Acupuncture for ischemic stroke:cerebellar activation may be a central mechanism following Deqi

The needling sensation of Deqi during acupuncture is a key factor of influencing acupuncture outcome.Recent studies have mainly focused on the brain function effects of Deqi in a physiological state.Functional magnetic resonance imaging(f MRI)on the effects of acupuncture at Waiguan(SJ5)in pathological and physiological states is controversial.In this study,12 patients with ischemic stroke received acupuncture at Waiguan(SJ5)and simultaneously underwent f MRI scanning of the brain,with imaging data of the activated areas obtained.Based on the patient’s sensation,imaging data were allocated to either the Deqi group or non-Deqi group.In the Deqi group,the activated/deactivated areas were the left superior temporal gyrus(BA39)/right anterior lobe of the cerebellum and left thalamus.In the non-Deqi group,the activated areas included the medial frontal gyrus of the right frontal lobe(BA11),right limbic lobe(BA30,35),and left frontal lobe(BA47),while the only deactivated area was the right parietal lobe(BA40).Compared with the non-Deqi group,the Deqi group exhibited marked activation of the right anterior lobe of the cerebellum and right limbic lobe(BA30).These findings confirm that the clinical effect of Deqi during acupuncture is based on brain functional changes.Cerebellar activation may be one of the central mechanisms of acupuncture in the treatment of ischemic stroke.     

Increased perfusion in motor areas after constraint-induced movement therapy in chronic stroke: a single-photon emission computerized tomography study.

Hemiparesis is the most common deficit after cerebral stroke. Constraint-induced movement therapy (CIMT) is a new neurorehabilitation method that emphasizes task-relevant repetitive training for the stroke hand. Twelve chronic stroke patients were studied with single-photon emission computerized tomography at rest before and after the two-week CIMT period. Increased perfusion was found in motor control related areas. The specific areas with an increase in perfusion in the affected hemisphere were in the precentral gyrus, premotor cortex (Brodmann's area 6 (BA6)), frontal cortex, and superior frontal gyrus (BA10). In the nonaffected hemisphere, perfusion was increased in the superior frontal gyrus (BA6) and cingulate gyrus (BA31). In the cerebellum increased perfusion was seen bilaterally. The brain areas with increased perfusion receive and integrate the information from different sensory systems and plan the movement execution. Regional cerebral perfusion decreased in the lingual gyrus (BA18) in the affected hemisphere. In the nonaffected frontal cortex, two areas with decreased perfusion were found in the middle frontal gyrus (BA8/10). Also, the fusiform gyrus (BA20) and inferior temporal gyrus (BA37) in the nonaffected hemisphere showed decreased perfusion. Intensive movement therapy appears to change local cerebral perfusion in areas known to participate in movement planning and execution. These changes might be a sign of active reorganization processes after CIMT in the chronic state of stroke.     

Activation of immediate-early response gene c-Fos protein in the rat paralimbic cortices after myocardial infarction

c-Fos is a good biological marker for detecting the pathogenesis of central nervous system disorders. Few studies are reported on the change in myocardial infarction-induced c-Fos expression in the paralimbic regions. Thus, in this study, we investigated the changes in c-Fos expression in the rat cingulate and piriform cortices after myocardial infarction. Neuronal degeneration in cingulate and piriform cortices after myocardial infarction was detected using cresyl violet staining, Neu N immunohistochemistry and Fluoro-Jade B histofluorescence staining. c-Fos-immunoreactive cells were observed in cingulate and piriform cortices at 3 days after myocardial infarction and peaked at 7 and 14 days after myocardial infarction. But they were hardly observed at 56 days after myocardial infarction. The chronological change of c-Fos expression determined by western blot analysis was basically the same as that of c-Fos immunoreactivity. These results indicate that myocardial infarction can cause the chronological change of immediate-early response gene c-Fos protein expression, which might be associated with the neural activity induced by myocardial infarction.     

Studies in schizophrenia: pathophysiology and treatment

Studies on the pathophysiology of schizophrenia have implicated the limbic cortex, using postmortem, structural, and functional data, especially in the hippocampus (HC) and the anterior cingulate cortex (ACC). We have made contributions to the literature consistent with this idea: first, we describe a positive significant correlation between psychotic symptoms in schizophrenia and neuronal activity in the ACC and HC, suggesting the involvement of limbic cortex in the mediation of symptoms in schizophrenia. Second, in the ACC and the anterior HC (but not in the posterior HC), regional cerebral blood flow (rCBF) is abnormal (ie, reduced in the ACC and elevated in the HC) in schizophrenia. Third, the relationship of rCBF to task difficulty in the ACC is altered in schizophrenia, suggesting a failure of participation of the ACC in effortful tasks. Lastly, connectivity between the ACC and HC during the performance of an auditory discrimination task is also lacking, suggesting that cognitive performance in schizophrenia lacks a functional limbic contribution. On the basis of these changes, we studied the effects of antipsychotic drugs in these abnormal areas in persons with schizophrenia. Both first- and second-generation antipsychotics produce functional alterations in these limbic cortical areas, in the direction of normals, putatively acting through the brain's own cortical-subcortical circuits.     

Changes of resting cerebral activities in subacute ischemic stroke patients

This study aimed to detect the difference in resting cerebral activities between ischemic stroke patients and healthy participants, define the abnormal site, and provide new evidence for pathological mechanisms, clinical diagnosis, prognosis prediction and efficacy evaluation of ischemic stroke. At present, the majority of functional magnetic resonance imaging studies focus on the motor dysfunction and the acute stage of ischemic stroke. This study recruited 15 right-handed ischemic stroke patients at subacute stage (15 days to 11.5 weeks) and 15 age-matched healthy participants. A resting-state functional magnetic resonance imaging scan was performed on each subject to detect cerebral activity. Regional homogeneity analysis was used to investigate the difference in cerebral activities between ischemic stroke patients and healthy participants. The results showed that the ischemic stroke patients had lower regional homogeneity in anterior cingulate and left cerebrum and higher regional homogeneity in cerebellum, left precuneus and left frontal lobe, compared with healthy participants. The experimental findings demonstrate that the areas in which regional homogeneity was different between ischemic stroke patients and healthy participants are in the cerebellum, left precuneus, left triangle inferior frontal gyrus, left inferior temporal gyrus and anterior cingulate. These locations, related to the motor, sensory and emotion areas, are likely potential targets for the neural regeneration of subacute ischemic stroke patients.     

卒中后吞咽障碍患者脑磁图下吞咽皮质环路预探索研究

目的 探讨卒中后吞咽障碍患者皮质吞咽中枢在脑磁图中的激活情况,为吞咽皮质中枢的功能探
讨提供资料。
方法 采用151通道Omega2000全头型生物磁仪（CTF.co,Canada）对6例卒中后吞咽障碍的患者进行
脑磁信号的采集。以等电流偶极（equivalent current dipole,ECD）记录肌电信号开始前－2500 ms内激
活脑区的部位及时间顺序。以每隔20 s、25 s、30 s、35 s时间不等的方式向受试者口腔注射室温纯净
水0.5～1 ml共10次。所有检查者均行头颅磁共振成像（magnetic resonance imaging,MRI）检查,并与脑
磁图的磁场变化结果融合,形成磁源性成像（magnetic source imaging,MSI）。
结果 5例患者得到磁源性影像。所激活的脑区包括岛叶、初级运动感觉皮质、扣带、丘脑等。部分
脑区呈现反复激活,脑内吞咽皮质激活存在3个相对较为固定的环路。中央前后回、岛叶、丘脑、扣带
回持续稳定激活,其初次激活发生在一定时间段内。后扣带较前扣带回及岛叶激活较晚。
结论 吞咽皮质在处理吞咽信息中可能存在一定的环路。后扣带回激活较晚可能是由于卒中后吞咽
皮质功能活动受损的表现。     

Correlating interleukin-10 promoter gene polymorphisms with human cerebral infarction onset

Evidence suggests that interleukin-10 (IL-10) deficiency exacerbates inflammation and worsens the outcome of brain ischemia. In view of the critical role of the single nucleotide polymorphic sites -1082 (A/G) and -819 (C/T) in the promoter region of the IL-10 gene, we hypothesized that they are associated with cerebral infarction morbidity in the Chinese Han population. We genotyped these allelic gene polymorphisms by amplification refractory mutation system-polymerase chain reaction methods in 181 patients with cerebral infarction (cerebral infarction group) and 115 healthy subjects (control group). We identified significant differences in genotype distribution and allele frequency of the IL-10-1082 A/G allele between cerebral infarction and control groups (χ² = 6.643, P = 0.010). The IL-10-1082 A allele frequency was significantly higher in the cerebral infarction group (92.3%) than in the control group (86.1%) (P = 0.015). Moreover, cerebral infarction risk of the AA genotype was 2-fold higher than with the AG genotype (OR = 2.031, 95%CI: 1.134–3.637). In addition, AA genotype together with hypertension was the independent risk factor of cerebral infarction (OR = 2.073, 95%CI: 1.278–3.364). No statistical difference in genotype distribution or allele frequency of IL-10-819 C/T was found between cerebral infarction and control groups (P > 0.05). These findings suggest that the IL-10-1082 A/G gene polymorphism is involved in cerebral infarction, and increased A allele frequency is closely associated with occurrence of cerebral infarction.     

Point application with Angong Niuhuang sticker protects hippocampal and cortical neurons in rats with cerebral ischemia

Angong Niuhuang pill, a Chinese materia medica preparation, can improve neurological functions after acute ischemic stroke. Because of its inconvenient application and toxic components(Cinnabaris and Realgar), we used transdermal enhancers to deliver Angong Niuhuang pill by modern technology, which expanded the safe dose range and clinical indications. In this study, Angong Niuhuang stickers administered at different point application doses(1.35, 2.7, and 5.4 g/kg) were administered to the Dazhui(DU14), Qihai(RN6) and Mingmen(DU4) of rats with chronic cerebral ischemia, for 4 weeks. The Morris water maze was used to determine the learning and memory ability of rats. Hematoxylin-eosin staining and Nissl staining were used to observe neuronal damage of the cortex and hippocampal CA1 region in rats with chronic cerebral ischemia. The middle- and high-dose point application of Angong Niuhuang stickers attenuated neuronal damage in the cortex and hippocampal CA1 region, and improved the memory of rats with chronic cerebral ischemia with an efficacy similar to interventions by electroacupuncture at Dazhui(DU14), Qihai(RN6) and Mingmen(DU4). Our experimental findings indicate that point application with Angong Niuhuang stickers can improve cognitive function after chronic cerebral ischemia in rats and is neuroprotective with an equivalent efficacy to acupuncture.     

Cortical neurogenesis in adult rats after ischemic brain injury: most new neurons fail to mature

The present study examines the hypothesis that endogenous neural progenitor cells isolated from the neocortex of ischemic brain can differentiate into neurons or glial cells and contribute to neural regeneration. We performed middle cerebral artery occlusion to establish a model of cerebral ischemia/reperfusion injury in adult rats. Immunohistochemical staining of the cortex 1, 3, 7, 14 or 28 days after injury revealed that neural progenitor cells double-positive for nestin and sox-2 appeared in the injured cortex 1 and 3 days post-injury, and were also positive for glial fibrillary acidic protein. New neurons were labeled using bromodeoxyuridine and different stages of maturity were identified using doublecortin, microtubule-associated protein 2 and neuronal nuclei antigen immunohistochemistry. Immature new neurons coexpressing doublecortin and bromodeoxyuridine were observed in the cortex at 3 and 7 days post-injury, and semi-mature and mature new neurons double-positive for microtubule-associated protein 2 and bromodeoxyuridine were found at 14 days post-injury. A few mature new neurons coexpressing neuronal nuclei antigen and bromodeoxyuridine were observed in the injured cortex 28 days post-injury. Glial fibrillary acidic protein/bromodeoxyuridine double-positive astrocytes were also found in the injured cortex. Our findings suggest that neural progenitor cells are present in the damaged cortex of adult rats with cerebral ischemic brain injury, and that they differentiate into astrocytes and immature neurons, but most neurons fail to reach the mature stage.     

The role of Rho/Rho-kinase pathway and the neuroprotective effects of fasudil in chronic cerebral ischemia

The Rho/Rho-kinase signaling pathway plays an important role in cerebral ischemia/reperfusion injury. However, very few studies have examined in detail the changes in the Rho/Rho-kinase signaling pathway in chronic cerebral ischemia. In this study, rat models of chronic cerebral ischemia were established by permanent bilateral common carotid artery occlusion and intragastrically administered 9 mg/kg fasudil, a powerful ROCK inhibitor, for 9 weeks. Morris water maze results showed that cognitive impairment progressively worsened as the cerebral ischemia proceeded. Immunohistochemistry, semi-quantitative RT-PCR and western blot analysis showed that the expression levels of Rho-kinase, its substrate myosin-binding subunit, and its related protein alpha smooth muscle actin, significantly increased after chronic cerebral ischemia. TUNEL staining showed that chronic cerebral ischemia could lead to an increase in neuronal apoptosis, as well as the expression level of caspase-3 in the frontal cortex of rats subjected to chronic cerebral ischemia. Fasudil treatment alleviated the cognitive impairment in rats with chronic cerebral ischemia, and decreased the expression level of Rho-kinase, myosin-binding subunit and alpha smooth muscle actin. Furthermore, fasudil could regulate cerebral injury by reducing cell apoptosis and decreasing caspase-3 expression in the frontal cortex. These findings demonstrate that fasudil can protect against cognitive impairment induced by chronic cerebral ischemia via the Rho/Rho-kinase signaling pathway and anti-apoptosis mechanism.     

Traumatic stress: effects on the brain

Brain areas implicated in the stress response include the amygdala, hippocampus, and prefrontal cortex. Traumatic stress can be associated with lasting changes in these brain areas. Traumatic stress is associated with increased cortisol and norepinephrine responses to subsequent stressors. Antidepressants have effects on the hippocampus that counteract the effects of stress. Findings from animal studies have been extended to patients with post-traumatic stress disorder (PTSD) showing smaller hippocampal and anterior cingulate volumes, increased amygdala function, and decreased medial prefrontal/anterior cingulate function. In addition, patients with PTSD show increased cortisol and norepinephrine responses to stress. Treatments that are efficacious for PTSD show a promotion of neurogenesis in animal studies, as well as promotion of memory and increased hippocampal volume in PTSD.     

Relative Changes in Regional Cerebral Blood Flow During Spinal Cord Stimulation in Patients with Refractory Angina Pectoris

Spinal cord stimulation applied at thoracic level 1 (T1) has a neurally mediated anti-anginal effect based on anti-ischaemic action in the myocardium. Positron emission tomography was used to study which higher brain centres are influenced by spinal cord stimulation. Nine patients with a spinal cord stimulator for angina pectoris were studied using H₂¹⁵O as a flow tracer. Relative changes in regional cerebral blood flow related to stimulation compared with non-stimulation were assessed and analysed using the method of statistical parametric mapping. Increased regional cerebral blood flow was observed in the left ventrolateral periaqueductal grey, the medial prefrontal cortex [Brodmann area (BA) 9/10], the dorsomedial thalamus bilaterally, the left medial temporal gyrus (BA 21), the left pulvinar of the thalamus, bilaterally in the posterior caudate nucleus, and the posterior cingulate cortex (BA 30). Relative decreases in rCBF were noticed bilaterally in the insular cortex (BA 20/21 and BA 38), the right inferior temporal gyrus (BA 19/37), the right inferior frontal gyrus (BA 45), the left inferior parietal lobulus (BA 40), the medial temporal gyrus (BA 39) and the right anterior cingulate cortex (BA 24). It is concluded that spinal cord stimulation used as an additional treatment for angina applied at TI modulates regional cerebral blood flow in brain areas known to be associated with nociception and in areas associated with cardiovascular control.     

MicroRNAs: a novel promising therapeutic target for cerebral ischemia/reperfusion injury?

To determine the molecular mechanism of cerebral ischemia/reperfusion injury, we examined the microRNA (miRNA) expression profile in rat cortex after focal cerebral ischemia/reperfusion injury using miRNA microarrays and bioinformatic tools to systematically analyze Gene Ontology (GO) function classifications, as well as the signaling pathways of genes targeted by these differentially expressed miRNAs. Our results show significantly changed miRNA expression profiles in the reperfusion period after focal cerebral ischemia, with a total of 15 miRNAs up-regulated and 44 miRNAs down-regulated. Target genes of these differentially expressed miRNAs were mainly involved in metabolic and cellular processes, which were identified as hub nodes of a miRNA-GO-network. The most correlated pathways included D-glutamine and D-glutamate metabolism, the renin-angiotensin system, peroxisomes, the PPAR signaling pathway, SNARE interactions in vesicular transport, and the calcium signaling pathway. Our study suggests that miRNAs play an important role in the pathological process of cerebral ischemia/reperfusion injury. Understanding miRNA expression and function may shed light on the molecular mechanism of cerebral ischemia/reperfusion injury.     

Plasticity of language networks in patients with brain tumors: a positron emission tomography activation study.

We investigated plasticity of language networks exposed to slowly evolving brain damage. Single subject 0-15-water language activation positron emission tomography studies were analyzed in 61 right-handed patients with brain tumors of the left hemisphere, and 12 normal controls. In controls, activations were found in left Brodmann's Area (BA)44 and BA45, superior posterior temporal gyrus bilaterally, and right cerebellum. Patients additionally activated left BA46, BA47, anterior insula, and left cerebellum. Superior temporal activation was less frequent, and activations in areas other than posterior temporal gyrus were found bilaterally. Frontolateral activations within the nondominant hemisphere were only seen in patients (63%) with frontal or posterior temporal lesions. Laterality indices of frontolateral cortex showed reversed language dominance in 18% of patients. Laterality indices of the cerebellum were negatively correlated with language performance. Two compensatory mechanisms in patients with slowly evolving brain lesions are described: An intrahemispheric mechanism with recruitment of left frontolateral regions other than classic language areas; and an interhemispheric compensatory mechanism with frontolateral activation in the nondominant hemisphere. The latter one was only found in patients with frontal or posterior temporal lesions, thus supporting the hypothesis that right frontolateral activations are a disinhibition phenomenon.     

Cerebral glucose metabolism abnormalities in patients with major depressive symptoms in pre-dialytic chronic kidney disease: statistical parametric mapping analysis of F-18-FDG PET, a preliminary study

Aims: The aim of the present study was to investigate the relationship between depressive symptoms and cerebral glucose metabolism in pre‐dialytic chronic kidney disease (PDCKD) patients. Methods: Twenty‐one patients with stage 5 CKD and 21 healthy volunteers underwent depressive mood assessment and statistical parametric mapping (SPM) using F‐18‐fluorodeoxyglucose (FDG) positron emission tomography (PET). Results: Several voxel clusters of significantly decreased cerebral glucose metabolism were found in PDCKD patients. The largest cluster was left prefrontal cortex (Brodmann area [BA] 9). The second largest cluster was also left prefrontal cortex (BA 9). The third largest clusters were right prefrontal cortex (BA 10) and right basolateral prefrontal cortex (BA 46). Other brain areas also showed decreased cerebral glucose metabolism including left anterior cingulate gyrus (BA 32), left premotor cortex (BA 6), left transverse temporal gyrus (BA 41), left superior temporal gyrus (BA 42), right basolateral prefrontal cortex (BA 44), right inferior parietal lobule (BA 39), left middle temporal gyrus (BA 19), and left angular gyrus (BA 39). Hypermetabolized brain areas, however, were not found in PDCKD patients compared to normal controls. For the right orbitofrontal cortex there was a negative correlation of cerebral glucose metabolism with Hamilton Depression Rating Scale (HDRS) in PDCKD patients (BA 11). Conclusion: PDCKD patients with depressive symptoms had decreased cerebral glucose metabolism in several brain areas. For the right orbitofrontal cortex there was a negative correlation with HDRS in PDCKD patients. The present findings provide functional neuroimaging support for abnormal cerebral glucose metabolism in PDCKD patients with depressive symptoms.     

Optimal concentration and time window for proliferation and differentiation of neural stem cells from embryonic cerebral cortex: 5% oxygen preconditioning for 72 hours

Hypoxia promotes proliferation and differentiation of neural stem cells from embryonic day 12 rat brain tissue, but the concentration and time of hypoxic preconditioning are controversial. To address this, we cultured neural stem cells isolated from embryonic day 14 rat cerebral cortex in 5% and 10% oxygen in vitro. MTT assay, neurosphere number, and immunofluorescent staining found that 5% or 10% oxygen preconditioning for 72 hours improved neural stem cell viability and proliferation. With prolonged hypoxic duration(120 hours), the proportion of apoptotic cells increased. Thus, 5% oxygen preconditioning for 72 hours promotes neural stem cell proliferation and neuronal differentiation. Our findings indicate that the optimal concentration and duration of hypoxic preconditioning for promoting proliferation and differentiation of neural stem cells from the cerebral cortex are 5% oxygen for 72 hours.     

Hydrogen sulfide intervention in focal cerebral ischemia/reperfusion injury in rats

The present study aimed to explore the mechanism underlying the protective effects of hydrogen sulfide against neuronal damage caused by cerebral ischemia/reperfusion. We established the middle cerebral artery occlusion model in rats via the suture method. Ten minutes after middle cerebral artery occlusion, the animals were intraperitoneally injected with hydrogen sulfide donor compound sodium hydrosulfide. Immunofluorescence revealed that the immunoreactivity of P2X₇ in the cerebral cortex and hippocampal CA1 region in rats with cerebral ischemia/reperfusion injury decreased with hydrogen sulfide treatment. Furthermore, treatment of these rats with hydrogen sulfide significantly lowered mortality, the Longa neurological deficit scores, and infarct volume. These results indicate that hydrogen sulfide may be protective in rats with local cerebral ischemia/reperfusion injury by down-regulating the expression of P2X₇ receptors.     

Motor function outcomes of pediatric patients with hemiplegic cerebral palsy after rehabilitation treatment:a diffusion tensor imaging study

Previous diffusion tensor imaging(DTI) studies regarding pediatric patients with motor dysfunction have confirmed the correlation between DTI parameters of the injured corticospinal tract and the severity of motor dysfunction. There is also evidence that DTI parameters can help predict the prognosis of motor function of patients with cerebral palsy. But few studies are reported on the DTI parameters that can reflect the motor function outcomes of pediatric patients with hemiplegic cerebral palsy after rehabilitation treatment. In the present study, 36 pediatric patients with hemiplegic cerebral palsy were included. Before and after rehabilitation treatment, DTI was used to measure the fiber number(FN), fractional anisotropy(FA) and apparent diffusion coefficient(ADC) of bilateral corticospinal tracts. Functional Level of Hemiplegia scale(Fx L) was used to assess the therapeutic effect of rehabilitative therapy on clinical hemiplegia. Correlation analysis was performed to assess the statistical interrelationship between the change amount of DTI parameters and Fx L. DTI findings obtained at the initial and follow-up evaluations demonstrated that more affected corticospinal tract yielded significantly decreased FN and FA values and significantly increased ADC value compared to the less affected corticospinal tract. Correlation analysis results showed that the change amount of Fx L was positively correlated to FN and FA values, and the correlation to FN was stronger than the correlation to FA. The results suggest that FN and FA values can be used to evaluate the motor function outcomes of pediatric patients with hemiplegic cerebral palsy after rehabilitation treatment and FN is of more significance for evaluation.     

Resveratrol inhibits matrix metalloproteinases to attenuate neuronal damage in cerebral ischemia:a molecular docking study exploring possible neuroprotection

The main pathophysiology of cerebral ischemia is the structural alteration in the neurovascular unit, coinciding with neurovascular matrix degradation. Resveratrol has been reported to be one of the most potent chemopreventive agents that can inhibit cellular processes associated with ischemic stroke. Matrix metalloproteinases(MMPs) has been considered as a potential drug target for the treatment of cerebral ischemia. To explore this, we tried to investigate the interaction of resveratrol with MMPs through molecular docking studies. At 30 minutes before and 2 hours after cerebral ischemia/reperfusion induced by occlusion of the middle cerebral artery, 40 mg/kg resveratrol was intraperitoneally administered. After resveratrol administration, neurological function and brain edema were significantly alleviated, cerebral infarct volume was significantly reduced, and nitrite and malondialdehyde levels in the cortical and striatal regions were significantly decreased. The molecular docking study of resveratrol and MMPs revealed that resveratrol occupied the active site of MMP-2 and MMP-9. The binding energy of the complexes was –37.848672 k J/mol and –36.6345 k J/mol for MMP-2 and MMP-9, respectively. In case of MMP-2, Leu 164, Ala 165 and Thr 227 were engaged in H-Bonding with resveratrol and in case of MMP-9, H-bonding was found with Glu 402, Ala 417 and Arg 424 residues. These findings collectively reveal that resveratrol exhibits neuroprotective effects on cerebral ischemia through inhibiting MMP-2 and MMP-9 activity.     

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.