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Prognostic power of the combination of MRI and structural network for the discrimination of conversion from mild cognitive impairment to probable Alzheimer's disease

Prognostic power of the combination of MRI and structural ne...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Ri-Zhen Wei Zhen-Lan Jing Ling Li Key Laboratory for Neuro Information of Ministry of Education School of Life Science and TechnologyUniversity of Electronic Science and Technology of China

Optimized magnetic resonance imaging(MRI) features may allow earlier detection and successful prediction of the progression from mild cognitive impairment(MCI) to Alzheimer's disease(AD). In addition to the cortical and subcortical features, abnormal changes of brain network architectures in MCI, which have been reported to be intermediate states between AD and normal control, are potentially promising for classification of imminent conversion. However, few studies have systematically and extensively assessed the predictive power of combination of MRI and structural network measures in discriminating MCI conversion so far. In this study, using 159 MCI subjectsobtained from baseline ADNI database, we examined whether combining MRI with structural network features, compared with either MRI or network features separately, improves the classification performances. According to the subsequent diagnosis status at follow-up evaluations, subjects were divided into two clinical groups: 1) 76 MCI subjects who converted to AD within 36 months(MCI converters, MCIc), and 2) 83 MCI subjects who did not convert to AD within 36 months(MCI non-converter, MCInc). Specifically, a thickness network matrix was established for each individual by employing a kernel function to calculate the difference in cortical thickness between every pair of regions, and then the weight matrix was thresholded into a binaries matrix using network connection cost. Finally, a total of 380 features were extracted for next classification(244 Free Surfer-derived MRI features including 204 cortical and 40 subcortical features and 136 network features including nodal degrees and nodal path length). To fully assess the combined prognostic power, different types of features were combined in iterative methods. A total of 63 combinations were extracted for next analysis. For each combination, features were selected by stepwise discriminant analysis and the remaining variables were taken as the selected features. M

关键词： mild cognitive impairment,MRI,structural network,classification

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Activation of cannabinoid type Ⅱ receptors modulates T-type voltage-gated calcium channels in rat retinal ganglion cells

Activation of cannabinoid type Ⅱ receptors modulates T-type...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Wen-Jing Qian Qian Li Fang Li Na Wu Xing-Huai Sun Xiong-Li Yang Zhongfeng Wang Institutes of Brain Science Institute of Neurobiology and State Key Laboratory of Medical NeurobiologyFudan University

Endocannabinoid signaling is involved in regulating multiple neuronal functions in the central nervous system, by activating two types of G-protein coupled cannabinoid receptors(CB1Rs and CB2Rs). Growing evidence has shown that CB1 Rs and CB2 Rs are both extensively distributed in the vertebrate retina. Specifically, CB2 Rs are expressed in rat retinal ganglion cells(RGCs). In the present work, we aimed to explore whether activation of CB2 Rs could modulate T-type voltage-gated calcium channels in acutely isolated RGCs using whole-cell patch-clamp techniques. We showed that extracellular application of either CB65 or HU308, two specific CB2 R agonists, significantly suppressed T-type calcium current amplitudes, and the effects could be blocked by co-application of AM630, a selective CB2 R antagonist, suggesting a modulation of CB2 Rs. Furthermore, intracellular c AMP/PKA and Ca M kinase II(Ca MKII) signaling pathways were involved in the CB2Rs-mediated suppression of T-type calcium channels because both c AMP/PKA inhibitors(Rp-c AMP and H-89) and Ca MKII inhibitor(KN-62) could block the CB65 effect. In contrast, neither PKC nor MAPK/ERK signaling pathway was involved since Bis-IV and cherelyrine chloride, two PKC inhibitors, and U0126, a MAPK/ERK inhibitor, did not affect the CB65-induced suppression of T-type calcium currents. As a comparison, CB65 or HU308 administration was found to suppressed L-type calcium currents as well, but the effect could not be blocked by AM630, suggesting a receptor-independent modulation. It seems likely that activation of CB2 Rs may specifically modulate the T-type calcium channels in RGCs.

关键词： retinal ganglion cells T-type calcium channels L-type calcium channels CB2Rs patch clamp

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Reduced cerebral oxygen content in DG and SVZ in situ promotes neurogenesis in adult rat brain in vivo

Reduced cerebral oxygen content in DG and SVZ in situ promot...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Kuan Zhang Yanzhao Zhou Tong Zhao Li-ying Wu Xin Huang Kuiwu Wu Dahu Li Shuhong Liu Yongqi Zhao Ming Fan Ling-ling Zhua Department of Cognitive Sciences Beijing Institute of Basic Medical Sciences Brain Research Center College of Basic Medical SciencesThird Military Medical University Co-innovation Center of Neuro-regeneration Nantong University Beijing Institute for Brain Disorders

Neurogenesis in the adult brain occurs mainly within the two neurogenic structures, the dentate gyrus(DG) of the hippocampus and the sub-ventricular zone(SVZ) of the forebrain. It has been reported that mild hypoxia promoted the proliferation of NSCs in vitro. Our previous study demonstrated that external hypoxic environment stimulates neurogenesis in the adult rat brain in vivo. However, it is unknown that how hypoxic environment affects the oxygen content in brain and result in neurogenesis. Here we use an optical fiber luminescent oxygen sensor to detect the oxygen content in adult rat brain in situ under normoxia and hypoxia. We found that the distribution of oxygen in cerebral regions is spatiotemporally heterogeneous. The Po2 value in the ventricles and DG of the brains are much higher than that in the other parts of the brain(Po2 level is about 10 torr in the DG, and 45～50 torr in the ventricles);While, in the other parts, like cortex and thalamus, the Po2 always remains about 2 torr. Interestingly, our in vivo studies evidenced that external hypoxia environment could change the intrinsic oxygen content in brain tissue, especially, reduced the oxygen levels in both DG and sub-ventricular zone which are the major parts where adult neurogenesis take place. Furthermore, hypoxic environment also increases the expressions of HIF-1/VEGF in DG and SVZ, which have been reported in regulation of neurogenesis. We first evidenced that along with the external environment of the oxygen content decreased, the PO2 levels in DG and SVZ were decreased. The reduced oxygen content in DG and SVZ could be the main causes to trigger neurogenesis in the adult brain. More importantly, we speculate this putative oxygen may be the physiological bases that maintain neurogenesis in restricted area in adult brain.

关键词： neurogenesis oxygen partial pressure cerebral regions intermittent hypoxia Optical fiber luminescent oxygen sensors in vivo

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Roles for the chromatin remodeler CHD7 in CNS patterning and neural stem cell proliferation and differentiation

Roles for the chromatin remodeler CHD7 in CNS patterning and...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Mark Durham Jennifer M.Skidmore Hui Yao Donna M.Martin Medical Scientist Training Program Baylor College of Medicine Departments of Pediatrics The University of Michigan Medical School Human Genetics The University of Michigan Medical School

Impairments in central nervous system(CNS) processing of peripheral sensory functions(vision, hearing, balance and olfaction) are common in autism spectrum disorders(ASDs). CHARGE syndrome, a congenital anomaly disorder and leading cause of multisensory impairment and deafblindness, is one genetic form of ASD. The underlying mechanisms leading to ASD behaviors in CHARGE are not known;however, CNS developmental abnormalities including arrhinencephaly, holoprosencephaly, corpus callosum defects and cerebellar defects are common. CHARGE is caused by heterozygous loss of CHD7, an ATP dependent chromodomain nucleosome remodeling protein that regulates gene expression. Chd7 heterozygous mutant mice exhibit defects in development of inner ear and craniofacial structures similar to those in humans with CHARGE. In mice, Chd7 is expressed in the developing and mature brain regions(olfactory bulb, hypothalamus, midbrain, hindbrain, and cerebellum), and in areas of adult neurogenesis(dentate gyrus of the hippocampus and subventricular zone). Prior studies identified roles for Chd7 in neurogenesis in the developing mouse inner ear and olfactory placode, where CHD7 is expressed in neural stem cells and regulates proneural gene expression, and in the CNS forebrain subventricular zone, where CHD7 regulates neural stem cell proliferation and fate. Here we present data from conditional mice with loss of one or both copies of in the brain. Nestin-Cre-mediated Chd7 deletion led to mild anxiety phenotypes, whereas Wnt1Cre-mediated conditional deletion of Chd7 in the midbrain/hindbrain was postnatal lethal and resulted in cerebellar hypoplasia and reduced foliation in postnatal day 1 cerebella. Loss of Chd7 by Wnt1-Cre also led to attenuation of Wnt1 and Fgf8 expression domains at the embryonic day 11.5 midbrain/hindbrain boundary, consistent with roles for Chd7 in early midbrain-hindbrain patterning. Our results provide novel insights into roles for Chd7 in cerebellar development, and s

关键词： CHD Roles for the chromatin remodeler CHD7 in CNS patterning and neural stem cell proliferation and differentiation CNS

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Nrf2-ARE signals mediated the anti-oxidative action of electro-acupuncture in an MPTP mouse model of Parkinson's disease

Nrf2-ARE signals mediated the anti-oxidative action of elect...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Jun Jia E Lv Jiahui Deng Yan Yu Xiaomin Wang Department of Physiology Key Laboratory for Neurodegenerative Disorders of the Ministry of EducationBeijing Key Laboratory for Parkinson's DiseaseCapital Medical University Beijing Institute for Brain Disorders

Oxidative stress and neuroinflammation are early events associated with dopaminergic neuronal degeneration in Parkinson's disease(PD). Previous studies indicated that electro-acupuncture(EA) stimulation is effective to protect dopaminergic neurons from degeneration in an 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine(MPTP) mouse model of PD. In this study, we further characterized the effect of EA on MPTP-induced oxidative responses in the mouse dopamine system. We found that subacute administration of MPTP enhanced lipid and protein oxidation and reduced expression of endogenous antioxidant enzymes(such as superoxide dismutase and catalase) in the striatum. MPTP also reduced expression of an antioxidant transcription factor, nuclear factor-E2-related factor-2(Nrf2), and Nrf2-regulated antioxidant enzymes(nicotinamide adenine dinucleotide phosphate quinone oxidorreductase-1 and heme oxygenase-1) in the striatum and/or midbrain. Using human placental alkaline phosphatase(h PAP) as a reporter of Nrf2-regulated gene expression in hP AP transgenic mice, we found that MPTP suppressed hP AP expression in the striatum and midbrain. Application of EA at an effective frequency(100 Hz) was sufficient to reverse these changes induced by MPTP. In addition, EA reduced microglia activation and astrogliosis in the striatum and midbrain, increased tyrosine hydroxylase levels in the striatum, and improved vertical movement in MPTP mice. These results provide further evidence supporting that EA produces a series of anti-oxidative effects that effectively counteract with the oxidative stress in the nigrostriatal dopamine system induced by MPTP in a mouse model of PD.

关键词： Parkinson's disease Electro-acupuncture anti-oxidative stress anti-inflammation Nrf2-ARE pathway

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The expression and role of hippocampal HDAC2 in contextual fear memory in rats

The expression and role of hippocampal HDAC2 in contextual f...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Juan Zhang Wen-Yu Cao Fu-Lian Huang Xiao-Ling Zhong Zhao-Lan Hu Hong-Tao Wang Wen-Juan Zhang Xiao-Qing Qiao Fang Li Chang-Qi Li The Department of Anatomy And Neurobiology Xiang Ya School of MedicineCentral South University

Objective Posttraumatic stress disorder(PTSD) is a significant manifestation of mental and behavioural disorders resulted by disaster and intense severe trauma. The present study is to explore the expression and role of hippocampal histone deacetylase2(HDAC2) in the contextual fear memory. Methods The contextual fear memory in rats was established by training rats to using inescapable electric shocks pairing with a neutral stimulus(training context).The expression of HDAC2 in the hippocampus was investigated 30min、2h、6h、24h after fear memory recall. At the peak period of HDAC2 expression, sodium butyrate(Na B) which is a kind of inhibitor of HDAC2 and saline were intraperitoneally administered to the rats respectively. The anxiety-like behaviour was assessed in the Open-Field and Light-Dark Box tests. The remote fear memory was studiedon the 7th day after contextual fear conditioning. Results(1) The expression of HDAC2 in the hippocampus was significantly increased compared with the control group at 30 min and 24 h after fear memory recall.(2)The expression of HDAC2 30 min after fear memory recall was inhibited by intraperitoneally injection of Na B in rats. Rats injected with Na B spent less time in the central of the open field than rats injected with saline did in the open-field test. The difference was statistically significant. In remote contextual fear memory test, there was no significant difference of the freezing level between the two groups on the 7th day.(3) The expression of HDAC2 24 h after fear memory recall was inhibited by intraperitoneally injection of Na B in rats. The number of entered into the white box in the NaB group was significantly less than that of the saline group in light-dark box test. In remote contextual fear memory test, the Na B group showed a higher level of freezing than that in the control group and the difference was statistically significant. Conclusion The expression of HDAC2 in the hippocampus is significantly higher than tha

关键词： PTSD HDAC2 anxiety fear memory.

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Effect of neuropeptide S on anxiety-like behavior and sleep

Effect of neuropeptide S on anxiety-like behavior and sleep

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Jun-Fan XIE Yi-Ping HOU Departments of Neuroscience AnatomyHistologyand EmbryologyKey Laboratory of Preclinical Study for New Drugs of Gansu ProvinceSchool of Basic Medical SciencesLanzhou University

Objective Insomnia induces anxiety and is also one of the most common symptoms of anxiety. However, the mechanism underlying anxiety and insomnia or sleep deprivation(SD) interaction remains to be elucidated. The newly identified neuropeptide S(NPS) and NPS receptor(NPSR) system has been found to be involved in sleep-waking and anxiolytic regulation. The present study was designed to explore the role and potential mechanism of NPS-NPSR system in SD-induced anxiety-like behavior and sleep in rats. Methods The SD-induced anxiety-like behaviors were induced by a modified multiple platform model for 24 h and detected by open field test(OFT) and light/dark(L/D) box. Sleep-wake profiles in vehicle- and NPS-treated rats after SD were assessed by EEG and EMG recording. NPSR m RNA in the amygdala of SD and control rats was respectivelydetected by real-time PCR. The active neurons related to anxiety regulation of NPS were analyzed with c-Fos immunohistochemistry. Results(1) SD caused anxiety-like behaviors in rats by significantly decreasing center time and rearing numbers, and increasing grooming time in OPT, and by significantly decreasing time in light and transition numbers in L/D box. NPS(1 nmol, i.c.v.) suppressed significantly SD-induced anxiety-like behaviors.(2) SD rats significantly increased sleep latency, the amount paradoxical sleep(PS) in light(8:00-20:00 h) and dark phase(20:00-8:00 h), and slow wave sleep(SWS) in dark phase. NPS(dosed at 8:00 h) promoted wakefulness for 3 h, and suppressed SD-induced PS in light phase, but did not influence the SD-induced PS and SWS in dark phase.(3) SD significantly enhanced the NPSR m RNA level in the amygdala by 57%.(4) NPS significantly increased the number of Fos-ir neurons by 4.5–fold in the basolateral amygdaloid complex, 4.2-fold in the central amygdala(Ce A) and 1.9-fold in the medial amygdala(MA). Conclusion A higher level of NPSR m RNA in the amygdala is related to SD-induced anxiety-like behaviors and sleep, sugges

关键词： anxiety neuropeptide S neuropeptide S receptor amygdala sleep deprivation sleep-wake cycle

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Amygdaloid PKA activation plays an anti-anxiety role in social defeat exposed animals

Amygdaloid PKA activation plays an anti-anxiety role in soci...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Liu Yang Lijun Shi Jin Yu Yuqiu Zhang Institute of Neurobiology Institutes of Brain Science and State Key Laboratory of Medical NeurobiologyCollaborative Innovation Center for Brain ScienceFudan University

Objective Social defeat stress(SDS) induces social avoidance and anxiety-like phenotypes. Amygdala is recognized as an emotion-related brain region such as fear, aversion and anxiety. It is conceivable to hypothesize that activation of amygdala is involved in SDS-dependent behavioral defects. The present study is designed to investigate a role of PKA activation in the amygdala on SDS. Methods SDS model was established using C57BL/6J mice that were physically defeated by different CD-1 mice for 10 days. Behavioral defects of stressed mice were observed, including social avoidance(assessed by social interaction test) and anxiety-like behaviors(assessed by elevated plus maze and open field test). Activations of PKA, CREB and FOS were determined by western blotting and immunofluorescence staining. To identify whether p-PKA is the upstream of CREB and FOS activation, 8-Br-c AMP(a PKA agonist) injection in bilateral amygdala and incubation for acute amygdaloid slices were performed. To address the role of PKA activation on SDS, 8-Br-c AMP or H-89(a PKA antagonist) was intra-amygdala injected on the first 4 days of SDS period. Results(1) Stressed mice exhibited decreased social interaction level and significant anxiety-like behaviors.(2) Stressed mice showed a higher phosphorylation of PKA and CREB(with a mutually linear correlation), and increased FOS labeled cells in the amygdala.(3) Activating PKA upregulated p CREB and FOS expression.(4) Neither H-89 nor 8-Br-c AMP influenced the social behavior, while they influenced the anxiety-like behaviors. H-89 slightly aggravated anxiety and 8-Br-c AMP significantly relieved anxiety.(5) Clomipramine, which exerted anti-avoidance and anti-anxiety like effects on stressed mice, up-regulated p-PKA level in the amygdala. Conclusion SDS-driven PKA activation in the amygdala is actually a counter-stress rather than pathogenic response in the homeostasis, and modulating amygdaloid PKA may exhibit potency in the therapy of social derive

关键词： Social defeat anxiety amygdala PKA CREB FOS

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How relevant is autophagy to neurodegeneration:two case studies of motor neuron disease-related DCTN1 and VAPB missense mutations

How relevant is autophagy to neurodegeneration:two case stud...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Jia Yu Carmelo Sgobio Leonardo Aliaga Chen Lai Hoon Shim Huaibin Cai Transgenics Section Laboratory of NeurogeneticsNational Institute on AgingNational Institutes of Health

Impairments of autophagy and lysosome-mediated degradation pathways have been becoming a common pathogenic mechanism of various neurodegenerative diseases. Many of the familial forms of diseases are caused by multitude missense mutations. When overexpressed in cell lines and transgenic mice, very often these mutant proteins form aggregates. These aggregates also co-stain with ubiquitin and P62, makers for the proteasome and autophagosome/lysosome pathways, suggesting the involvement of protein degradation deficiency in the neurodegeneration. However, it remains controversial whether the impairment of autophagy serves as a genuine cause in the process of disease-related neuronal loss or a mere byproduct of the protein overexpression. For example, motor protein dynactin p150 glued has been indicated in the transport of autophagosome to lysosome, while the G59 S missense mutation in p150 glued leads to a rare slow progressive form of motor neuron diseases. Transgenic mice overexpressing p150 glued G59S mutation show formation of p150glued-positive inclusion bodies and accumulation of autophagosomes in the spinal cord motor neurons, implying autophagic cell death in the pathogenesis of motor neurodegeneration. In a parallel study using p150 glued G59S knock-in(KI) mice, the missense mutation seems to destabilize p150 glued proteins rather than induce protein aggregation and autophagy deficiency, suggesting a loss-of-function mechanism for the neuronal loss. To further explore the role of p150 glued in motor neuron disease, we generated and characterized p150 glued conditional knockout mice(c KO) that deleted p150 glued gene from the postnatal motor neurons. The mutant mice developed progressive motor neuron loss similarly to the G59 S KI mice, but showed no evidence of autophagy dysfunction. Together these findings suggest that the autophagy impairments observed in the transgenic mice is likely attributable to the artificial overexpression of mutant proteins, which may

关键词： Autophagy p150glued motor neuron diseases vesicle-associated membrane protein-associated protein B(VAPB) mice

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Disorders of motor coordination ability and spatial learning ability in chronic iron-intoxicated mice

Disorders of motor coordination ability and spatial learning...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Fengjv Jia Ning Song Junxia Xie Hong Jiang Department of Physiology Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: PhysiologyShandong Provincial Collaborative Innovation Center for Neurodegenerative DisordersMedical College of Qingdao University

Environmental factors contribute to the development of Parkinson's disease(PD). High iron intake might be associated with an increased risk of PD. In the present study, we observed the motor symptom and non-motor symptom(spatial learning and memory abilities) in one-year-old C57/BL6 mice with dietary supplements of 3% carbony iron for 1 and 3 months, respectively. The residence time on rotarod treadmills was shorter in 3-month-treated female mice in rotarod test, whereas there was no change in 1-month-treated mice. However, there were no changes of the residence time in the male mice treated for both 1 and 3 months. The contents of dopamine(DA), dihydroxy-phenylaceticacid(DOPAC) and homovanillic acid(HVA) were measured by HPLC. The contents of DA and HVA were decreased by 55.6% and 29.6% respectively, in 3-month-treated female mice. The DA turnover rate was decreased by 38.1%. Interestingly, in 1-month-treated male group, the content of HVA and the level of DA turnover rate were increased by 36.7% and 61.1%. For 3-month-treated male group, the contents of DA, DOPAC and HVA were decreased by 46.3%, 40.6% and 37.3%, respectively. The DA turnover rate was decreased by 27.2% in this group. Spatial learning and memory ability was measured using Morris water maze. The latency to escape on the hidden platform was reduced in iron-intoxicated male mice for 1 month in the training session. Yet, no changes were detected in all the groups in any of the parameters of the probe session(average speed, time to destination, average proximity, platform crossings, relative time in the training and opposite quadrant). In conclusion, the results showed that dietary iron supplement for 1 month and 3 months could alter both motor symptom and spatial learning ability.

关键词： iron motor symptom spatial learning and memory abilities Parkinson's disease

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