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Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration最新文献

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Lack of association of apolipoprotein E epsilon 4 allele with progressive supranuclear palsy. 载脂蛋白E ε 4等位基因与进行性核上性麻痹缺乏关联。
Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration Pub Date : 1996-06-01
H Arai, S Higuchi, T Muramatsu, S Matsushita, S Itabashi, H Sasaki
{"title":"Lack of association of apolipoprotein E epsilon 4 allele with progressive supranuclear palsy.","authors":"H Arai, S Higuchi, T Muramatsu, S Matsushita, S Itabashi, H Sasaki","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":19109,"journal":{"name":"Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration","volume":"5 2","pages":"194-5"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19788106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Normal natural killer cell activity in a patient with adrenoleukodystrophy treated with Lorenzo's oil. 洛伦佐油治疗肾上腺脑白质营养不良患者的正常自然杀伤细胞活性。
Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration Pub Date : 1996-06-01
M Tanaka, R Koike, T Kuwabara
{"title":"Normal natural killer cell activity in a patient with adrenoleukodystrophy treated with Lorenzo's oil.","authors":"M Tanaka, R Koike, T Kuwabara","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":19109,"journal":{"name":"Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration","volume":"5 2","pages":"192-4"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19788105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Dystrophic neurites define diffuse as well as core-containing senile plaques in Alzheimer's disease. 在阿尔茨海默病中，营养不良的神经突定义了弥漫性和含核心的老年斑。
Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration Pub Date : 1995-06-01
R P Rifenburg, G Perry
{"title":"Dystrophic neurites define diffuse as well as core-containing senile plaques in Alzheimer's disease.","authors":"R P Rifenburg, G Perry","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":19109,"journal":{"name":"Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration","volume":"4 2","pages":"235-7"},"PeriodicalIF":0.0,"publicationDate":"1995-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18588251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Brain aminobutyrate aminotransferase activity in Alzheimer's disease. 阿尔茨海默病的脑氨基丁酸氨基转移酶活性。
Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration Pub Date : 1995-03-01
F Sherif, S S Ahmed, L Eriksson
{"title":"Brain aminobutyrate aminotransferase activity in Alzheimer's disease.","authors":"F Sherif, S S Ahmed, L Eriksson","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":19109,"journal":{"name":"Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration","volume":"4 1","pages":"114-5"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18606851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Clusterin as a marker for ischaemic Purkinje cells in human brain. 聚簇素作为人脑缺血浦肯野细胞的标志物。
Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration Pub Date : 1994-12-01
O Yasuhara, Y Aimi, T Yamada, A Matsuo, E G McGeer, P L McGeer
{"title":"Clusterin as a marker for ischaemic Purkinje cells in human brain.","authors":"O Yasuhara,&nbsp;Y Aimi,&nbsp;T Yamada,&nbsp;A Matsuo,&nbsp;E G McGeer,&nbsp;P L McGeer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Clusterin has been implicated in cell death both in peripheral tissues and in the central nervous system. In the present study, expression of clusterin in the cerebellar cortex was examined in two cases with hypoxic brain damage and in one case with cerebellar infarction. Intense staining of Purkinje cells was observed in each case, and these cells showed the shrunken and pyknotic appearance characteristic of irreversible ischaemic damage. In the cerebella of neurologically normal control cases, as well as in those of some other neurodegenerative diseases, no staining or only punctate staining of Purkinje cells was observed. The results provide additional evidence supporting an association of clusterin with dying neurons in human brain.</p>","PeriodicalId":19109,"journal":{"name":"Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration","volume":"3 4","pages":"325-9"},"PeriodicalIF":0.0,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18843655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
HLA antigens in paraneoplastic cerebellar degeneration associated with anti-Yo antibody. HLA抗原与副肿瘤小脑变性相关的抗yo抗体。
Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration Pub Date : 1994-12-01
M Tanaka, K Tanaka, S Tsuji
{"title":"HLA antigens in paraneoplastic cerebellar degeneration associated with anti-Yo antibody.","authors":"M Tanaka,&nbsp;K Tanaka,&nbsp;S Tsuji","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":19109,"journal":{"name":"Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration","volume":"3 4","pages":"341-2"},"PeriodicalIF":0.0,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18843658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Automatic quantification of amyloid plaque formation in human spongiform encephalopathy. 人海绵状脑病中淀粉样斑块形成的自动定量。
Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration Pub Date : 1994-12-01
K Sutherland, C Barrie, J W Ironside
{"title":"Automatic quantification of amyloid plaque formation in human spongiform encephalopathy.","authors":"K Sutherland,&nbsp;C Barrie,&nbsp;J W Ironside","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This study compared a panel of three different prion protein antibodies with conventional plaque staining methods--Congo Red, Periodic acid Schiff and sulphated Alcian blue--to investigate amyloid plaque formation in cases of human spongiform encephalopathy (HSE). Tissue samples were taken from the cerebellum in nine sporadic cases of Creutzfeldt-Jakob Disease, with plaque formation noted on routine histology, and one case of Gerstmann-Straussler Scheinker syndrome. Using image analysis techniques, a semi-automatic system of plaque quantification was devised to measure the relative performance of these different staining methods. A total figure of percentage tissue area stained positively was returned by the system in each case analysed. A significant statistical correlation was observed among all three antibodies (r > 0.9, P < 0.01, in all comparisons) and a significant improvement was observed when the average antibody staining figures were compared to those of the Alcian blue technique (P < 0.05). The distribution of plaques across the cerebellar layers observed here appears to confirm earlier research findings. A strong correlation was found between staining in the two cerebellar hemispheres (r = 0.97, P < 0.01). This novel image analysis system has considerable potential for objective assessment of the pathology of HSE.</p>","PeriodicalId":19109,"journal":{"name":"Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration","volume":"3 4","pages":"293-300"},"PeriodicalIF":0.0,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18538728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Topographic investigation of brain atrophy in parkinsonism-dementia complex of Guam: a comparison with Alzheimer's disease and progressive supranuclear palsy. 关岛帕金森-痴呆综合征脑萎缩的地形学研究:与阿尔茨海默病和进行性核上麻痹的比较。
Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration Pub Date : 1994-12-01
K Oyanagi, T Makifuchi, T Ohtoh, F Ikuta, K M Chen, T N Chase, D C Gajdusek
{"title":"Topographic investigation of brain atrophy in parkinsonism-dementia complex of Guam: a comparison with Alzheimer's disease and progressive supranuclear palsy.","authors":"K Oyanagi,&nbsp;T Makifuchi,&nbsp;T Ohtoh,&nbsp;F Ikuta,&nbsp;K M Chen,&nbsp;T N Chase,&nbsp;D C Gajdusek","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The topographic distribution of brain atrophy in nine patients with parkinsonism-dementia complex of Guam (Guam PDC) was evaluated quantitatively, and compared with that in six Japanese patients with Alzheimer's disease or senile dementia of Alzheimer type (AD), five Japanese patients with progressive supranuclear palsy (PSP), and nine Japanese control subjects. Characteristic features of Guam PDC were as follows: (1) severe atrophy of the frontal and temporal cortex with relative preservation of the white matter; (2) atrophy of the tectum, tegmentum and cerebral peduncle of the midbrain, and (3) atrophy of the tegmentum and base of the upper pons. In contrast, sectional areas of the tectum and cerebral peduncle of the midbrain were relatively well preserved in PSP, while in AD there was no significant atrophy in the brain stem.</p>","PeriodicalId":19109,"journal":{"name":"Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration","volume":"3 4","pages":"301-4"},"PeriodicalIF":0.0,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18840598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Aging and the nigrostriatal dopamine system: a non-human primate study. 衰老与黑质纹状体多巴胺系统:一项非人类灵长类动物研究。
Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration Pub Date : 1994-12-01
I Irwin, L E DeLanney, T McNeill, P Chan, L S Forno, G M Murphy, D A Di Monte, M S Sandy, J W Langston
{"title":"Aging and the nigrostriatal dopamine system: a non-human primate study.","authors":"I Irwin,&nbsp;L E DeLanney,&nbsp;T McNeill,&nbsp;P Chan,&nbsp;L S Forno,&nbsp;G M Murphy,&nbsp;D A Di Monte,&nbsp;M S Sandy,&nbsp;J W Langston","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The present study examined neurochemical, morphological and functional markers of the nigrostriatal dopamine system in young, intermediate-aged and old squirrel monkeys. Striking reductions in motoric activity were observed with advancing age. significant age-related loss of dopamine occurred in the substantia nigra (70%) and the putamen (30%) but not in the caudate. There was a strong correlation between the reductions in motoric activity and the loss of putamen dopamine. However, nigrostriatal dopamine loss did not appear to be the consequence of age-related loss of dopaminergic nigral neurons since the number of tyrosine immunoreactive cells was not significantly different among the three age groups. These results suggest that the aging squirrel monkey demonstrates the age-related loss of nigrostriatal dopamine thought to occur in humans and identify this non-human primate as a useful model to further investigate the underlying mechanism(s) and functional consequences of age-related decline of the nigrostriatal dopamine system. In addition, the selective loss of dopamine in the putamen but not the caudate parallels the regional vulnerability observed in Parkinson's disease, an age-related neurodegenerative disorder, raising the possibility of a relationship between normal aging and the development of this disease. Finally, because the number of tyrosine hydroxylase (TH) positive cells remains constant with age, these results raise the possibility that therapeutic strategies aimed at increasing dopamine concentrations may benefit elderly individuals.</p>","PeriodicalId":19109,"journal":{"name":"Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration","volume":"3 4","pages":"251-65"},"PeriodicalIF":0.0,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18538727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Expression of the neural cell adhesion molecule (NCAM) in Alzheimer's disease. 神经细胞粘附分子(NCAM)在阿尔茨海默病中的表达
Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration Pub Date : 1994-12-01
A M Gillian, J P Brion, K C Breen
{"title":"Expression of the neural cell adhesion molecule (NCAM) in Alzheimer's disease.","authors":"A M Gillian,&nbsp;J P Brion,&nbsp;K C Breen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Expression of the nerve cell adhesion molecule, NCAM, was examined in post-mortem brain samples from patients with Alzheimer's disease (AD) and from age-matched controls. Four major isoforms of NCAM were identified by Western blot analysis 195, 185, 145 and 120 kDa with no differences being observed in either the intensity of individual band staining or in the expression of the constituent NCAM isoforms in AD when compared with controls. Immunohistochemical staining revealed star-shaped NCAM-positive structures with numerous radiating 'processes' or a more protoplasmic shape with short and thick 'processes'. These structures were not obviously more abundant in AD and there was no NCAM immunoreactivity in neuritic plaques or neurofibrillary tangles. This evidence suggests there is no change in NCAM expression in AD.</p>","PeriodicalId":19109,"journal":{"name":"Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration","volume":"3 4","pages":"283-91"},"PeriodicalIF":0.0,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18840597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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