Parkinsonism by unilateral,intranigralβ-sitosterolβ-D-glucoside administration in rats is distinguished in that theα-synuclein insult begins unilaterally but spreads bilaterally and increases in severity over time,...Parkinsonism by unilateral,intranigralβ-sitosterolβ-D-glucoside administration in rats is distinguished in that theα-synuclein insult begins unilaterally but spreads bilaterally and increases in severity over time,thus replicating several clinical features of Parkinson’s disease,a typicalα-synucleinopathy.As Nurr1 repressesα-synuclein,we evaluated whether unilateral transfected of rNurr1-V5 transgene via neurotensin-polyplex to the substantia nigra on day 30 after unilateralβ-sitosterolβ-D-glucoside lesion could affect bilateral neuropathology and sensorimotor deficits on day 30 post-transfection.This study found that rNurr1-V5 expression but not that of the green fluorescent protein(the negative control)reducedβ-sitosterolβ-D-glucoside-induced neuropathology.Accordingly,a bilateral increase in tyrosine hydroxylase-positive cells and arborization occurred in the substantia nigra and increased tyrosine hydroxylase-positive ramifications in the striatum.In addition,tyrosine hydroxylase-positive cells displayed less senescence markerβ-galactosidase and more neuron-cytoskeleton markerβIII-tubulin and brain-derived neurotrophic factor.A significant decrease in activated microglia(positive to ionized calcium-binding adaptor molecule 1)and neurotoxic astrocytes(positive to glial fibrillary acidic protein and complement component 3)and increased neurotrophic astrocytes(positive to glial fibrillary acidic protein and S100 calcium-binding protein A10)also occurred in the substantia nigra.These effects followed the bilateral reduction inα-synuclein aggregates in the nigrostriatal system,improving sensorimotor behavior.Our results show that unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neurodegeneration(senescence and loss of neuron-cytoskeleton and tyrosine hydroxylase-positive cells),neuroinflammation(activated microglia,neurotoxic astrocytes),α-synuclein aggregation,and sensorimotor deficits.Increased neurotrophic astrocytes and brain-derived neurotrophic factor can mediate the rNurr1-V5 effect,supporting its potential clinical use in the treatment of Parkinson’s disease.展开更多
Background:Recent research showed that the NLRP3 inflammasome was activated in the central nervous system of mice administered chronic ethanol(EtOH).Dictyophora polysaccharides(DIPs)are essential components of the val...Background:Recent research showed that the NLRP3 inflammasome was activated in the central nervous system of mice administered chronic ethanol(EtOH).Dictyophora polysaccharides(DIPs)are essential components of the valuable edible fungus Dictyophora,which has antioxidant properties that can delay the aging process of the body.This study aimed to investigate the roles of NLRP3 in chronic EtOH-induced cerebellar Purkinje cell(PC)degeneration and behavioral changes.Methods:C57BL/6J normal and NLRP3 knockout mice were exposed to EtOH for 14 days.Dictyophora polysaccharide(DIP)and NLRP3 inhibitor were administered to the EtOH mice.The pathology and NLRP3-ASC-caspase-1 signaling pathway proteins were analyzed in EtOH mice cerebellar tissues and behavioral performance was assessed in the mice.Results:In the EtOH mouse model,we observed increases in the NLRP3 inflammasome proteins,including NLRP3,ASC,caspase-1,mature IL-1βand pro IL-1β,loss of PCs,and motor coordination disorders.We found that DIPs could suppress the NLRP3-ASC-caspase-1 signaling pathway,and alleviate the motor deficits and cerebellar pathological changes in chronic EtOH mice.Next,we used MCC950,a NLRP3 inhibitor,and an NLRP3 knockout strategy to further verify the effects of NLRP3-ASC-caspase-1 signaling in chronic EtOH mice.MCC950 or NLRP3 knockout alleviated the EtOH-induced latency to decreases in fall time,increases in stride width and decreases in stride length.MCC950 or NLRP3 knockout also attenuated PC number loss and suppressed NLRP3 inflammation induced by EtOH.Taken together,pharmacologically or genetically inhibiting NLRP3 alleviated EtOH-induced cerebellar degeneration and behavioral deficits.Conclusion:These findings indicated that DIPs might diminish EtOH-induced cerebellar degeneration and behavioral deficits through the NLRP3-ASC-caspase-1 signaling pathway,which provides a potential therapeutic target for the prevention and treatment of alcoholism and EtOH-induced cerebellar pathology.展开更多
The mirror neuron system consists of a set of brain areas capable of matching action observation with action execution. One core feature of the mirror neuron system is the activation of motor areas by action observati...The mirror neuron system consists of a set of brain areas capable of matching action observation with action execution. One core feature of the mirror neuron system is the activation of motor areas by action observation alone. This unique capacity of the mirror neuron system to match action perception and action execution stimulated the idea that mirror neuron system plays a crucial role in the understanding of the content of observed actions and may participate in procedural learning. These features bear a high potential for neurorehabilitation of motor deficits and of aphasia following stroke. Since the first articles exploring this principle were published, a growing number of follow-up studies have been conducted in the last decade. Though, the combination of action observation with practice of the observed actions seems to constitute the most powerful approach. In the present review, we present the existing studies analyzing the effects of this neurorehabJlitative approach in clinical settings especially in the rehabilitation of stroke associated motor deficits and give a perspective on the ongoing trials by our research group. The data obtained up to date showed significant positive effect of action observation on recovery of motor functions of the upper limbs even in the chronic state after stroke, indicating that our approach might become a new standardized add-on feature of modern neurorehabilitative treatment schemes.展开更多
Progressive motor deficits are relatively common in acute pontine infarction and frequently associated with increased functional disability. However, the factors that affect the progression of clinical motor weakness ...Progressive motor deficits are relatively common in acute pontine infarction and frequently associated with increased functional disability. However, the factors that affect the progression of clinical motor weakness are largely unknown. Previous studies have suggested that pontine infarctions are caused mainly by basilar artery stenosis and penetrating artery disease. Recently, lower pons lesions in patients with acute pontine infarctions have been reported to be related to progressive motor deficits, and ensuing that damage to the corticospinal tracts may be respon- sible for the worsening of neurological symptoms. Here, we review studies on motor weakness progression in pontine infarction and discuss the mechanisms that may underlie the neurologic worsening.展开更多
Norepinephrine plays an important role in motor functional recovery after a brain injury caused by ferrous chloride.Inhibition of norepinephrine release by clonidine is correlated with motor deficits after motor corte...Norepinephrine plays an important role in motor functional recovery after a brain injury caused by ferrous chloride.Inhibition of norepinephrine release by clonidine is correlated with motor deficits after motor cortex injury.The aim of this study was to analyze the role ofα-adrenergic receptors in the restoration of motor deficits in recovering rats after brain damage.The rats were randomly assigned to the sham and injury groups and then treated with the following pharmacological agents at 3 hours before and 8 hours,3 days,and 20 days after ferrous chloride-induced cortical injury:saline,clonidine,efaroxan(a selective antagonist ofα-adrenergic receptors)and clonidine+efaroxan.The sensorimotor score,the immunohistochemical staining forα-adrenergic receptors,and norepinephrine levels were evaluated.Eight hours post-injury,the sensorimotor score and norepinephrine levels in the locus coeruleus of the injured rats decreased,and these effects were maintained 3 days post-injury.However,20 days later,clonidine administration diminished norepinephrine levels in the pons compared with the sham group.This effect was accompanied by sensorimotor deficits.These effects were blocked by efaroxan.In conclusion,an increase inα-adrenergic receptor levels was observed after injury.Clonidine restores motor deficits in rats recovering from cortical injury,an effect that was prevented by efaroxan.The underlying mechanisms involve the stimulation of hypersensitiveα-adrenergic receptors and inhibition of norepinephrine activity in the locus coeruleus.The results of this study suggest thatαreceptor agonists might restore deficits or impede rehabilitation in patients with brain injury,and therefore pharmacological therapies need to be prescribed cautiously to these patients.展开更多
BACKGROUND Several studies have reported that the walking trail making test(WTMT)completion time is significantly higher in patients with developmental coordination disorders and mild cognitive impairments.We hypothes...BACKGROUND Several studies have reported that the walking trail making test(WTMT)completion time is significantly higher in patients with developmental coordination disorders and mild cognitive impairments.We hypothesized that WTMT performance would be altered in older adults with white matter hyperintensities(WMH).AIM To explore the performance in the WTMT in older people with WMH.METHODS In this single-center,observational study,25 elderly WMH patients admitted to our hospital from June 2019 to June 2020 served as the WMH group and 20 participants matched for age,gender,and educational level who were undergoing physical examination in our hospital during the same period served as the control group.The participants completed the WTMT-A and WTMT-B to obtain their gait parameters,including WTMT-A completion time,WTMT-B completion time,speed,step length,cadence,and stance phase percent.White matter lesions were scored according to the Fazekas scale.Multiple neuropsychological assessments were carried out to assess cognitive function.The relationships between WTMT performance and cognition and motion in elderly patients with WMH were analyzed by partial Pearson correlation analysis.RESULTS Patients with WMH performed significantly worse on the choice reaction test(CRT)(0.51±0.09 s vs 0.44±0.06 s,P=0.007),verbal fluency test(VFT,14.2±2.75 vs 16.65±3.54,P=0.012),and digit symbol substitution test(16.00±2.75 vs 18.40±3.27,P=0.010)than participants in the control group.The WMH group also required significantly more time to complete the WTMT-A(93.00±10.76 s vs 70.55±11.28 s,P<0.001)and WTMT-B(109.72±12.26 s vs 82.85±7.90 s,P<0.001).WTMT-A completion time was positively correlated with CRT time(r=0.460,P=0.001),while WTMT-B completion time was negatively correlated with VFT(r=-0.391,P=0.008).On the WTMT-A,only speed was found to statistically differ between the WMH and control groups(0.803±0.096 vs 0.975±0.050 m/s,P<0.001),whereas on the WTMT-B,the WMH group exhibited a significantly lower speed(0.778±0.111 vs 0.970±0.053 m/s,P<0.001)and cadence(82.600±4.140 vs 85.500±5.020 steps/m,P=0.039),as well as a higher stance phase percentage(65.061±1.813%vs 63.513±2.465%,P=0.019)relative to controls.CONCLUSION Older adults with WMH showed obviously poorer WTMT performance.WTMT could be a potential indicator for cognitive and motor deficits in patients with WMH.展开更多
Dear Editor Aging is linked to changes in brain function that lead to physical decline,including motor deficits and skeletal muscle loss.while maintaining motor activity is crucial for improving the quality of life in...Dear Editor Aging is linked to changes in brain function that lead to physical decline,including motor deficits and skeletal muscle loss.while maintaining motor activity is crucial for improving the quality of life in the elderly,there is limited research on strategies to prevent motor function decline and preserve skeletal muscle.Additionally.approaches to preserving the function of critical neural systems to mitigate age-related motor decline remain underexplored.展开更多
Background:Rapid eye movement sleep behavior disorder(RBD)and Parkinson’s disease(PD)are two distinct clinical diseases but they share some common pathological and anatomical characteristics.This study aims to confir...Background:Rapid eye movement sleep behavior disorder(RBD)and Parkinson’s disease(PD)are two distinct clinical diseases but they share some common pathological and anatomical characteristics.This study aims to confirm the clinical features of RBD in Chinese PD patients.Methods:One hundred fifty PD patients were enrolled from the Parkinson`s disease and Movement Disorders Center in Department of Neurology,Shanghai General Hospital from January 2013 to August 2014.This study examined PD patients with or without RBD as determined by the REM Sleep Behavior Disorder Screening Questionnaire(RBDSQ),assessed motor subtype by Unified PD Rating Scale(UPDRS)III at“on”state,and compared the sub-scale scores representing tremor,rigidity,appendicular and axial.Investigators also assessed the Hamilton Anxiety Scale(HAMA),Hamilton Depression Scale(HAMD),Mini-Mental State Examination(MMSE),Clinical Dementia Rating(CDR),and Parkinson’s disease Sleep Scale(PDSS).Results:One hundred fourty one PD patients entered the final study.30(21.28%)PD patients had probable RBD(pRBD)diagnosed with a RBDSQ score of 6 or above.There were no significant differences for age,including age of PD onset and PD duration,gender,smoking status,alcohol or coffee use,presence of anosmia or freezing,UPDRS III,and H-Y stages between the pRBD+and pRBD−groups.pRBD+group had lower MMSE scores,higher PDSS scores,and pRBD+PD patients had more prominent proportion in anxiety,depression,constipation,hallucination and a greater prevalence of orthostatic hypotension.Conclusion:pRBD+PD patients exhibited greater changes in non-motor symptoms.However,there was no increase in motor deficits.展开更多
Objective:The objective of this study was to investigate whether 70%aqueous ethanol extract of San-Jia-Fu-Mai decoction extract(SJFMDE)could protect against 1-methyl-4-phenylpyridinium(MPP+)-induced oxidative stress i...Objective:The objective of this study was to investigate whether 70%aqueous ethanol extract of San-Jia-Fu-Mai decoction extract(SJFMDE)could protect against 1-methyl-4-phenylpyridinium(MPP+)-induced oxidative stress in PC12 cells and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced motor function deficits in mice.Materials and Methods:The cell viability,the levels of intracellular reactive oxygen species(ROS),malondialdehyde(MDA),and glutathione(GSH)in the MPP+-treated PC12 cells were measured.Motor function deficits and dopamine(DA)level in the brain striatum and tyrosine hydroxylase(TH)-positive cells in substantia nigra pars compacta(SNc)of the MPTP-treated mice were determined.Results:The results showed that SJFMDE could reduce cell death and the levels of ROS and MDA while increase the level of GSH in the MPP+-treated PC12 cells.In addition,in vivo studies showed that oral administration of SJFMDE(3,6,and 12 g/kg)significantly improved the motor function deficits induced by MPTP and enhanced the DA level in the striatum and TH-positive neuronal cells in SNc of the MPTP-treated mice.Conclusions:Our results revealed that SJFMDE possessed neuroprotective effects against neurotoxicity induced by MPP+and motor function deficits induced by MPTP via suppressing oxidative stress and increasing the levels of DA and TH,indicating that SJFMDE might be a promising Chinese medicine formula for the treatment of Parkinson’s disease.展开更多
文摘Parkinsonism by unilateral,intranigralβ-sitosterolβ-D-glucoside administration in rats is distinguished in that theα-synuclein insult begins unilaterally but spreads bilaterally and increases in severity over time,thus replicating several clinical features of Parkinson’s disease,a typicalα-synucleinopathy.As Nurr1 repressesα-synuclein,we evaluated whether unilateral transfected of rNurr1-V5 transgene via neurotensin-polyplex to the substantia nigra on day 30 after unilateralβ-sitosterolβ-D-glucoside lesion could affect bilateral neuropathology and sensorimotor deficits on day 30 post-transfection.This study found that rNurr1-V5 expression but not that of the green fluorescent protein(the negative control)reducedβ-sitosterolβ-D-glucoside-induced neuropathology.Accordingly,a bilateral increase in tyrosine hydroxylase-positive cells and arborization occurred in the substantia nigra and increased tyrosine hydroxylase-positive ramifications in the striatum.In addition,tyrosine hydroxylase-positive cells displayed less senescence markerβ-galactosidase and more neuron-cytoskeleton markerβIII-tubulin and brain-derived neurotrophic factor.A significant decrease in activated microglia(positive to ionized calcium-binding adaptor molecule 1)and neurotoxic astrocytes(positive to glial fibrillary acidic protein and complement component 3)and increased neurotrophic astrocytes(positive to glial fibrillary acidic protein and S100 calcium-binding protein A10)also occurred in the substantia nigra.These effects followed the bilateral reduction inα-synuclein aggregates in the nigrostriatal system,improving sensorimotor behavior.Our results show that unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neurodegeneration(senescence and loss of neuron-cytoskeleton and tyrosine hydroxylase-positive cells),neuroinflammation(activated microglia,neurotoxic astrocytes),α-synuclein aggregation,and sensorimotor deficits.Increased neurotrophic astrocytes and brain-derived neurotrophic factor can mediate the rNurr1-V5 effect,supporting its potential clinical use in the treatment of Parkinson’s disease.
基金Guizhou Provincial Science and Technology Projects,Grant/Award Number:Qian Science Foundation-ZK[2023]General 328Guizhou Provincial Education Department Young Scientific Talent,Grant/Award Number:Qianjiaoji[2024]93+3 种基金National Natural Science Foundation of China,Grant/Award Number:42077313Natural Science Foundation of Guizhou Medical University Incubation Program,Grant/Award Number:20NSP084Research Foundation for Advanced Talents of Guizhou Medical University,Grant/Award Number:University Contract of Doctors J[2021]014Guizhou Provincial 2020 Science and Technology Subsidies,Grant/Award Number:GZ 2020SIG。
文摘Background:Recent research showed that the NLRP3 inflammasome was activated in the central nervous system of mice administered chronic ethanol(EtOH).Dictyophora polysaccharides(DIPs)are essential components of the valuable edible fungus Dictyophora,which has antioxidant properties that can delay the aging process of the body.This study aimed to investigate the roles of NLRP3 in chronic EtOH-induced cerebellar Purkinje cell(PC)degeneration and behavioral changes.Methods:C57BL/6J normal and NLRP3 knockout mice were exposed to EtOH for 14 days.Dictyophora polysaccharide(DIP)and NLRP3 inhibitor were administered to the EtOH mice.The pathology and NLRP3-ASC-caspase-1 signaling pathway proteins were analyzed in EtOH mice cerebellar tissues and behavioral performance was assessed in the mice.Results:In the EtOH mouse model,we observed increases in the NLRP3 inflammasome proteins,including NLRP3,ASC,caspase-1,mature IL-1βand pro IL-1β,loss of PCs,and motor coordination disorders.We found that DIPs could suppress the NLRP3-ASC-caspase-1 signaling pathway,and alleviate the motor deficits and cerebellar pathological changes in chronic EtOH mice.Next,we used MCC950,a NLRP3 inhibitor,and an NLRP3 knockout strategy to further verify the effects of NLRP3-ASC-caspase-1 signaling in chronic EtOH mice.MCC950 or NLRP3 knockout alleviated the EtOH-induced latency to decreases in fall time,increases in stride width and decreases in stride length.MCC950 or NLRP3 knockout also attenuated PC number loss and suppressed NLRP3 inflammation induced by EtOH.Taken together,pharmacologically or genetically inhibiting NLRP3 alleviated EtOH-induced cerebellar degeneration and behavioral deficits.Conclusion:These findings indicated that DIPs might diminish EtOH-induced cerebellar degeneration and behavioral deficits through the NLRP3-ASC-caspase-1 signaling pathway,which provides a potential therapeutic target for the prevention and treatment of alcoholism and EtOH-induced cerebellar pathology.
文摘The mirror neuron system consists of a set of brain areas capable of matching action observation with action execution. One core feature of the mirror neuron system is the activation of motor areas by action observation alone. This unique capacity of the mirror neuron system to match action perception and action execution stimulated the idea that mirror neuron system plays a crucial role in the understanding of the content of observed actions and may participate in procedural learning. These features bear a high potential for neurorehabilitation of motor deficits and of aphasia following stroke. Since the first articles exploring this principle were published, a growing number of follow-up studies have been conducted in the last decade. Though, the combination of action observation with practice of the observed actions seems to constitute the most powerful approach. In the present review, we present the existing studies analyzing the effects of this neurorehabJlitative approach in clinical settings especially in the rehabilitation of stroke associated motor deficits and give a perspective on the ongoing trials by our research group. The data obtained up to date showed significant positive effect of action observation on recovery of motor functions of the upper limbs even in the chronic state after stroke, indicating that our approach might become a new standardized add-on feature of modern neurorehabilitative treatment schemes.
文摘Progressive motor deficits are relatively common in acute pontine infarction and frequently associated with increased functional disability. However, the factors that affect the progression of clinical motor weakness are largely unknown. Previous studies have suggested that pontine infarctions are caused mainly by basilar artery stenosis and penetrating artery disease. Recently, lower pons lesions in patients with acute pontine infarctions have been reported to be related to progressive motor deficits, and ensuing that damage to the corticospinal tracts may be respon- sible for the worsening of neurological symptoms. Here, we review studies on motor weakness progression in pontine infarction and discuss the mechanisms that may underlie the neurologic worsening.
基金supported by Consejo Nacional de Ciencia y Tecnología(CONACy T)project CB 2016-287614(to RGP and ABN)by Scholarship Programa de Apoyo a Proyectos de Investigación e Innovación Tecnológica de la Universidad Nacional Autónoma de México(PAPIIT-UNAM)IA203319 and PAPIIT-UNAM IN216221 to(LERL)。
文摘Norepinephrine plays an important role in motor functional recovery after a brain injury caused by ferrous chloride.Inhibition of norepinephrine release by clonidine is correlated with motor deficits after motor cortex injury.The aim of this study was to analyze the role ofα-adrenergic receptors in the restoration of motor deficits in recovering rats after brain damage.The rats were randomly assigned to the sham and injury groups and then treated with the following pharmacological agents at 3 hours before and 8 hours,3 days,and 20 days after ferrous chloride-induced cortical injury:saline,clonidine,efaroxan(a selective antagonist ofα-adrenergic receptors)and clonidine+efaroxan.The sensorimotor score,the immunohistochemical staining forα-adrenergic receptors,and norepinephrine levels were evaluated.Eight hours post-injury,the sensorimotor score and norepinephrine levels in the locus coeruleus of the injured rats decreased,and these effects were maintained 3 days post-injury.However,20 days later,clonidine administration diminished norepinephrine levels in the pons compared with the sham group.This effect was accompanied by sensorimotor deficits.These effects were blocked by efaroxan.In conclusion,an increase inα-adrenergic receptor levels was observed after injury.Clonidine restores motor deficits in rats recovering from cortical injury,an effect that was prevented by efaroxan.The underlying mechanisms involve the stimulation of hypersensitiveα-adrenergic receptors and inhibition of norepinephrine activity in the locus coeruleus.The results of this study suggest thatαreceptor agonists might restore deficits or impede rehabilitation in patients with brain injury,and therefore pharmacological therapies need to be prescribed cautiously to these patients.
基金Supported by The Wu Jieping Medical Foundation,No.320.6750.18456.
文摘BACKGROUND Several studies have reported that the walking trail making test(WTMT)completion time is significantly higher in patients with developmental coordination disorders and mild cognitive impairments.We hypothesized that WTMT performance would be altered in older adults with white matter hyperintensities(WMH).AIM To explore the performance in the WTMT in older people with WMH.METHODS In this single-center,observational study,25 elderly WMH patients admitted to our hospital from June 2019 to June 2020 served as the WMH group and 20 participants matched for age,gender,and educational level who were undergoing physical examination in our hospital during the same period served as the control group.The participants completed the WTMT-A and WTMT-B to obtain their gait parameters,including WTMT-A completion time,WTMT-B completion time,speed,step length,cadence,and stance phase percent.White matter lesions were scored according to the Fazekas scale.Multiple neuropsychological assessments were carried out to assess cognitive function.The relationships between WTMT performance and cognition and motion in elderly patients with WMH were analyzed by partial Pearson correlation analysis.RESULTS Patients with WMH performed significantly worse on the choice reaction test(CRT)(0.51±0.09 s vs 0.44±0.06 s,P=0.007),verbal fluency test(VFT,14.2±2.75 vs 16.65±3.54,P=0.012),and digit symbol substitution test(16.00±2.75 vs 18.40±3.27,P=0.010)than participants in the control group.The WMH group also required significantly more time to complete the WTMT-A(93.00±10.76 s vs 70.55±11.28 s,P<0.001)and WTMT-B(109.72±12.26 s vs 82.85±7.90 s,P<0.001).WTMT-A completion time was positively correlated with CRT time(r=0.460,P=0.001),while WTMT-B completion time was negatively correlated with VFT(r=-0.391,P=0.008).On the WTMT-A,only speed was found to statistically differ between the WMH and control groups(0.803±0.096 vs 0.975±0.050 m/s,P<0.001),whereas on the WTMT-B,the WMH group exhibited a significantly lower speed(0.778±0.111 vs 0.970±0.053 m/s,P<0.001)and cadence(82.600±4.140 vs 85.500±5.020 steps/m,P=0.039),as well as a higher stance phase percentage(65.061±1.813%vs 63.513±2.465%,P=0.019)relative to controls.CONCLUSION Older adults with WMH showed obviously poorer WTMT performance.WTMT could be a potential indicator for cognitive and motor deficits in patients with WMH.
基金supported by grants from the National Research Foundation of Korea(MSIT:RS-2024-00408736,NRF-2020R1A2C2007954,and2017R1A2B4002675)funded by the Korean government.
文摘Dear Editor Aging is linked to changes in brain function that lead to physical decline,including motor deficits and skeletal muscle loss.while maintaining motor activity is crucial for improving the quality of life in the elderly,there is limited research on strategies to prevent motor function decline and preserve skeletal muscle.Additionally.approaches to preserving the function of critical neural systems to mitigate age-related motor decline remain underexplored.
基金This work was supported by the National Natural Science Foundation of China(NSFC)(81171205,81371410)the Biomedical Multidisciplinary Program of Shanghai Jiao Tong University(YG2014MS31,YG2015QN21,YG2016QN25).
文摘Background:Rapid eye movement sleep behavior disorder(RBD)and Parkinson’s disease(PD)are two distinct clinical diseases but they share some common pathological and anatomical characteristics.This study aims to confirm the clinical features of RBD in Chinese PD patients.Methods:One hundred fifty PD patients were enrolled from the Parkinson`s disease and Movement Disorders Center in Department of Neurology,Shanghai General Hospital from January 2013 to August 2014.This study examined PD patients with or without RBD as determined by the REM Sleep Behavior Disorder Screening Questionnaire(RBDSQ),assessed motor subtype by Unified PD Rating Scale(UPDRS)III at“on”state,and compared the sub-scale scores representing tremor,rigidity,appendicular and axial.Investigators also assessed the Hamilton Anxiety Scale(HAMA),Hamilton Depression Scale(HAMD),Mini-Mental State Examination(MMSE),Clinical Dementia Rating(CDR),and Parkinson’s disease Sleep Scale(PDSS).Results:One hundred fourty one PD patients entered the final study.30(21.28%)PD patients had probable RBD(pRBD)diagnosed with a RBDSQ score of 6 or above.There were no significant differences for age,including age of PD onset and PD duration,gender,smoking status,alcohol or coffee use,presence of anosmia or freezing,UPDRS III,and H-Y stages between the pRBD+and pRBD−groups.pRBD+group had lower MMSE scores,higher PDSS scores,and pRBD+PD patients had more prominent proportion in anxiety,depression,constipation,hallucination and a greater prevalence of orthostatic hypotension.Conclusion:pRBD+PD patients exhibited greater changes in non-motor symptoms.However,there was no increase in motor deficits.
基金supported by the Innovation and Technology Commission Funding Administrative System of Hong Kong(Project No.:ITS/122/19FP)the Natural Science Fund of Guangdong(project no.2019A1515011257)
文摘Objective:The objective of this study was to investigate whether 70%aqueous ethanol extract of San-Jia-Fu-Mai decoction extract(SJFMDE)could protect against 1-methyl-4-phenylpyridinium(MPP+)-induced oxidative stress in PC12 cells and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced motor function deficits in mice.Materials and Methods:The cell viability,the levels of intracellular reactive oxygen species(ROS),malondialdehyde(MDA),and glutathione(GSH)in the MPP+-treated PC12 cells were measured.Motor function deficits and dopamine(DA)level in the brain striatum and tyrosine hydroxylase(TH)-positive cells in substantia nigra pars compacta(SNc)of the MPTP-treated mice were determined.Results:The results showed that SJFMDE could reduce cell death and the levels of ROS and MDA while increase the level of GSH in the MPP+-treated PC12 cells.In addition,in vivo studies showed that oral administration of SJFMDE(3,6,and 12 g/kg)significantly improved the motor function deficits induced by MPTP and enhanced the DA level in the striatum and TH-positive neuronal cells in SNc of the MPTP-treated mice.Conclusions:Our results revealed that SJFMDE possessed neuroprotective effects against neurotoxicity induced by MPP+and motor function deficits induced by MPTP via suppressing oxidative stress and increasing the levels of DA and TH,indicating that SJFMDE might be a promising Chinese medicine formula for the treatment of Parkinson’s disease.
