A hallmark of all forms of neurodegenerative diseases is impairment of neuronal functions,and in many cases neuronal cell death.Although the etiology of neurodegenerative diseases may be distinct,different diseases di...A hallmark of all forms of neurodegenerative diseases is impairment of neuronal functions,and in many cases neuronal cell death.Although the etiology of neurodegenerative diseases may be distinct,different diseases display a similar pathogenesis,for example abnormal immunity within the central nervous system(CNS),activation of macrophage/microglia and the involvement of proinflammatory cytokines.Recent studies show that neurons in a neurodegenerative state undergo a highly regulated programmed cell death,also called apoptosis.TNF-related apoptosis-inducing ligand(TRAIL),a member of the TNF family,has been shown to be involved in apoptosis during many diseases.As one member of a death ligand family,TRAIL was originally thought to target only tumor cells and was not present in CNS.However,recent data showed that TRAIL was unregulated in HIV-1-infected and immune-activated macrophages,a major disease inducing cell during HIV-1-assoeiated dementia(HAD).TRAIL is also induced on neuron by β-amyloid protein,an important pathogen for Alzheimer's disease.In this review,we summarize the possible common aspects that TRAIL involved those neurodegenerative diseases,TRAIL induced apoptosis signaling in the CNS cells,and specific role of TRAIL in individual diseases.Cellular & Molecular Immunology.2005;2(2):113-122.展开更多
AIM To investigate the expression change of α-synuclein in the brain of different age AD-like an-imal model and to explore the pathology mechanism of α-synuclein in neural degeneration and protective effect of 2 kin...AIM To investigate the expression change of α-synuclein in the brain of different age AD-like an-imal model and to explore the pathology mechanism of α-synuclein in neural degeneration and protective effect of 2 kinds of Chinese components. METHODS A generally accepted animal model of Alzheimer' s disease-APP V717I transgenic (Tg) mouse was observed from 4 to 16 month old. The Tg mice wererandomly divided into model group(4 month, 10 month and 16 month old), Shen-wu capsule with the dose of 0.4g and 1.2g/kg/d, 2,3,5,4’-tetrahydroxystilbene-2-O-β-D-glucoside(TSG), one of effective components in Polygonum muhiflorum, at dose of 0. 05,0.1 and 0.2g/kg/d.展开更多
文摘A hallmark of all forms of neurodegenerative diseases is impairment of neuronal functions,and in many cases neuronal cell death.Although the etiology of neurodegenerative diseases may be distinct,different diseases display a similar pathogenesis,for example abnormal immunity within the central nervous system(CNS),activation of macrophage/microglia and the involvement of proinflammatory cytokines.Recent studies show that neurons in a neurodegenerative state undergo a highly regulated programmed cell death,also called apoptosis.TNF-related apoptosis-inducing ligand(TRAIL),a member of the TNF family,has been shown to be involved in apoptosis during many diseases.As one member of a death ligand family,TRAIL was originally thought to target only tumor cells and was not present in CNS.However,recent data showed that TRAIL was unregulated in HIV-1-infected and immune-activated macrophages,a major disease inducing cell during HIV-1-assoeiated dementia(HAD).TRAIL is also induced on neuron by β-amyloid protein,an important pathogen for Alzheimer's disease.In this review,we summarize the possible common aspects that TRAIL involved those neurodegenerative diseases,TRAIL induced apoptosis signaling in the CNS cells,and specific role of TRAIL in individual diseases.Cellular & Molecular Immunology.2005;2(2):113-122.
文摘AIM To investigate the expression change of α-synuclein in the brain of different age AD-like an-imal model and to explore the pathology mechanism of α-synuclein in neural degeneration and protective effect of 2 kinds of Chinese components. METHODS A generally accepted animal model of Alzheimer' s disease-APP V717I transgenic (Tg) mouse was observed from 4 to 16 month old. The Tg mice wererandomly divided into model group(4 month, 10 month and 16 month old), Shen-wu capsule with the dose of 0.4g and 1.2g/kg/d, 2,3,5,4’-tetrahydroxystilbene-2-O-β-D-glucoside(TSG), one of effective components in Polygonum muhiflorum, at dose of 0. 05,0.1 and 0.2g/kg/d.
