Neurodegeneration最新文献_第6页

Microglial Reaction in MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) Induced Parkinson's Disease Mice Model MPTP(1-甲基-4-苯基-1,2,3,6-四氢吡啶)诱导帕金森病小鼠模型的小胶质细胞反应

Neurodegeneration Pub Date : 1996-06-01 DOI: 10.1006/neur.1996.0020

Anna Członkowska , Małgorzata Kohutnicka , Iwona Kurkowska-Jastrzębska , Andrzej Członkowski

引用次数: 279

Improved Selectivity and Sensitivity in the Visualization of Neurofibrillary Tangles, Plaques and Neuropil Threads 提高了神经纤维缠结、斑块和神经纤维线可视化的选择性和灵敏度

Neurodegeneration Pub Date : 1996-06-01 DOI: 10.1006/neur.1996.0025

Cullen K.M. , Halliday G.M. , Cartwright H. , Kril J.J.

{"title":"Improved Selectivity and Sensitivity in the Visualization of Neurofibrillary Tangles, Plaques and Neuropil Threads","authors":"Cullen K.M. , Halliday G.M. , Cartwright H. , Kril J.J.","doi":"10.1006/neur.1996.0025","DOIUrl":"10.1006/neur.1996.0025","url":null,"abstract":"<div><p>Stain sensitivity is a key factor in estimating the frequency of plaques and neurofibrillary tangles in Alzheimer's disease (AD), making it essential that the sensitivity and selectivity of detection methods for identifying these lesions is maximized. Several new, improved techniques have recently been described, although these methods have not been compared quantitatively with those techniques currently recommended for use in standardized diagnostic protocols. In the present study, eight different stains were examined for their selectivity and sensitivity in detecting plaques and tangles in serial tissue sections from AD and control brains. Techniques compared were immunohistochemistry for tau and β-amyloid, thioflavin S, nickel peroxidase method, and four silver impregnation techniques (Gallyas silver iodide, Campbell-Switzer-Martin, Garvey's modified Bielschowsky and methenamine silver methods). Among these eight staining techniques, the nickel peroxidase proved the most reliable method for the demonstration of the histopathological lesions of AD. This method labels all morphological types of plaques and tangles within a single tissue section, and provides several advantages for the analysis of lesion progression and distribution.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 2","pages":"Pages 177-187"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19788834","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: 20

Synaptic Plasticity in the Caudate Nucleus of Patients with Parkinson's Disease 帕金森病患者尾状核的突触可塑性

Neurodegeneration Pub Date : 1996-06-01 DOI: 10.1006/neur.1996.0018

Philippe Anglade, Annick Mouatt-Prigent, Yves Agid, Etienne C. Hirsch

{"title":"Synaptic Plasticity in the Caudate Nucleus of Patients with Parkinson's Disease","authors":"Philippe Anglade, Annick Mouatt-Prigent, Yves Agid, Etienne C. Hirsch","doi":"10.1006/neur.1996.0018","DOIUrl":"10.1006/neur.1996.0018","url":null,"abstract":"<div><p>The loss of dopaminergic neurons from the substantia nigra in Parkinson's disease (PD) may provoke a reorganization of cellular interactions in the nigrostriatal pathway. Indeed, a plasticity of putative corticostriatal synapses has been evidenced in the striatum of rats with a 6-hydroxydopamine-induced lesion of the substantia nigra. However, to our knowledge, synaptic plasticity in the striatum has not previously been investigated in human PD. In this study, we have analysed, at electron microscope level, the morphological characteristics of the synapses formed by afferents in asymmetric contact with dendritic spines of neurons in the caudate nucleus of three patients with PD and three matched controls. The length of the postsynaptic densities and the number of perforated synapses were both significantly increased (24 and 88%, respectively) in the PD patients; the size of these afferents and the surface area occupied by their mitochondria also showed an increase (24 and 50%, respectively), although not statistically significant. The size and density of dendritic spines and the size of postsynaptic density perforations were unchanged. These data indicate the presence of plasticity of the putative corticostriatal synapses in PD and suggest a hyperactivity of cortical afferents to GABAergic neurons.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 2","pages":"Pages 121-128"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19788827","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: 117

The Effects of an RNA Synthesis Inhibitor on the Survival and Regeneration of Rat Motoneurones Injured at Birth RNA合成抑制剂对出生时损伤大鼠运动神经元存活和再生的影响

Neurodegeneration Pub Date : 1996-03-01 DOI: 10.1006/neur.1996.0009

Clowry G.J., Sen P., Vrbová G.

{"title":"The Effects of an RNA Synthesis Inhibitor on the Survival and Regeneration of Rat Motoneurones Injured at Birth","authors":"Clowry G.J., Sen P., Vrbová G.","doi":"10.1006/neur.1996.0009","DOIUrl":"10.1006/neur.1996.0009","url":null,"abstract":"<div><p>This preliminary study aimed to test the proposal that neuronal death is triggered by expression of specific genes. In rat pups, the sciatic nerve was injured unilaterally on the first day after birth and actinomycin D, an RNA synthesis inhibitor, was administered 3 days later in a lower and higher dose to rat pups just prior to onset of motoneurone death induced by the lesion. Four weeks later, sciatic motoneurones from operated and contralateral pools were counted and their size measured. Significantly fewer motoneurones (16.7% ± 2.9 SD) survived when the animals were treated with a lower dose of the inhibitor compared to saline treated controls (36.6% ± 12.7 SD). Experiments recording tension generated in soleus muscle in response to sciatic nerve stimulation, at different ages following nerve crush, suggested that the treatment with the RNA synthesis inhibitor may have delayed regeneration of motor axons back to the muscle. However, survival of motoneurones after treatment with the higher dose did not differ significantly from controls (27.5% ± 1.3 SD. Nevertheless, the higher dose significantly reduced growth of motoneurones after 4 weeks. Therefore, the higher dose, although impeding normal development of motoneurones, is less neurotoxic than a lower dose. This suggests that a balancing of conflicting effects may have occurred. The neurodegenerative effects of delayed reinnervation induced by RNA synthesis inhibition may be balanced by some neuroprotective effects at a higher dose. More extensive studies are required to validate these pilot findings.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 1","pages":"Pages 65-71"},"PeriodicalIF":0.0,"publicationDate":"1996-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19704026","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: 2

Substantia Nigra Pars Reticulata Neurons in Parkinson's Disease 帕金森病的黑质网状部神经元

Neurodegeneration Pub Date : 1996-03-01 DOI: 10.1006/neur.1996.0007

Hardman C.D. , McRitchie D.A. , Halliday G.M. , Cartwright H.R. , Morris J.G.L.

引用次数: 58

Association of Aβ40-positive Senile Plaques with Microglial Cells in the Brains of Patients with Alzheimer's Disease and in Non-demented Aged Individuals 阿尔茨海默病患者和非痴呆老年人大脑中a β40阳性老年斑与小胶质细胞的关系

Neurodegeneration Pub Date : 1996-03-01 DOI: 10.1006/neur.1996.0002

Hiroaki Fukumoto , Asano Asami-Odaka , Nobuhiro Suzuki , Takeshi Iwatsubo

{"title":"Association of Aβ40-positive Senile Plaques with Microglial Cells in the Brains of Patients with Alzheimer's Disease and in Non-demented Aged Individuals","authors":"Hiroaki Fukumoto , Asano Asami-Odaka , Nobuhiro Suzuki , Takeshi Iwatsubo","doi":"10.1006/neur.1996.0002","DOIUrl":"10.1006/neur.1996.0002","url":null,"abstract":"<div><p>To gain insight into the role of microglia in the formation of senile plaques (SP), especially in the generation of the two major molecular species of amyloid β protein (Aβ) with different carboxyl (C)-termini, Aβ40 and Aβ42(43), we conducted double immunolabelling studies on tissue sections from the brains of Alzheimer's disease (AD) and non-demented aged individuals using antibodies to the C-termini of Aβ and ferritin, a marker for microglia. All SP were Aβ42(43)-positive in AD as well as in non-demented individuals, only a proportion of which were Aβ40-positive. Both in AD and in non-demented individuals, approximately 2/3 of the Aβ40-positive SP were typical SP with amyloid cores, these being almost invariably associated with microglia. Aβ40-positive, uncored SP were also frequently associated with microglia (mean, 74%), whereas only 24% of Aβ40-negative, uncored SP contained microglia. These results suggest that microglia may play a role in the maturation of SP, especially in the generation of Aβ40.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 1","pages":"Pages 13-17"},"PeriodicalIF":0.0,"publicationDate":"1996-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19704730","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: 68

Cytotoxicity of Prion Protein Peptide (PrP106–126) Differs in Mechanism from the Cytotoxic Activity of the Alzheimer's Disease Amyloid Peptide, Aβ25–35 朊病毒蛋白肽（PrP106-126）的细胞毒性与阿尔茨海默病淀粉样肽Aβ25-35的细胞毒性作用机制不同

Neurodegeneration Pub Date : 1996-03-01 DOI: 10.1006/neur.1996.0001

James Hope , Mark S. Shearman , Helen C. Baxter , Angela Chong , Sharon M. Kelly , Nicholas C. Price

引用次数: 67

Ultrastructural Immuno-localization of Synthetic Prion Protein Peptide Antibodies in 87V Murine Scrapie 合成朊蛋白肽抗体在87V鼠痒病中的超微结构免疫定位

Neurodegeneration Pub Date : 1996-03-01 DOI: 10.1006/neur.1996.0014

Jeffrey M. , Goodsir C.M. , Fowler N. , Hope J. , Bruce M.E. , McBride P.A.

{"title":"Ultrastructural Immuno-localization of Synthetic Prion Protein Peptide Antibodies in 87V Murine Scrapie","authors":"Jeffrey M. , Goodsir C.M. , Fowler N. , Hope J. , Bruce M.E. , McBride P.A.","doi":"10.1006/neur.1996.0014","DOIUrl":"10.1006/neur.1996.0014","url":null,"abstract":"<div><p>Disease specific forms of a host encoded cell surface sialoglycoprotein called prion protein (PrP) accumulate during the incubation period of the transmissible spongiform encephalopathies. A 33–35 kDa disease specific form of PrP is partially resistant to protease digestion whereas the normal form of PrP can be completely digested. Proteinase K digestion of the murine disease specific form of PrP produces diverse forms of low molecular weight PrP, some of which are N-terminally truncated at amino acid residue 49 or 57 within the octapeptide repeat segment. Amyloid plaques are a pathological feature of many of the transmissible spongiform encephalopathies and are composed of PrP. Using synthetic peptide antibodies to the N-terminus of PrP (which is not present in truncated disease specific PrP) and antibodies to the protease resistant fraction of PrP we have immunostained plaques and pre-amyloid deposits in the brains of mice, experimentally infected with the 87V strain of scrapie, for examination by light and electron microscopy. Classical fibrillar amyloid deposits in plaques as well as pre-amyloid deposits were both immunostained by antibodies to the N-terminus of PrP and to the protease resistant core of the PrP molecule. This suggests that both N-terminal and core amino acid residues are present in disease specific PrP released from scrapie infected cells in vivo. The results also suggest that N-terminal truncation of PrP may not be essential for formation of amyloid fibrils.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 1","pages":"Pages 101-109"},"PeriodicalIF":0.0,"publicationDate":"1996-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19704031","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: 31

Acetylcholine Muscarinic M2 Receptor Stimulated [35S]GTPγS Binding Shows Regional Selective Changes in Alzheimer's Disease Postmortem Brain 乙酰胆碱毒蕈碱M2受体刺激[35S]GTPγS结合在阿尔茨海默病死后大脑中显示区域选择性变化

Neurodegeneration Pub Date : 1996-03-01 DOI: 10.1006/neur.1996.0003

Richard F. Cowburn , Birgitta Wiehager , Rivka Ravid , Bengt Winblad

{"title":"Acetylcholine Muscarinic M2 Receptor Stimulated [35S]GTPγS Binding Shows Regional Selective Changes in Alzheimer's Disease Postmortem Brain","authors":"Richard F. Cowburn , Birgitta Wiehager , Rivka Ravid , Bengt Winblad","doi":"10.1006/neur.1996.0003","DOIUrl":"https://doi.org/10.1006/neur.1996.0003","url":null,"abstract":"<div><p>Oxotremorine-M stimulated [<sup>35</sup>S]GTPγS binding was used to assess acetylcholine muscarinic M2 receptor mediated G-protein function in superior frontal cortical, superior temporal cortical and hippocampal membranes from a series of Alzheimer's disease and matched control subjects. No significant differences were seen in basal [<sup>35</sup>S]GTPγS binding between the groups. The maximal level of oxotremorine-M stimulated [<sup>35</sup>S]GTPγS binding over basal was significantly increased in Alzheimer's disease superior temporal cortex, suggesting an enhanced muscarinic M2 receptor-G-protein coupling efficiency in this region. In contrast, the maximal level of oxotremorine-M stimulated [<sup>35</sup>S]GTPγS binding over basal was unaltered in Alzheimer's disease superior frontal cortex and significantly reduced in Alzheimer's disease hippocampus. Western immunoblotting using antisera towards the α-subunits of those G-protein types known to couple muscarinic receptors, revealed that G<sub>qα</sub>and G<sub>iα</sub>, but not G<sub>oα</sub>, levels were significantly reduced in Alzheimer's disease superior temporal cortex. Neither G<sub>qα</sub>, G<sub>iα</sub>nor G<sub>oα</sub>levels were significantly altered in Alzheimer's disease superior frontal cortex or hippocampus. These results suggest that the efficacy of muscarinic M<sub>2</sub>receptor G-protein coupling shows regional selective changes in Alzheimer's disease postmortem brain with deficits occurring only in a region that shows severe pathology.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 1","pages":"Pages 19-26"},"PeriodicalIF":0.0,"publicationDate":"1996-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72252218","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: 21

Immunoreactive Levels of α-ketoglutarate Dehydrogenase Subunits in Friedreich's Ataxia and Spinocerebellar Ataxia Type 1 Friedreich共济失调和1型棘角肌共济失调患者α-酮戊二酸脱氢酶亚单位的免疫反应水平

Neurodegeneration Pub Date : 1996-03-01 DOI: 10.1006/neur.1996.0004

Frank Mastrogiacomo , Jacques LaMarche , Slobodan Dožić , Gordon Lindsay , Lucien Bettendorff , Yves Robitaille , Lawrence Schut , Stephen J. Kish

{"title":"Immunoreactive Levels of α-ketoglutarate Dehydrogenase Subunits in Friedreich's Ataxia and Spinocerebellar Ataxia Type 1","authors":"Frank Mastrogiacomo , Jacques LaMarche , Slobodan Dožić , Gordon Lindsay , Lucien Bettendorff , Yves Robitaille , Lawrence Schut , Stephen J. Kish","doi":"10.1006/neur.1996.0004","DOIUrl":"https://doi.org/10.1006/neur.1996.0004","url":null,"abstract":"<div><p>Enzyme activities of α-ketoglutarate dehydrogenase complex (αKGDHC) and one of its constituent subunits, dihydrolipoamide dehydrogenase (E3), are reported to be reduced in non-CNS tissues of some patients with Friedreich's ataxia (FA); however, the results are highly confliicting. To determine whether an enzyme abnormality occurs in brain, we measured immunoreactive levels of the three αKGDHC subunits, namely, α-ketoglutarate dehydrogenase (E1), dihydro-lipoamide succinyltransferase (E2) and E3 in postmortem frontal, occipital and cerebellar cortices of 18 control subjects, 9 patients with FA and, for comparison, 12 patients with spinocerebellar ataxia type 1 (SCA1). Decreased (−20 to −31%) levels of E3 were observed in all three examined areas of the patients with FA with the changes statistically significant in cerebellar and frontal cortices. The E3 reduction could be explained by a loss of αKGDHC or other dehydrogenase complexes (e.g. pyruvate dehydrogenase complex) which utilize this subunit. In SCA1, enzyme changes were limited to E2 in cerebellar (−26%) and frontal (−19%) cortices. Although the E3 and E2 reductions are only slight, and may represent secondary events, the changes in this key Krebs cycle enzyme could exacerbate degenerative processes in both of the spinocerebellar ataxia disorders.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 1","pages":"Pages 27-33"},"PeriodicalIF":0.0,"publicationDate":"1996-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72252219","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: 37