Brain Functional Network Changes in Patients with Poststroke Cognitive Impairment Following Acupuncture Therapy

Background: The mechanisms by which acupuncture affects poststroke cognitive impairment (PSCI) remain unclear. Objective: To investigate brain functional network (BFN) changes in patients with PSCI after acupuncture therapy. Methods: Twenty-two PSCI patients who underwent acupuncture therapy in our hospital were enrolled as research subjects. Another 14 people matched for age, sex, and education level were included in the normal control (HC) group. All the subjects underwent resting-state functional magnetic resonance imaging (rs-fMRI) scans;the PSCI patients underwent one scan before acupuncture therapy and another after. The network metric difference between PSCI patients and HCs was analyzed via the independent-sample t test, whereas the paired-sample t test was employed to analyze the network metric changes in PSCI patients before vs. after treatment. Results: Small-world network attributes were observed in both groups for sparsities between 0.1 and 0.28. Compared with the HC group, the PSCI group presented significantly lower values for the global topological properties (γ, Cp, and Eloc) of the brain;significantly greater values for the nodal attributes of betweenness centrality in the CUN. L and the HES. R, degree centrality in the SFGdor. L, PCG. L, IPL. L, and HES. R, and nodal local efficiency in the ORBsup. R, ORBsupmed. R, DCG. L, SMG. R, and TPOsup. L;and decreased degree centrality in the MFG. R, IFGoperc. R, and SOG. R. After treatment, PSCI patients presented increased degree centrality in the LING.L, LING.R, and IOG. L and nodal local efficiency in PHG. L, IOG. R, FFG. L, and the HES. L, and decreased betweenness centrality in the PCG. L and CUN. L, degree centrality in the ORBsupmed. R, and nodal local efficiency in ANG. R. Conclusion: Cognitive decline in PSCI patients may be related to BFN disorders;acupuncture therapy may modulate the topological properties of the BFNs of PSCI patients.

Modulatory effects of acupuncture on brain networks in mild cognitive impairment patients

Functional magnetic resonance imaging has been widely used to investigate the effects of acupuncture on neural activity. However, most functional magnetic resonance imaging studies have focused on acute changes in brain activation induced by acupuncture. Thus, the time course of the therapeutic effects of acupuncture remains unclear. In this study, 32 patients with amnestic mild cognitive impairment were randomly divided into two groups, where they received either Tiaoshen Yizhi acupuncture or sham acupoint acupuncture. The needles were either twirled at Tiaoshen Yizhi acupoints, including Sishencong（EX-HN1）, Yintang（EX-HN3）, Neiguan（PC6）, Taixi（KI3）, Fenglong（ST40）, and Taichong（LR3）, or at related sham acupoints at a depth of approximately 15 mm, an angle of ± 60°, and a rate of approximately 120 times per minute. Acupuncture was conducted for 4 consecutive weeks, five times per week, on weekdays. Resting-state functional magnetic resonance imaging indicated that connections between cognition-related regions such as the insula, dorsolateral prefrontal cortex, hippocampus, thalamus, inferior parietal lobule, and anterior cingulate cortex increased after acupuncture at Tiaoshen Yizhi acupoints. The insula, dorsolateral prefrontal cortex, and hippocampus acted as central brain hubs. Patients in the Tiaoshen Yizhi group exhibited improved cognitive performance after acupuncture. In the sham acupoint acupuncture group, connections between brain regions were dispersed, and we found no differences in cognitive function following the treatment. These results indicate that acupuncture at Tiaoshen Yizhi acupoints can regulate brain networks by increasing connectivity between cognition-related regions, thereby improving cognitive function in patients with mild cognitive impairment.

Brain Functional Networks with Dynamic Hypergraph Manifold Regularization for Classification of End-Stage Renal Disease Associated with Mild Cognitive Impairment

The structure and function of brain networks have been altered in patients with end-stage renal disease(ESRD).Manifold regularization(MR)only considers the pairing relationship between two brain regions and cannot represent functional interactions or higher-order relationships between multiple brain regions.To solve this issue,we developed a method to construct a dynamic brain functional network(DBFN)based on dynamic hypergraph MR(DHMR)and applied it to the classification of ESRD associated with mild cognitive impairment(ESRDaMCI).The construction of DBFN with Pearson’s correlation(PC)was transformed into an optimization model.Node convolution and hyperedge convolution superposition were adopted to dynamically modify the hypergraph structure,and then got the dynamic hypergraph to form the manifold regular terms of the dynamic hypergraph.The DHMR and L_(1) norm regularization were introduced into the PC-based optimization model to obtain the final DHMR-based DBFN(DDBFN).Experiment results demonstrated the validity of the DDBFN method by comparing the classification results with several related brain functional network construction methods.Our work not only improves better classification performance but also reveals the discriminative regions of ESRDaMCI,providing a reference for clinical research and auxiliary diagnosis of concomitant cognitive impairments.

Study of brain morphology change in Alzheimer’s disease and amnestic mild cognitive impairment compared with normal controls

Background With an aggravated social ageing level, the number of patients with Alzheimer's disease (AD) is gradually increasing, and mild cognitive impairment (MCI) is considered to be an early form of Alzheimer's disease. How to distinguish diseases in the early stage for the purposes of early diagnosis and treatment is an important topic. Aims The purpose of our study was to investigate the differences in brain cortical thickness and surface area among elderly patients with AD, elderly patients with amnestic MCI (aMCI) and normal controls (NC). Methods 20 AD patients, 21 aMCIs and 25 NC were recruited in the study. FreeSurfer software was used to calculate cortical thickness and surface area among groups. Results The patients with AD had less cortical thickness both in the left and right hemisphere in 17 of the 36 brain regions examined than the patients with aMCI or NC. The patients with AD also had smaller cerebral surface area both in the left and right hemisphere in 3 of the 36 brain regions examined than the patients with aMCI or NC. Compared with the NC, the patients with aMCI only had slight atrophy in the inferior parietal lobe of the left hemisphere, and no significant difference was found. Conclusion AD, as well as aMCI (to a lesser extent), is associated with reduced cortical thickness and surface area in a few brain regions associated with cognitive impairment. These results suggest that cortical thickness and surface area could be used for early detection of AD.

Is Goshinjo therapy effective in cognitive impairment after severe traumatic brain injury?

We report a case of a 21-year-old man who had severe traumatic brain injury as a result of an accident at the age of 16 years. Two years and 4 months after the trauma, at the age of 19 years, he still had severe right hemiplegia and cognitive dysfunction including aphasia and attention and memory disturbance. Conventional rehabilitation programs cou（d not resolve all of the neuropsychological problems. He started receiving Goshinjo therapy over a period of 22 months. Following the therapy, significant improvements in verbal intelligence quotient （assessed by the Wechsler Adult Intelligence Scale-Third Edition） and attention and concentration function （using the Wechsler Memory Scale-Revised）, and remission of traumatic epilepsy were observed. Goshinjo therapy is suspected to be effective in the treatment of cognitive dysfunction in the chronic stage after severe traumatic brain injury.

Brain-derived neurotrophic factor plasma levels and premature cognitive impairment/dementia in type 2 diabetes

AIM To assess the relationship of brain-derived neurotrophic factor(BDNF) with cognitive impairment in patients with type 2 diabetes. METHODS The study included 40 patients with diabetes mellitus type 2(DM2), 37 patients with chronic kidney disease in hem dialysis hemodialysis therapy(HD) and 40 healthy subjects. BDNF in serum was quantified by ELISA. The Folstein Mini-Mental State Examination was used to evaluate cognitive impairment.RESULTS The patients with DM2 and the patients in HD were categorized into two groups, with cognitive impairment and without cognitive impairment. The levels of BDNF showed significant differences between patients with DM2(43.78 ± 9.05 vs 31.55 ± 10.24, P = 0.005). There were no differences between patients in HD(11.39 ± 8.87 vs 11.11 ± 10.64 P = 0.77); interestingly, ferritin levels were higher in patients with cognitive impairment(1564 ± 1335 vs 664 ± 484 P = 0.001). The comparison of BDNF values, using a Kruskal Wallis test, between patients with DM2, in HD and healthy controls showed statistical differences(P < 0.001).CONCLUSION Low levels of BDNF are associated with cognitive impairment in patients with DM2. The decrease of BDNF occurs early and progressively in patients in HD.

Correlation of brain-derived neurotrophic factor to cognitive impairment following traumatic brain injury in rats

BACKGROUND： In vitro and in vivo studies have confirmed that brain-derived neurotrophic factor （BDNF） can promote survival and differentiation of cholinergic, dopaminergic and motor neurons, and axonal regeneration. BDNF has neuroprotective effects on the nervous system. OBJECTIVE： To explore changes in BDNF expression and cognitive function in rats after brain injury. DESIGN, TIME AND SETTING： The neuropathology experiment was performed at the Second Research Room, Department of Neurosurgery, Fujian Medical University （China） from July 2007 to July 2008. MATERIALS： A total of 72 healthy, male, Sprague Dawley, rats were selected for this study. METHODS： Rat models of mild and moderate traumatic brain injury were created by percussion, according to Feeney＇s method （n = 24, each group）. A bone window was made in rats from the sham operation group （n = 24）, but no attack was conducted. MAIN OUTCOME MEASURES： At days 1, 2, 4 and 7 following injury, BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was examined by immunohistochemistry （streptavidin-biotin-peroxidase complex method）. Changes in rat cognitive function were assessed by the walking test, balance-beam test and memory function detection. RESULTS： Cognitive impairment was aggravated at day 2, and recovered to normal at days 3 and 7 in rats from the mild and moderate traumatic brain injury groups. BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was increased at 1 day, decreased at day 2, and then gradually increased in the mild and moderate traumatic brain injury groups. BDNF expression was greater in rats from the moderate traumatic brain injury group than in the sham operation and mild traumatic brain injury groups （P 〈 0.05）. CONCLUSION： BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain is correlated to cognitive impairment after traumatic brain injury. BDNF has a protective effect on cognitive function in rats following injury.

The Diagnostic Role of Brain MRI in Detection of Multiple Sclerosis Related Cognitive Impairment

Background: Cognitive impairment (CI) is a common manifestation of multiple sclerosis (MS), which can severely affect patients’ and their families’ life. Early suspicion and detection of CI can improve general medical management of MS patients. Objectives: To correlate MS related CI to cortical brain lesions using brain magnetic resonance imaging (MRI). Materials and Methods: Cognitive impairment was detected using mini mental state examination (MMSE);Neurological examination and brain MRI were performed for all patients. Correlation was calculated between disease cortical burden detected by MRI and CI. Results: Fifty-three patients with proven MS were scanned by brain MRI;69.8% of them had cognitive impairment diagnosed with MMSE. The presence and severity of cognitive impairment was correlated to cortical brain lesion. Cognitive impairment was not correlated with non-cortical brain lesions or neurological physical disability measured by Expanded Disability Status Scale (EDSS). Conclusions: Presence of brain frontal cortical lesions detected by MRI in MS patients can predict subsequent development of MS-related CI.

Acupuncture at the Taixi(KI3) acupoint activates cerebral neurons in elderly patients with mild cognitive impairment

Our previous ifndings have demonstrated that acupuncture at the Taixi （KI3） acupoint in healthy youths can activate neurons in cognitive-related cerebral cortex. Here, we investigated whether acupuncture at this acupoint in elderly patients with mild cognitive impairment can also activate neurons in these regions. Resting state and task-related functional magnetic resonance imaging showed that the pinprick senstation of acupuncture at the Taixi acupoint differed signiifcantly between elderly patients with mild cognitive impairment and healthy elderly controls. Results showed that 20 brain regions were activated in both groups of participants, including the bi-lateral anterior cingulate gyrus （Brodmann areas [BA] 32, 24）, left medial frontal cortex （BA 9, 10, 11）, left cuneus （BA 19）, left middle frontal gyrus （BA 11）, left lingual gyrus （BA 18）, right medial frontal gyrus （BA 11）, bilateral inferior frontal gyrus （BA 47）, left superior frontal gyrus （BA11）, right cuneus （BA 19, 18）, right superior temporal gyrus （BA 38）, left subcallosal gyrus （BA 47）, bilateral precuneus （BA 19）, right medial frontal gyrus （BA 10）, right superior frontal （BA 11）, left cingulate gyrus （BA 32）, left precentral gyrus （BA 6）, and right fusiform gyrus （BA 19）. These results suggest that acupuncture at the Taixi acupoint in elderly patients with mild cogni-tive impairment can also activate some brain regions.

Spinal cord injury-induced cognitive impairment: a narrative review

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.

Efficacy of enhanced extracorporeal counterpulsation combined with atorvastatin in the treatment of cognitive impairment after stroke

BACKGROUND Cerebral apoplexy patients are prone to cognitive impairment,and it is very important to choose appropriate treatment methods to improve their cognitive impairment after stroke.AIM To evaluate the effects of enhanced external counterpulsation(EECP)in con-junction with atorvastatin on cognitive function,neurotransmitter levels,and the repair of brain tissue damage in patients with cognitive impairment due to stroke.METHODS In this retrospective study,data from 60 patients with poststroke cognitive impairment due to stroke who were treated in our hospital from February 2021 to July 2022 were analyzed and divided into a treatment group(n=30)and a control group(n=30)according to the different nursing methods applied.Patients in the treatment group received EECP in addition to atorvastatin,while those in the control group received atorvastatin alone.Mini-Mental State Examination(MMSE),Montreal Cognitive Assessment(MoCA)and activities of daily living(ADL)scale scores were compared between the two groups.Additionally,the two groups were compared in terms of serum acetylcholine(ACh),acetylcholin-esterase(AChE),nitric oxide(NO),endothelin-1(ET-1),β2-microglobulin(β2-MG),glial fibrillary acidic protein(GFAP),and visinin-like protein 1(VILIP-1)in the serum.Blood flow measurements from the anterior cerebral artery(ACA),middle cerebral artery(MCA)and posterior cerebral artery(PCA)were compared between the two groups before and after treatment,and the pulsatility index(PI)and resistance index(RI)of each artery were determined.RESULTS MMSE,MoCA,and ADL scores all improved in both groups following treatment,with the study group showing more improvement than the control group(P<0.05).After treatment,there were statistically significant increases in both ACh and NO levels,whereas decreases occurred in AChE,ET-1,β2-MG,VILIP-1,and GFAP,levels and the PI and RI of the left-ACA,right-ACA,left-MCA,right-MCA,left-PCA,and right-PCA.The study group showed greater gains in all metrics than the control group(P<0.05).CONCLUSION EECP combined with atorvastatin is effective in the treatment of cognitive impairment after stroke and can effectively improve the cognitive function,neurotransmitter levels,and brain tissue damage status of patients.

The Role of Gut Microbiota in the Mechanism of Cognitive Impairment in the Elderly

With the aging in whole world, it has become a great challenge to explore the relationship between the cognitive and behavioral performance of senile dementia and the underlying pathology of the brain. Alzheimer’s disease (AD) is a common age-related and progressive neurodegenerative disease characterized and one of the main causes of senile dementia. The pathogenesis and treatment mechanism of AD are not completely clear. In recent years, it has been found that the Gut microbiota (GM) disorder is related to nervous system diseases. The objective of this review is to summarize the etiology and pathogenyon the role of GM in the development of AD, metabolites of GM and the occurrence of AD, and GM, diabetes and occurrence of AD. Understanding the relationship between GM and AD will help provide possible interventions to improve the structure of GM and prevent AD through different treatments, and it may provide clinicians with a new and more effective way for early diagnosis, prevention and treatment of AD.

Treadmill exercise in combination with acousto-optic and olfactory stimulation improves cognitive function in APP/PS1 mice through the brain-derived neurotrophic factor-and Cygb-associated signaling pathways

A reduction in adult neurogenesis is associated with behavioral abnormalities in patients with Alzheimer's disease.Consequently,enhancing adult neurogenesis represents a promising therapeutic approach for mitigating disease symptoms and progression.Nonetheless,nonpharmacological interventions aimed at inducing adult neurogenesis are currently limited.Although individual non-pharmacological interventions,such as aerobic exercise,acousto-optic stimulation,and olfactory stimulation,have shown limited capacity to improve neurogenesis and cognitive function in patients with Alzheimer's disease,the therapeutic effect of a strategy that combines these interventions has not been fully explored.In this study,we observed an age-dependent decrease in adult neurogenesis and a concurrent increase in amyloid-beta accumulation in the hippocampus of amyloid precursor protein/presenilin 1 mice aged 2-8 months.Amyloid deposition became evident at 4 months,while neurogenesis declined by 6 months,further deteriorating as the disease progressed.However,following a 4-week multifactor stimulation protocol,which encompassed treadmill running(46 min/d,10 m/min,6 days per week),40 Hz acousto-optic stimulation(1 hour/day,6 days/week),and olfactory stimulation(1 hour/day,6 days/week),we found a significant increase in the number of newborn cells(5'-bromo-2'-deoxyuridine-positive cells),immature neurons(doublecortin-positive cells),newborn immature neurons(5'-bromo-2'-deoxyuridine-positive/doublecortin-positive cells),and newborn astrocytes(5'-bromo-2'-deoxyuridine-positive/glial fibrillary acidic protein-positive cells).Additionally,the amyloid-beta load in the hippocampus decreased.These findings suggest that multifactor stimulation can enhance adult hippocampal neurogenesis and mitigate amyloid-beta neuropathology in amyloid precursor protein/presenilin 1 mice.Furthermore,cognitive abilities were improved,and depressive symptoms were alleviated in amyloid precursor protein/presenilin 1 mice following multifactor stimulation,as evidenced by Morris water maze,novel object recognition,forced swimming test,and tail suspension test results.Notably,the efficacy of multifactor stimulation in consolidating immature neurons persisted for at least 2weeks after treatment cessation.At the molecular level,multifactor stimulation upregulated the expression of neuron-related proteins(NeuN,doublecortin,postsynaptic density protein-95,and synaptophysin),anti-apoptosis-related proteins(Bcl-2 and PARP),and an autophagyassociated protein(LC3B),while decreasing the expression of apoptosis-related proteins(BAX and caspase-9),in the hippocampus of amyloid precursor protein/presenilin 1 mice.These observations might be attributable to both the brain-derived neurotrophic factor-mediated signaling pathway and antioxidant pathways.Furthermore,serum metabolomics analysis indicated that multifactor stimulation regulated differentially expressed metabolites associated with cell apoptosis,oxidative damage,and cognition.Collectively,these findings suggest that multifactor stimulation is a novel non-invasive approach for the prevention and treatment of Alzheimer's disease.

Cognitive disorder in brain concussion

This paper presented original study results concerning the prevalence and clinical characteristics of cognitive impairment associated with brain concussion. The cognitive functions of 80 consecutive patients （mean age = 37.40±1l.74years; 50 men and 30 women） admitted to the hospital with brain concussions were evaluated. Their cognitive scores were compared with 40 age- and education-matched healthy volunteers without history of cranial trauma. Cognitive impairment without dementia was found in 93% of the patients. Cognitive impairment in brain concussion was also characterized by prominent cognitive slowness （bradyphrenia）, concentration decrease, free recall insufficiency, and visual-spatial dysfunction. Age and severity of anxiety significantly influence the cognitive performance of patients.

Icariin Improves Cognitive Impairment after Traumatic Brain Injury by Enhancing Hippocampal Acetylation

Objective: To examine the effect of icariin(ICA) on the cognitive impairment induced by traumatic brain injury(TBI) in mice and the underlying mechanisms related to changes in hippocampal acetylation level. Methods: The modified free-fall method was used to establish the TBI mouse model. Mice with post-TBI cognitive impairment were randomly divided into 3 groups using the randomised block method(n=7): TBI(vehicle-treated), low-dose(75 mg/kg) and high-dose(150 mg/kg) of ICA groups. An additional sham-operated group(vehicle-treated) was employed. The vehicle or ICA was administrated by gavage for 28 consecutive days. The Morris water maze(MWM) test was conducted. Acetylcholine(ACh) content, m RNA and protein levels of choline acetyltransferase(Ch AT), and protein levels of acetylated H3(Ac-H3) and Ac-H4 were detected in the hippocampus. Results: Compared with the sham-operated group, the MWM performance, hippocampal ACh content, m RNA and protein levels of Ch AT, and protein levels of Ac-H3 and Ac-H4 were significantly decreased in the TBI group(P<0.05). High-dose of ICA significantly ameliorated the TBI-induced weak MWM performance, increased hippocampal ACh content, and m RNA and protein levels of Ch AT, as well as Ac-H3 protein level compared with the TBI group(P<0.05). Conclusion: ICA improved post-TBI cognitive impairment in mice by enhancing hippocampal acetylation, which improved hippocampal cholinergic function and ultimately improved cognition.

Tetrahedral framework nucleic acids promote cognitive impairment recovery post traumatic brain injury

Cognitive impairment often occurs after post traumatic brain injury. In addition, recovery of cognitive impairment is largely dependent on spontaneous repair and the severity of secondary insult. The tetrahedral framework nucleic acid is a novel nanostructure has been shown to have a positive biological effect in promoting regeneration and anti-inflammation. To explore the treatment effect of tetrahedral framework nucleic acids for cognitive impairment recovery post traumatic brain injury, we established a mouse model of traumatic brain injury and verified the efficacy of tetrahedral framework nucleic acids in promoting cognitive impairment recovery post traumatic brain injury. The results show that the tetrahedral framework nucleic acids promoted the recovery of post-traumatic cognitive function by enhancing the proliferation of endogenous neural stem cells. Besides, tetrahedral framework nucleic acids modulated the neuroinflammatory response in the acute phase by inhibiting excessive astrocyte and microglial activation. Taken together, the results of the study indicate tetrahedral framework nucleic acids for treatment of cognitive impairment post traumatic brain injury.

Altered regional homogeneity of prefrontal cortex in Parkinson's disease with mild cognitive impairment

Background:Mild cognitive impairment (MCI) is a common non-motor symptom of early Parkinson's disease (PD),but the neural mechanisms underlying it remain poorly understood.The aim of the present study was to investigate the characteristics of cognition-related brain activities in the PD patients with MCI.Methods:The brain fMRIs and cognition tests were acquired in 39 PD patients and 22 healthy controls (HC) from September 2013 to January 2015.The patients were divided into two groups:PD-MCI (n--18) and PD with normal cognition (PDNC,n =19).we used resting state fMRI and a regional homogeneity (ReHo) method to explore patterns of intrinsic brain activity in patients with PD-MCI as compared with PDNC subjects and HC.Results:Compared with the PDNC group,the PD-MCI group exhibited significantly increased ReHo in parts of the prefrontal cortex regions (e.g.right superior frontal gyrus,right middle frontal gyrus and orbitofrontal cortex).Compared to the HC group,a decrease of ReHo value in left thalamus was found in PD-MCI.However,this reduction was not found in the left thalamus of PDNC group,but in the above prefrontal regions (p ＜ 0.05,with Bonferroni correction).Conclusions:These results demonstrate that the ReHo of prefrontal cortex in resting state is changed in PD patients with MCI.The presence of MCI in PD may be attributed to abnormal regional activity in prefrontal cortex regions.

Selective impairment of musical emotion recognition in patients with amnesic mild cognitive impairment and mild to moderate Alzheimer disease

Background:Patients with Alzheimer disease(AD)and amnesic mild cognitive impairment(aMCI)have deficits in emotion recognition.However,it has not yet been determined whether patients with AD and aMCI also experience difficulty in recognizing the emotions conveyed by music.This study was conducted to investigate whether musical emotion recognition is impaired or retained in patients with AD and aMCI.Methods:All patients were recruited from the First Affiliated Hospital of Anhui Medical University between March 1,2015 and January 31,2017.Using the musical emotion recognition test,patients with AD(n=16),patients with aMCI(n=19),and healthy controls(HCs,n=16)were required to choose one of four emotional labels(happy,sad,peaceful,and fearful)that matched each musical excerpt.Emotion recognition scores in three groups were compared using one-way analysis of variance(ANOVA)test.We also investigated the relationship between the emotion recognition scores and Mini-Mental State Examination(MMSE)using Pearson’s correlation analysis test in patients with AD and aMCI.Results:Compared to the HC group,both of the patient groups showed deficits in the recognition of fearful musical emotions(HC:7.88±1.36;aMCI:5.05±2.34;AD:3.69±2.02),with results of a one-way ANOVA confirming a significant main effect of group(F(2,50)=18.70,P<0.001).No significant differences were present among the three groups for the happy(F(2,50)=2.57,P=0.09),peaceful(F(2,50)=0.38,P=0.09),or sad(F(2,50)=2.50,P=0.09)musical emotions.The recognition of fearful musical emotion was positively associated with general cognition,which was evaluated by MMSE in patients with AD and aMCI(r=0.578,P<0.001).The correlations between the MMSE scores and recognition of the remaining emotions were not significant(happy,r=0.228,P=0.11;peaceful,r=0.047,P=0.74;sad,r=0.207,P=0.15).Conclusion:This study showed that both patients with AD and aMCI had decreased ability to distinguish fearful emotions,which might be correlated with diminished cognitive function.

Changes of inflammatory factors, reactive oxygen species and cognitive function in mice after brain-blast injury

Objective: To study the changes of cognitive function in mouse after brain-blast injury. Methods: Fourty healthy male C57BL/6 mice were randomly divided into model group and control group. After 24 h of injury, histopathological changesc and reactive oxygen species changes were observed under microscope;while changes of inflammatory cytokines content were determined by Western-blot. Four weeks later, Morris water maze method was used to detect the cognition impairment. Results: HE staining showed blast induced brain injury in C57BL/6 mice. Compared with normal control group, the expression of IL-1β,IL-4, IL-6 were significantly increased in brain tissue of model group whereas IL-10 was significantly decreased (P<0.05);ROS expression in the hippocampus of model group mice was significantly increased compared with that in the control group. Morris water maze showed cognition impairment in mice after brain-blast injury. Conclusions: Brain-blast injury causes cognition impairment in mice, which may be related to the occur of inflammatory change and oxidative stress in the early stage.

A review of the neurotransmitter system associated with cognitive function of the cerebellum in Parkinson's disease

The dichotomized brain system is a concept that was generalized from the‘dual syndrome hypothesis’to explain the heterogeneity of cognitive impairment,in which anterior and posterior brain systems are independent but partially overlap.The dopaminergic system acts on the anterior brain and is responsible for executive function,working memory,and planning.In contrast,the cholinergic system acts on the posterior brain and is responsible for semantic fluency and visuospatial function.Evidence from dopaminergic/cholinergic imaging or functional neuroimaging has shed significant insight relating to the involvement of the cerebellum in the cognitive process of patients with Parkinson’s disease.Previous research has reported evidence that the cerebellum receives both dopaminergic and cholinergic projections.However,whether these two neurotransmitter systems are associated with cognitive function has yet to be fully elucidated.Furthermore,the precise role of the cerebellum in patients with Parkinson’s disease and cognitive impairment remains unclear.Therefore,in this review,we summarize the cerebellar dopaminergic and cholinergic projections and their relationships with cognition,as reported by previous studies,and investigated the role of the cerebellum in patients with Parkinson’s disease and cognitive impairment,as determined by functional neuroimaging.Our findings will help us to understand the role of the cerebellum in the mechanisms underlying cognitive impairment in Parkinson’s disease.