.Here,we utilized in vivo PAI to analyze the changes in vascular structure during the progression of AD,elucidating the spatial and temporal correlation with cognitive impairment,which will provide more intuitive data for the study of the correlation between cerebrovascular and the development of AD.

Sevoflurane effects on cyclic adenosine monophosphate response element binding protein,phosphorylated cyclic adenosine monophosphate response element binding protein,and Livin expression in the cortex and hippocampus of a vascular cognitive impairment rat

BACKGROUND： Neuronal necrosis and apoptosis play important roles in the pathophysiology of cerebral ischemia and resulting cognitive impairment. However, inhibition of neuronal necrosis and apoptosis has been shown to attenuate cognitive impairment following cerebral ischemia. OBJECTIVE： To investigate the effects of sevoflurane on cyclic adenosine monophosphate response element binding protein （CREB）, phosphorylated CREB （pCREB）, and Livin expression in the cortex and hippocampus of a rat model of vascular cognitive impairment.DESIGN, TIME AND SETTING： A randomized, controlled experiment was performed in the Chongqing Key Laboratory of Neurology between June 2007 and July 2008.MATERIALS： Sevoflurane was provided by Abbott Laboratory, UK; Morris water maze was provided by Chinese Academy of Medical Sciences, China; goat anti-rat CREB, goat anti-rat pCREB and goat anti-rat Livin antibodies were provided by Biosource International, USA. METHODS： A total of 42 female, Wistar rats were randomly assigned to the following groups： sham operation, vascular cognitive impairment, and sevoflurane treatment. The vascular cognitive impairment rat model was established by permanent bilateral occlusion of both common carotid arteries, and 1.0 MAC sevoflurane was immediately administered by inhalation for 2 hours. MAIN OUTCOME MEASURES： CREB, pCREB, and Livin expression was measured in the cortex and hippocampus by Western blot and reverse transcription-polymerase chain reaction. Behavior was evaluated with Morris water maze. RESULTS： CREB, pCREB, and Livin expression in the sevoflurane treatment group was significantly greater than the vascular cognitive impairment group （P 〈 0.01）. However, expression of CREB and pCREB was significantly less in the sevoflurane treatment and vascular cognitive impairment groups, compared with the sham operation group （P 〈 0.01）. Livin expression in the sevoflurane treatment and vascular cognitive impairment groups was significantly greater than the sham operation group （P 〈 0.01）. Learning, memory, and behavior disorders were observed in the vascular cognitive impairment group. Sevoflurane treatment significantly improved these observed disorders. CONCLUSION： Sevoflurane improved cognitive impairment due to permanent bilateral occlusion of both common carotid arteries. Improved function was associated with increased CREB, pCREB, and Livin expression in the cortex and hippocampus.

Information entropy-based fitting of the disease trajectory of brain ischemia-induced vascular cognitive impairment

The present study investigated the disease trajectory of vascular cognitive impairment using the entropy of information in a neural network mathematical simulation based on the free radical and excitatory amino acids theories. Glutamate, malondialdehyde, and inducible nitric oxide synthase content was significantly elevated, but acetylcholine, catalase, superoxide dismutase, glutathione peroxidase and constitutive nitric oxide synthase content was significantly decreased in our vascular cognitive impairment model. The fitting curves for each factor were obtained using Matlab software. Nineteen, 30 and 49 days post ischemia were the main output time frames of the influence of these seven factors. Our results demonstrated that vascular cognitive impairment involves multiple factors. These factors include excitatory amino acid toxicity and nitric oxide toxicity. These toxicities disrupt the dynamic equilibrium of the production and removal of oxygen free radicals after cerebral ischemia, reducing the ability to clear oxygen free radicals and worsening brain injury.

Expert Consensus on the Clinical Application of Tianma Xingnao Capsule in the Treatment of Vascular Cognitive Impairment and Neuropathic Headache

The prescription of Tianma Xingnao Capsule is composed of Gastrodiae Rhizoma,Pheretima,Acori Tatarinowii Rhizoma,Polygalae Radix,Rehmanniae Radix Praeparata,and Cistanches Herba.It has effects of nourishing liver and kidney,dredging collaterals and relieving pain.More than 20 years of clinical application and evidence-based medical research have shown that Tianma Xingnao Capsule has a significant therapeutic effect on vascular cognitive impairment and neuropathic headache.In order to further guide the proper clinical use of this prescription,the consensus expert group conducted a comprehensive analysis of the prescription of Tianma Xingnao Capsule.Combining the existing evidence-based medicine evidence and the experience of clinical experts,this consensus report standardized the usage,dosage,duration and safety of Tianma Xingnao Capsule in the treatment of vascular cognitive impairment and neuropathic headache.It is expected to provide a theoretical basis for clinically reasonable and safe use of Tianma Xingnao Capsule.

Advances in multimodal magnetic resonance imaging of vascular mild cognitive impairment

Vascular mild cognitive impairment(VaMCI)represents the early stage of symptoms of vascular cognitive impairment(VCI).There are many intervention factors in this period.If the active treatment can delay the further development of the disease and even reduce the risk of transforming into vascular dementia(VaD).As a widely used imaging method,multi-mode magnetic resonance imaging can evaluate the brain structure and function of patients with VaMCI noninvasively and explore the relationship between brain structure,function and cognitive function change.It is beneficial to provide an idea for early diagnosis of VaMCI and to further understand the neuropathologic mechanism of its occurrence,which has broad application prospects.In this paper,the research status and new methods of VaMCI are reviewed by using multi-mode magnetic resonance imaging in recent years.

Disrupted functional connectivity of default mode network and executive control network in patients with vascular cognitive impairment, no dementia

Objective： To investigate functional connectivity within default mode network （DMN） and ex-ecutive control network （ECN） in vascular cognitive im-pairment, no dementia （VCIND）. Methods： Twenty-eight VCIND patients and sixteen healthy controls were recruit-ed. A seed-based connectivity analysis was performed us-ing data from resting-state functional magnetic resonance imaging （fMRI）. Based on previous fndings, posteriorcingulate cortex （PCC） and dorsolateral prefrontal cortex （DLPFC） were chosen as regions of interest to study these networks.One-sample t-test and two-sample t-test were used for statistical analysis. Results： Compared with thecontrols, the VCIND group exhibited increased functional activity in such DMN regions as the left inferior temporal gyrus, parahippocampal gyrus, and medial frontal gyrus. The VCIND group had decreased functional connectivity of DMN at right superior frontal gyrus, left mid-cingu-late area, the medial part of left superior frontal gyrus, and bilateral medial frontal gyrus. The VCIND group also showed decreased functional connectivity of ECN pri-marilyat left inferior parietal gyrus, right angular gyrus, right middle occipital gyrus, and right middle frontal cor-tex. Conclusions： Increased functional connectivity with-in DMN and decreased functional connectivity within ECN suggested dysfunction of these two networks, which mightbe associated with the cognitive defcitsin patients with VCIND. These fndingsmay help usunderstandthe pathogenesis and clinical characteristics of VCIND.

Advances in the Pathogenesis of Vascular Cognitive Impairment

As the population ages,the number of patients with vascular cognitive impairment(VCI)increases,which increases the burden on patient's family and social.At present,the treatment and pathogenesis of VCI is still unclear.This paper reviews the literature on VCI pathogenesis,especially the molecular mechanism(oxidative stress,endoplasmic reticulum stress,inflammation,autophagy.),aiming to provide direction and reference for VCI pathogenesis research and target therapy.

Clinical Study of Endovascular Treatment of Severe Middle Cerebral Artery Stenosis or Occlusion and Vascular Cognitive Impairment

It is very important to study the factors affecting the incidence,progress and prognosis of patients with vascular dementia.50 cases of severe middle cerebral artery stenosis or occlusion underwent endovascular treatment(25 cases of mild cognitive dysfunction,25 cases of moderate cognitive dysfunction)were divided into two groups,where a medical drug treatment group and a control group established with 25 cases in each group.The cognitive function of each group of patients was evaluated before operation,7 days after operation,30 days after operation,and 180 days after operation.CTP was used to compare the hemodynamic changes in patients before and after operation.The severe stenosis or occlusion of the middle cerebral artery in patients can be improved,and the intracranial blood supply of patients with poorly compensated medial cranial circulation and hypoperfusion can be restored to a certain extent.Meanwhile,improvement of cognitive function was definitive in some patients with cognitive dysfunction.To guide the formulation of treatment plans for patients with severe middle cerebral artery stenosis or occlusion.

Changes in HIF-1α, VEGF, NGF and BDNF Levels in Cerebrospinal Fluid and TheirRelationship with Cognitive Impairment in Patients with Cerebral Infarction

Summary： This study was carried out to investigate the role of intrinsic neuroprotective mechanisms in the occurrence and development of vascular cognitive impairment （VCI） with the goal of providing a target for the treatment and prevention of VCI. Inpatients with proven cerebral infarction on cranial computed tomography （CT） were recruited as the ischemic cerebrovascular diseases （ICVD） group, and the patients with mixed stroke were excluded. In ICVD group, 12 patients were diagnosed as having VCI and served as VCI group. Inpatients undergoing surgical operation in our hospital were enrolled as control group. Double-antibody sandwich enzyme-linked immunosorbent assay （ELISA） was employed to detect the levels of hypoxia-inducible factor 1-alpha （HIF-1α）, vascular endothelial growth factor （VEGF）, nerve growth factor （NGF） and brain-derived neurotrophic factor （BDNF） in the cerebrospinal fluid of patients with ICVD. Associations between the levels of these factors and the Mini-Mental State Examination （MMSE） score were evaluated. In ICVD and VCI groups, the levels of HIF-1α and NGF in the cerebrospinal fluid were markedly lower than those in control group （P=-0.037 and P=0.000; P=0.023 and P=-0.005）. In ICVD and VCI groups, the MMSE score was negatively related to VEGF level in the cerebrospinal fluid （r=-0.327, P=0.021; r=-0.585, P=0.046）. In VCI group, HIF-1α level was correlated with NGF level （r=0.589, P=0.044）. HIF-1α and NGF are involved in ischemic and hy- poxic cerebral injury. The HIF signaling pathway plays an important role in intrinsic neuroprotection. Upregulation and maintenance of HIF-1α and NGF expression may attenuate VCI. Changes in VEGF levels are related to the occurrence and development of cognitive impairment.

阿托伐他汀联合胞磷胆碱治疗脑小血管病轻度认知障碍疗效观察

目的 分析阿托伐他汀联合胞磷胆碱治疗脑小血管病(CSVD)轻度认知障碍(MCI)的疗效及对患者血-脑屏障功能和炎症因子的影响。方法 选取2021-03—2023-03自贡市第四人民医院收治的102例CSVD合并MCI患者为研究对象,分为观察组与对照组各51例。对照组口服胞磷胆碱钠片,观察组在对照组基础上加用阿托伐他汀钙片口服,2组均持续治疗3个月。治疗结束后比较2组患者临床疗效,以及治疗前、治疗3个月后蒙特利尔评定量表(MoCA)评分、血-脑屏障功能、炎症因子水平[血清C反应蛋白(CRP)、白细胞介素-6(IL-6)]和血脂水平[总胆固醇(TC)、甘油三酯(TG)和低密度脂蛋白(LDL-C)],记录治疗期间不良反应。结果 治疗后观察组总有效率优于对照组(94.12%比78.43%,P<0.05)。2组患者MoCA评分较治疗前均显著升高,观察组为(27.07±1.05)分,高于对照组的(25.89±1.54)分(P<0.05)。2组患者治疗后伊文思蓝水平、血清CRP、IL-6水平、血清TC、TG和LDL-C水平较治疗前均降低,观察组分别为(10.29±1.17)μg/g、(4.67±1.03)mg/L、(101.76±10.54)ng/L、(2.06±0.46)mmol/L、(1.65±0.32)mmol/L、(1.84±0.30)mmol/L,均低于对照组的(13.87±1.56)μg/g、(6.93±1.78)mg/L、(109.34±11.12)ng/L、(3.24±0.49)mmol/L、(2.24±0.48)mmol/L、(2.39±0.46)mmol/L(P<0.05)。2组患者治疗期间相关不良反应发生率无统计学差异(7.84%比5.88%,P>0.05)。结论 阿托伐他汀联合胞磷胆碱治疗CSVD合并MCI疗效确切,有利于改善患者认知功能、血-脑屏障功能,并降低炎症因子和脂质代谢水平。

糖尿病前期对皮质下缺血性血管性认知障碍的影响

目的探讨糖尿病前期对皮质下缺血性血管性认知障碍(SIVCI)的影响。方法回顾性分析2017年4月至2022年7月于作者医院就诊的皮质下缺血性脑血管病(SIVD)患者242例。依据认知功能分为血管性痴呆组(VaD),轻度认知障碍组(vMCI)以及无认知障碍组(NoCI),记录并应用单因素分析比较各组一般临床资料以及空腹血糖、糖化血红蛋白等生化指标,以及颅内脑白质病变(WMLs)的Fazekas评分、腔隙性脑梗死评级等影像学指标的差异,并将组间差异有统计学意义(P<0.05)的指标纳入有序Logistic回归方程,分析SIVD发生SIVCI的危险因素。结果VaD组及vMCI组的受教育程度低于NoCI组,高血压、糖代谢异常的患者比例高于NoCI组,而VaD组糖尿病患者比例高于vMCI组(均P<0.05),VaD组与vMCI组的受教育程度、高血压、糖尿病前期患者比例差异无统计学意义(P>0.05);VaD组的MMSE评分低于vMCI组及NoCI组,重度WMLs患者比例高于vMCI组及NoCI组,vMCI组MMSE评分低于NoCI组(均P<0.05),vMCI组与NoCI组的重度WMLs比例差异无统计学意义(P>0.05)。有序Logistic回归分析提示糖尿病〔OR(95%CI)=2.921(1.636~5.215),P=0.001〕及糖尿病前期〔OR(95%CI)=2.743(1.461~5.150),P=0.002〕均是SIVD患者发生SIVCI的危险因素。受教育程度低〔OR(95%CI)=0.861(0.811~0.914),P=0.001〕、有高血压史〔OR(95%CI)=1.867(1.089~3.201),P=0.023〕、重度WMLs〔OR(95%CI)=2.227(1.344~3.690),P=0.002〕也是发生SIVCI的危险因素。结论除了受教育程度低、高血压史以及重度WMLs以外,糖尿病前期及糖尿病也是SIVD患者发生认知障碍的危险因素。对SIVD患者早期进行糖代谢筛查,在糖尿病前期进行血糖干预有助于预防SIVCI发生。

静息态功能磁共振成像在血管性认知障碍患者默认网络研究中的应用进展

血管性认知障碍是由脑血管疾病导致的一种从轻度认知功能障碍至痴呆的综合征,由于缺乏敏感性和特异性生物标志物,早期不易鉴别和诊断。血管性认知障碍患者脑网络连接异常的脑区多位于默认网络,其异常变化的功能连接与患者的认知障碍程度相关。静息态功能磁共振成像技术是一种常用的检测静息态大脑内在活动的方法,应用静息态磁共振不同分析技术探索血管性认知障碍患者默认网络异常变化有助于深入研究血管性认知障碍的发病机制,并提供客观的影像依据。该文主要综述静息态功能磁共振成像技术在血管性认知障碍患者默认网络研究中的应用成果,为血管性认知障碍的精准诊断和评估提供新思路。