目的研究寡聚化α-突触核蛋白(oligomer-α-synuclein,oligo-α-Syn)在不同年龄段食蟹猴消化道中的表达差异。方法 Western blotting和ELISA方法检测oligo-α-Syn在不同年龄段食蟹猴消化道中的表达。结果在老年食蟹猴的食管、胃底、十...目的研究寡聚化α-突触核蛋白(oligomer-α-synuclein,oligo-α-Syn)在不同年龄段食蟹猴消化道中的表达差异。方法 Western blotting和ELISA方法检测oligo-α-Syn在不同年龄段食蟹猴消化道中的表达。结果在老年食蟹猴的食管、胃底、十二指肠、空肠、回肠和结肠中,寡聚化α-Syn浓度较青年与中年猴显著增加,且差异有统计学意义(P<0.01)。结论食蟹猴消化道的各部位中α-Syn寡聚体表达具有增龄性变化。展开更多
Parkinson’s disease(PD)is a common age-related neurodegenerative disease characterized by movement disorders.The hallmark pathological lesions of PD are the formation of Lewy pathology in selected populations of neur...Parkinson’s disease(PD)is a common age-related neurodegenerative disease characterized by movement disorders.The hallmark pathological lesions of PD are the formation of Lewy pathology in selected populations of neurons throughout the nervous system.Braak and his colleagues created a staging system for PD describing the connection between Lewy pathology and disease severity.They proposed that Lewy pathology might be initially triggered by exogenous pathogens targeting the enteric or olfactory nervous system,then spread in a prion-like propagation manner from the peripheral nerves to the lower brainstem and midbrain,before finally reaching higher cortical structures,causing a sequential occurrence of the non-motor and motor symptoms,depending on the lesioned neurons.However,emerging evidence also supports a functional threshold hypothesis proposed by Engelender and Isacson in which Lewy pathology may occur parallelly in the central and peripheral nervous systems and the symptoms only begin when the functional reserve of the affected neurons(and their connecting brain regions)is unable to allow for network compensation.Consequently,early symptoms of PD reflect the loss of function in the least compensated systems,such as the enteric and olfactory nervous systems,rather than the spread of Lewy pathology from the peripheral to the central nervous systems.The current review article provides a comprehensive overview of the evidence supporting a merged mechanism that the neurodegeneration in PD happens to those neurons that are not only intrinsically vulnerable but also affected by the spread of Lewy pathology.展开更多
文摘目的研究寡聚化α-突触核蛋白(oligomer-α-synuclein,oligo-α-Syn)在不同年龄段食蟹猴消化道中的表达差异。方法 Western blotting和ELISA方法检测oligo-α-Syn在不同年龄段食蟹猴消化道中的表达。结果在老年食蟹猴的食管、胃底、十二指肠、空肠、回肠和结肠中,寡聚化α-Syn浓度较青年与中年猴显著增加,且差异有统计学意义(P<0.01)。结论食蟹猴消化道的各部位中α-Syn寡聚体表达具有增龄性变化。
基金the authors were supported by grants from Natural Science Foundation of China(81671244,81371200,and 81401042)Beijing Municipal Science and Technology Commission(Z161100005116011,Z171100000117013)+1 种基金Beijing Municipal Commission of Health and Family Planning(PXM2017_026283_000002)Beijing Nova Program(Z181100006218052,xx2018096)to Yang WW.
文摘Parkinson’s disease(PD)is a common age-related neurodegenerative disease characterized by movement disorders.The hallmark pathological lesions of PD are the formation of Lewy pathology in selected populations of neurons throughout the nervous system.Braak and his colleagues created a staging system for PD describing the connection between Lewy pathology and disease severity.They proposed that Lewy pathology might be initially triggered by exogenous pathogens targeting the enteric or olfactory nervous system,then spread in a prion-like propagation manner from the peripheral nerves to the lower brainstem and midbrain,before finally reaching higher cortical structures,causing a sequential occurrence of the non-motor and motor symptoms,depending on the lesioned neurons.However,emerging evidence also supports a functional threshold hypothesis proposed by Engelender and Isacson in which Lewy pathology may occur parallelly in the central and peripheral nervous systems and the symptoms only begin when the functional reserve of the affected neurons(and their connecting brain regions)is unable to allow for network compensation.Consequently,early symptoms of PD reflect the loss of function in the least compensated systems,such as the enteric and olfactory nervous systems,rather than the spread of Lewy pathology from the peripheral to the central nervous systems.The current review article provides a comprehensive overview of the evidence supporting a merged mechanism that the neurodegeneration in PD happens to those neurons that are not only intrinsically vulnerable but also affected by the spread of Lewy pathology.
