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cognitive impairment in two subtypes of a single subcortical infarction

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Chinese Medical Journal 2021年第24期134卷 2992-2998页

作者： Tang Yang Qiao Deng Shuai Jiang Yu-Ying Yan Ye Yuan Si-Miao Wu Shu-Ting Zhang Jia-Yu Sun Bo Wu Department of Neurology West China HospitalSichuan UniversityChengduSichuan 610041China Department of Radiology Affiliated Hospital of North Sichuan Medical CollegeNanchongSichuan 637000China Department of Radiology West China HospitalSichuan UniversityChengduSichuan 610041China

Background:Single subcortical infarction(SSI)is caused by two main etiological subtypes,which are branch atheromatous disease(BAD)and cerebral small vessel disease(CSVD)-related SSI.We applied the Beijing version of the Montreal cognitive Assessment(MoCA-BJ),the Shape Trail Test(STT),and the Stroop Color and Word Test(SCWT)to investigate the differences in cognitive performance between these two subtypes of SSI.Methods:Patients with acute SSIs were prospectively enrolled.The differences of MoCA-BJ,STT,and SCWT between the BAD group and CSVD-related SSI group were analyzed.A generalized linear model was used to analyze the associations between SSI patients with different etiological mechanisms and cognitive function.We investigated the correlations between MoCA-BJ,STT,and SCWT using Spearman’s correlation analysis and established cut-off scores for Shape Trail Test A(STT-A)and STT-B to identify cognitive impairment in patients with SSI.Results:This study enrolled a total of 106 patients,including 49 and 57 patients with BAD and CSVD-related SSI,respectively.The BAD group performances were worse than those of the CSVD-related SSI group for STT-A(83[60.5-120.0]vs.68[49.0-86.5],P=0.01),STT-B(204[151.5-294.5]vs.153[126.5-212.5],P=0.015),and the number of correct answers on Stroop-C(46[41-49]vs.49[45-50],P=0.035).After adjusting for age,years of education,National Institutes of Health Stroke Scale and lesion location,the performance of SSI patients with different etiological mechanisms still differed significantly for STT-A and STT-B.Conclusions:BAD patients were more likely to perform worse than CSVD-related SSI patients in the domains of language,attention,executive function,and memory.The mechanism of cognitive impairment after BAD remains unclear.

关键词： Brain cognitive impairment Cerebral small vessel disease Subcortical infarction Stroke

cognitive impairment in multiple sclerosis: lessons from cerebrospinal fluid biomarkers

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Neural Regeneration Research 2021年第1期16卷 36-42页

作者： Lorenzo Gaetani Nicola Salvadori Elena Chipi Lucia Gentili Angela Borrelli Lucilla Parnetti Massimiliano Di Filippo Section of Neurology Department of MedicineUniversity of PerugiaPerugiaItaly

cognitive impairment is a common clinical manifestation of multiple sclerosis,but its pathophysiology is not completely understood.White and grey matter injury together with synaptic dysfunction do play a role.The measurement of biomarkers in the cerebrospinal fluid and the study of their association with cognitive impairment may provide interesting in vivo evidence of the biological mechanisms underlying multiple sclerosis-related cognitive impairment.So far,only a few studies on this topic have been published,giving interesting results that deserve further investigation.Cerebrospinal fluid biomarkers of different pathophysiological mechanisms seem to reflect different neuropsychological patterns of cognitive deficits in multiple sclerosis.The aim of this review is to discuss the studies that have correlated cerebrospinal fluid markers of immune,glial and neuronal pathology with cognitive impairment in multiple sclerosis.Although preliminary,these findings suggest that cerebrospinal fluid biomarkers show some correlation with cognitive performance in multiple sclerosis,thus providing interesting insights into the mechanisms underlying the involvement of specific cognitive domains.

关键词： biomarkers cerebrospinal fluid cognitive impairment information processing speed memory multiple sclerosis

cognitive impairment in cerebral small vessel disease induced by hypertension

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Neural Regeneration Research 2024年第7期19卷 1454-1462页

作者： Weipeng Wei Denglei Ma Lin Li Lan Zhang Department of Pharmacy Xuanwu Hospital of Capital Medical UniversityBeijingChina Beijing Geriatric Medical Research Center Beijing Engineering Research Center for Nervous System DrugsNational Center for Neurological DisordersNational Clinical Research Center for Geriatric DiseasesBeijingChina

Hypertension is a primary risk factor for the progression of cognitive impairment caused by cerebral small vessel disease,the most common cerebrovascular disease.Howeve r,the causal relationship between hypertension and cerebral small vessel disease remains unclear.Hypertension has substantial negative impacts on brain health and is recognized as a risk factor for cerebrovascular disease.Chronic hypertension and lifestyle factors are associated with risks for stro ke and dementia,and cerebral small vessel disease can cause dementia and stroke.Hypertension is the main driver of cerebral small vessel disease,which changes the structure and function of cerebral vessels via various mechanisms and leads to lacunar infarction,leukoaraiosis,white matter lesions,and intracerebral hemorrhage,ultimately res ulting in cognitive decline and demonstrating that the brain is the to rget organ of hypertension.This review updates our understanding of the pathogenesis of hypertensioninduced cerebral small vessel disease and the res ulting changes in brain structure and function and declines in cognitive ability.We also discuss drugs to treat cerebral small vessel disease and cognitive impairment.

关键词： blood-brain barrier cerebral small vessel disease cognitive impairment dementia endothelial dysfunction enlarged perivascular space hypertension lacunar infarction neuroinflammation treatment white matter high signal intensity

Comparative efficacy of various exercise interventions on cognitive function in patients with mild cognitive impairment or dementia:A systematic review and network meta-analysis

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Journal of Sport and Health Science 2022年第2期11卷 212-223页

作者： Xiuxiu Huang Xiaoyan Zhao Bei Li Ying Cai Shifang Zhang Qiaoqin Wan Fang Yu School of Nursing Peking UniversityBeijing 100191China Edson College of Nursing and Health Innovation Arizona State UniversityPhoenixAZ 85004USA

Background:Exercise is a promising nonpharmacological therapy for cognitive dysfunction,but it is unclear which type of exercise is most effective.The objective of this study was to compare and rank the effectiveness of various exercise interventions on cognitive function in patients with mild cognitive impairment(MCI)or dementia and to examine the effects of exercise on the symptoms relevant to cognitive impairment.Methods:We searched PubMed,Web of Science,Embase,Cochrane Central Register of Controlled Trials,SPORTDiscus,and PsycInfo through September 2019 and included randomized controlled trials that examined the effectiveness of exercise interventions in patients with MCI or dementia.Primary outcomes included global cognition,executive cognition,and memory cognition.Secondary outcomes included activities of daily living,neuropsychiatric symptoms,and quality of life.Pairwise analyses and network meta-analyses were performed using a random effects model.Results:A total of 73 articles from 71 trials with 5606 participants were included.All types of exercise were effective in increasing or maintaining global cognition,and resistance exercise had the highest probability of being the most effective intervention in slowing the decrease in global cognition(standard mean difference(SMD)=1.05,95%confidence interval(95%CI):0.56-1.54),executive function(SMD=0.85,95%CI:0.21-1.49),and memory function(SMD=0.32,95%CI:0.01-0.63)in patients with cognitive dysfunction.Subgroup analyses for patients with MCI revealed different effects,and multicomponent exercise was most likely to be the optimal exercise therapy for preventing the decline of global cognition(SMD=0.99,95%CI:0.44-1.54)and executive function(SMD=0.72,95%CI:0.06-1.38).However,only resistance exercise showed significant effects on memory function for patients with MCI(SMD=0.35,95%CI:0.01-0.69).Exercise interventions also showed various effects on the secondary outcomes.Conclusion:Resistance exercise has the highest probability of being the optimal exercise type for s

关键词： cognitive function cognitive impairment Exercise Network meta-analysis

Enhancement of oligodendrocyte autophagy alleviates white matter injury and cognitive impairment induced by chronic cerebral hypoperfusion in rats

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Acta Pharmaceutica Sinica B 2023年第5期13卷 2107-2123页

作者： Huiyang Wang Yueyang Liu Zhenkun Guo Minghui Cui Peng Pang Jingyu Yang Chunfu Wu Department of Pharmacology Shenyang Pharmaceutical UniversityShenyang 110016China

cognitive impairment caused by chronic cerebral hypoperfusion(CCH)is associated with white matter injury(WMI),possibly through the alteration of autophagy.Here,the autophagy—lysosomal pathway(ALP)dysfunction in white matter(WM)and its relationship with cognitive impairment were investigated in rats subjected to two vessel occlusion(2VO).The results showed that cognitive impairment occurred by the 28th day after 2VO.Injury and autophagy activation of mature oligodendrocytes and neuronal axons sequentially occurred in WM by the 3rd day.By the 14th day,abnormal accumulation of autophagy substrate,lysosomal dysfunction,and the activation of mechanistic target of rapamycin(MTOR)pathway were observed in WM,paralleled with mature oligodendrocyte death.This indicates autophagy activation was followed by ALP dysfunction caused by autophagy inhibition or lysosomal dysfunction.To target the ALP dysfunction,enhanced autophagy by systemic rapamycin treatment or overexpression of Beclin1(BECN1)in oligodendrocytes reduced mature oligodendrocyte death,and subsequently alleviated the WMI and cognitive impairment after CCH.These results reveal that early autophagy activation was followed by ALP dysfunction in WM after 2VO,which was associated with the aggravation of WMI and cognitive impairment.This study highlights that alleviating ALP dysfunction by enhancing oligodendrocyte autophagy has benefits for cognitive recovery after CCH.

关键词： Chronic cerebral hypoperfusion Two vessel occlusion White matter cognitive impairment Oligodendrocyte Myelin sheath Autophagy-lysosomal pathway Mechanistic target of rapamycin

Spinal cord injury-induced cognitive impairment: a narrative review

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Neural Regeneration Research 2022年第12期17卷 2649-2654页

作者： Oscar V.Alcántar-Garibay Diego Incontri-Abraham Antonio Ibarra Centro de Investigación en Ciencias de la Salud(CICSA) Facultad de Ciencias de la SaludUniversidad Anáhuac México Campus NorteHuixquilucanEstado de MéxicoMéxico

Spinal cord injury is a serious damage to the spinal cord that can lead to life-long disability.Based on its etiology,spinal cord injury can be classified as traumatic or non-traumatic spinal cord injury.Furthermore,the pathology of spinal cord injury can be divided into two phases,a primary injury phase,and a secondary injury phase.The primary spinal cord injury phase involves the initial mechanical injury in which the physical force of impact is directly imparted to the spinal cord,disrupting blood vessels,axons,and neural cell membranes.After the primary injury,a cascade of secondary events begins,expanding the zone of neural tissue damage,and exacerbating neurological deficits.Secondary injury is a progressive condition characterized by pro-inflammatory cytokines,reactive oxygen species,oxidative damage,excitatory amino acids such as glutamate,loss of ionic homeostasis,mitochondrial dysfunction,and cell death.This secondary phase lasts for several weeks or months and can be further subdivided into acute,subacute,and chronic.One of the most frequent and devastating complications developed among the spinal cord injury population is cognitive impairment.The risk of cognitive decline after spinal cord injury has been reported to be 13 times higher than in healthy individuals.The exact etiology of this neurological complication remains unclear,however,many factors have been proposed as potential contributors to the development of this disorder,such as concomitant traumatic brain injury,hypoxia,anoxia,autonomic dysfunction,sleep disorders such as obstructive sleep apnea,body temperature dysregulation,alcohol abuse,and certain drugs.This review focuses on a deep understanding of the pathophysiology of spinal cord injury and its relationship to cognitive impairment.We highlight the main mechanisms that lead to the development of this neurological complication in patients with spinal cord injury.

关键词： autonomic dysfunction cognitive impairment spinal cord injury traumatic brain injury

Blunt dopamine transmission due to decreased GDNF in the PFC evokes cognitive impairment in Parkinson’s disease

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Neural Regeneration Research 2023年第5期18卷 1107-1117页

作者： Chuan-Xi Tang Jing Chen Kai-Quan Shao Ye-Hao Liu Xiao-Yu Zhou Cheng-Cheng Ma Meng-Ting Liu Ming-Yu Shi Piniel Alphayo Kambey Wei Wang Abiola Abdulrahman Ayanlaja Yi-Fang Liu Wei Xu Gang Chen Jiao Wu Xue Li Dian-Shuai Gao Department of Neurobiology Xuzhou Key Laboratory of NeurobiologyXuzhou Medical UniversityXuzhouJiangsu ProvinceChina Experinental Teaching Center of Morphology Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Neurology Affiliated Suqian Hospital of Xuzhou Medical UniversitySuqianJiangsu ProvinceChina Department of Rehabilitation Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Neurology Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Medicine Jiangnan UniversityWuxiJiangsu ProvinceChina Department of Nursing Care the Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina

Studies have found that the absence of glial cell line-derived neurotrophic factor may be the primary risk factor for Parkinson’s disease. However, there have not been any studies conducted on the potential relationship between glial cell line-derived neurotrophic factor and cognitive performance in Parkinson’s disease. We first performed a retrospective case-control study at the Affiliated Hospital of Xuzhou Medical University between September 2018 and January 2020 and found that a decreased serum level of glial cell line-derived neurotrophic factor was a risk factor for cognitive disorders in patients with Parkinson’s disease. We then established a mouse model of Parkinson’s disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and analyzed the potential relationships among glial cell line-derived neurotrophic factor in the prefrontal cortex, dopamine transmission, and cognitive function. Our results showed that decreased glial cell line-derived neurotrophic factor in the prefrontal cortex weakened dopamine release and transmission by upregulating the presynaptic membrane expression of the dopamine transporter, which led to the loss and primitivization of dendritic spines of pyramidal neurons and cognitive impairment. In addition, magnetic resonance imaging data showed that the long-term lack of glial cell line-derived neurotrophic factor reduced the connectivity between the prefrontal cortex and other brain regions, and exogenous glial cell line-derived neurotrophic factor significantly improved this connectivity. These findings suggested that decreased glial cell line-derived neurotrophic factor in the prefrontal cortex leads to neuroplastic degeneration at the level of synaptic connections and circuits, which results in cognitive impairment in patients with Parkinson’s disease.

关键词： cognitive impairment degree centrality dendritic spine dopamine transmission dopamine transporter glial cell line-derived neurotrophic factor Parkinson’s disease prefrontal cortex synaptic plasticity

β2-Microglobulin exacerbates neuroinflammation,brain damage,and cognitive impairment after stroke in rats

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Neural Regeneration Research 2023年第3期18卷 603-608页

作者： Feng Chen Jing Liu Fa-Qiang Li Shuai-Shuai Wang Yan-Yan Zhang Yun-Yun Lu Fang-Fang Hu Rui-Qin Yao Department of Neurology Xuzhou Cancer HospitalXuzhouJiangsu ProvinceChina Department of Neurobiology Xuzhou Key Laboratory of NeurobiologyXuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Neurology Xuzhou No.1 People’s Hospitalthe Affiliated Xuzhou Municipal Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina

β2-Microglobulin(β2M),a component of the major histocompatibility complex class I molecule,is associated with aging-related cognitive impairment and Alzheimer’s disease.Although upregulation ofβ2M is considered to be highly related to ischemic stroke,the specific role and underlying mechanistic action ofβ2M are poorly understood.In this study,we established a rat model of focal cerebral ischemia by occlusion of the middle cerebral artery.We found thatβ2M levels in the cerebral spinal fluid,serum,and brain tissue were significantly increased in the acute period but gradually decreased during the recovery period.RNA interference was used to inhibitβ2M expression in the acute period of cerebral stroke.Tissue staining with 2,3,5-triphenyltetrazolium chloride and evaluation of cognitive function using the Morris water maze test demonstrated that decreasedβ2M expression in the ischemic penumbra reduced infarct volume and alleviated cognitive deficits,respectively.Notably,glial cell,caspase-1(p20),and Nod-like receptor pyrin domain containing 3(NLRP3)inflammasome activation as well as production of the inflammatory cytokines interleukin-1β,interleukin-6,and tumor necrosis factor-αwere also effectively inhibited byβ2M silencing.These findings suggest thatβ2M participates in brain injury and cognitive impairment in a rat model of ischemic stroke through activation of neuroinflammation associated with the NLRP3 inflammasome.

关键词： cognitive impairment cognitive improvement glial activation infarct volume ischemia middle cerebral artery occlusion neuroinflammation NLRP3 inflammasome stroke β2 microglobulin

Echinacoside Alleviates cognitive impairment in Cerebral Ischemia Rats through α7nAChR-Induced Autophagy

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Chinese Journal of Integrative Medicine 2022年第9期28卷 809-816页

作者： DING Ling YE Hong GU Long-dian DU An-qing YUAN Xin-lu Department of Endocrinology and Metabolic Diseases Shanghai Pudong HospitalFudan University Pudong Medical CenterShanghai201399China

Objectives:To evaluate the effect of echinacoside(ECH)on cognitive dysfunction in post cerebral stroke model rats.Methods:The post stroke cognitive impairment rat model was created by occlusion of the transient middle cerebral artery(MCAO).The rats were randomly divided into 3 groups by a random number table:the sham group(sham operation),the MCAO group(received operation for focal cerebral ischemia),and the ECH group(received operation for focal cerebral ischemia and ECH50 mg/kg per day),with 6 rats in each group,The infarct volume and spatial learning were evaluated by triphenyl tetrazolium chloride staining and Morris water maze.The expression of α7 nAChR in the hippocampus was detected by immunohistochemistry.The contents of acetylcholine(ACh),malondialdehyde(MDA),glutathione(GSH),superoxide dismutase(SOD),activities of choline acetyltransferase(ChAT),acetylcholinesterase(AChE),and catalase(CAT)were evaluated by enzyme linked immunosorbent assay.The neural apoptosis and autophagy were determined by TUNEL staining and LC3 staining,respectively.Results:ECH significantly lessened the brain infarct volume and ameliorated neurological deficit in infarct volume and water content(both Pcognitive impairment by attenuating neurological damage and enhancing autophagy in MCAO rats.

关键词： cerebral ischemia cognitive impairment autophagy echinacoside cholinergic activity