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[PMID]:26857919
[Au] Autor:Wharton SB; Minett T; Drew D; Forster G; Matthews F; Brayne C; Ince PG; MRC Cognitive Function and Ageing Neuropathology Study Group
[Ad] Endereço:Sheffield Institute for Translational Neuroscience, University of Sheffield, 385A Glossop Road, Sheffield, S10 2HQ, UK.
[Ti] Título:Epidemiological pathology of Tau in the ageing brain: application of staging for neuropil threads (BrainNet Europe protocol) to the MRC cognitive function and ageing brain study.
[So] Source:Acta Neuropathol Commun;4:11, 2016 Feb 08.
[Is] ISSN:2051-5960
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Deposition of abnormally phosphorylated tau (phospho-tau) occurs in Alzheimer's disease but also with brain ageing. The Braak staging scheme focused on neurofibrillary tangles, but abundant p-tau is also present in neuropil threads, and a recent scheme has been proposed by the BrainNet Europe consortium for staging tau pathology based on neuropil threads. We determined the relationship of threads to tangles, and the value of staging for threads in an unselected population-representative ageing brain cohort. We also determined the prevalence of astroglial tau pathologies, and their relationship to neuronal tau. Phospho-tau pathology was determined by immunohistochemistry (AT8 antibody) in the MRC-CFAS neuropathology cohort. Neuropil threads were staged using the BrainNet Europe protocol for tau pathology, and compared with Braak tangle stages. Astroglial tau pathology was assessed in neo-cortical, mesial temporal and subcortical areas. RESULTS: Cases conformed well to the hierarchical neuropil threads staging of the BrainNet Europe protocol and correlated strongly with Braak staging (r=0.84, p < 0.001). Based on the areas under the receiver operator curves (AUC), incorporating either threads or tangle staging significantly improved dementia case identification to a similar degree over age alone (Braak stage X (2)(1)=10.1, p=0.002; BNE stage X (2)(1)=9.7, p=0.002). Thorn-shaped astrocytes, present in 40 % of cases, were most common in mesial temporal lobe, then brainstem, and were associated with subpial tau-positive neurites (mesial temporal: X (2)(1)=61.3, p < 0.001; brainstem: X (2)(1)=47.9, p < 0.001). Adding thorn astrocytes did not improve dementia prediction (AUC: X (2)(1)=0.77, p=0.381), but there was a weak relationship between numbers of areas involved and staging for threads or tangles (r=0.17, p=0.023). Neuropil threads develop hierarchically in parallel with neurofibrillary tangles. CONCLUSIONS: The BrainNet Europe staging protocol is straightforward to apply, and offers similar predictive value for dementia to Braak tangle staging. Astroglial tauopathy, particularly thorn shaped astrocyte formation, does not relate to dementia status, but the association with phospho-tau neurites may suggest a pathogenic relationship to neuronal tau pathology.
[Mh] Termos MeSH primário: Envelhecimento/patologia
Encéfalo/patologia
Filamentos do Neurópilo/patologia
Tauopatias
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Estudos de Coortes
Progressão da Doença
Europa (Continente)/epidemiologia
Feminino
Seres Humanos
Masculino
Emaranhados Neurofibrilares/patologia
Fosforilação
Escalas de Graduação Psiquiátrica
Tauopatias/epidemiologia
Tauopatias/metabolismo
Tauopatias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (tau Proteins)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160210
[St] Status:MEDLINE
[do] DOI:10.1186/s40478-016-0275-x


  2 / 67 MEDLINE  
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[PMID]:26293308
[Au] Autor:Mizukami K; Akatsu H; Abrahamson EE; Mi Z; Ikonomovic MD
[Ad] Endereço:Faculty of Health and Sport Sciences, Tsukuba, Japan.
[Ti] Título:Immunohistochemical analysis of hippocampal butyrylcholinesterase: Implications for regional vulnerability in Alzheimer's disease.
[So] Source:Neuropathology;36(2):135-45, 2016 Apr.
[Is] ISSN:1440-1789
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Studies of acetylcholine degrading enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) in Alzheimer's disease (AD) have suggested their potential role in the development of fibrillar amyloid-ß (Aß) plaques (amyloid plaques). A recent genome-wide association study analysis identified a novel association between genetic variations in the BCHE locus and amyloid burden. We studied BChE immunoreactivity in hippocampal tissue sections from AD and control cases, and examined its relationship with amyloid plaques, neurofibrillary tangles (NFT), dystrophic neurites (DN) and neuropil threads (NT). Compared to controls, AD cases had greater BChE immunoreactivity in hippocampal neurons and neuropils in CA2/3, but not in the CA1, CA4 and dentate gyrus. The majority of amyloid plaques (> 80%, using a pan-amyloid marker X-34) contained discrete neuritic clusters which were dual-labeled with antibodies against BChE and phosphorylated tau (clone AT8). There was no association between overall regional BChE immunoreaction intensity and amyloid plaque burden. In contrast to previous reports, BChE was localized in only a fraction (~10%) of classic NFT (positive for X-34). A similar proportion of BChE-immunoreactive pyramidal cells were AT8 immunoreactive. Greater NFT and DN loads were associated with greater BChE immunoreaction intensity in CA2/3, but not in CA1, CA4 and dentate gyrus. Our results demonstrate that in AD hippocampus, BChE accumulates in neurons and plaque-associated neuritic clusters, but only in a small proportion of NFT. The association between greater neurofibrillary pathology burden and markedly increased BChE immunoreactivity, observed selectively in CA2/3 region, could reflect a novel compensatory mechanism. Since CA2/3 is generally considered more resistant to AD pathology, BChE upregulation could impact the cholinergic modulation of glutamate neurotransmission to prevent/reduce neuronal excitotoxicity in AD hippocampus.
[Mh] Termos MeSH primário: Doença de Alzheimer/enzimologia
Butirilcolinesterase/biossíntese
Hipocampo/enzimologia
Hipocampo/patologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Doença de Alzheimer/patologia
Butirilcolinesterase/análise
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Emaranhados Neurofibrilares/enzimologia
Emaranhados Neurofibrilares/patologia
Neurônios/enzimologia
Neurônios/patologia
Filamentos do Neurópilo/enzimologia
Filamentos do Neurópilo/patologia
Placa Amiloide/enzimologia
Placa Amiloide/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.1.1.8 (Butyrylcholinesterase)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150822
[St] Status:MEDLINE
[do] DOI:10.1111/neup.12241


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[PMID]:26028203
[Au] Autor:Aoki Y; Mochizuki Y; Isozaki E; Bando M; Oyanagi K; Mizutani T
[Ad] Endereço:Home Rehabilitation Center Seijyo.
[Ti] Título:[An autopsy case of frontotemporal lobar degeneration with motor neuron disease associated with numerous diffuse plaques, pretangles and neuropil threads].
[So] Source:Rinsho Shinkeigaku;55(5):362-3, 2015.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/patologia
Autopsia
Encéfalo/patologia
Filamentos do Neurópilo/patologia
Placa Amiloide/patologia
[Mh] Termos MeSH secundário: Degeneração Lobar Frontotemporal
Seres Humanos
[Pt] Tipo de publicação:LETTER
[Em] Mês de entrada:1609
[Cu] Atualização por classe:150601
[Lr] Data última revisão:
150601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150602
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-000662


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[PMID]:24529280
[Au] Autor:Perez SE; He B; Nadeem M; Wuu J; Scheff SW; Abrahamson EE; Ikonomovic MD; Mufson EJ
[Ad] Endereço:Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois.
[Ti] Título:Resilience of precuneus neurotrophic signaling pathways despite amyloid pathology in prodromal Alzheimer's disease.
[So] Source:Biol Psychiatry;77(8):693-703, 2015 Apr 15.
[Is] ISSN:1873-2402
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Reduction of precuneus choline acetyltransferase activity co-occurs with greater beta-amyloid (Aß) in Alzheimer's disease (AD). Whether this cholinergic deficit is associated with alteration in nerve growth factor (NGF) signaling and its relation to Aß plaque and neurofibrillary tangle (NFT) pathology during disease onset is unknown. METHODS: Precuneus NGF upstream and downstream signaling levels relative to Aß and NFT pathology were evaluated using biochemistry and histochemistry in 62 subjects with a premortem diagnosis of non-cognitively impaired (NCI; n = 23), mild cognitive impairment (MCI; n = 21), and mild to moderate AD (n = 18). RESULTS: Immunoblots revealed increased levels of proNGF in AD subjects but not MCI subjects, whereas cognate receptors were unchanged. There were no significant differences in protein level for the downstream survival kinase-signaling proteins Erk and phospho-Erk among groups. Apoptotic phospho-JNK, phospho-JNK/JNK ratio, and Bcl-2 were significantly elevated in AD subjects. Soluble Aß1-42 and fibrillar Aß measured by [(3)H] Pittsburgh compound-B ([(3)H]PiB) binding were significantly higher in AD subjects compared with MCI and NCI subjects. The density of plaques showed a trend to increase, but only 6-CN-PiB-positive plaques reached significance in AD subjects. AT8-positive, TOC-1-positive, and Tau C3-positive NFT densities were unchanged, whereas only AT8-positive neuropil thread density was statistically higher in AD subjects. A negative correlation was found between proNGF, phospho-JNK, and Bcl-2 levels and phospho-JNK/JNK ratio and cognition, whereas proNGF correlated positively with 6-CN-PiB-positive plaques during disease progression. CONCLUSIONS: Data indicate that precuneus neurotrophin pathways are resilient to amyloid toxicity during the onset of AD.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Doença de Alzheimer/patologia
Fator de Crescimento Neural/metabolismo
Lobo Parietal/metabolismo
Sintomas Prodrômicos
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Peptídeos beta-Amiloides/metabolismo
Compostos de Anilina/farmacocinética
Colina O-Acetiltransferase
Disfunção Cognitiva/patologia
Feminino
Seres Humanos
Técnicas In Vitro
Masculino
Entrevista Psiquiátrica Padronizada
Filamentos do Neurópilo/patologia
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Transdução de Sinais/efeitos dos fármacos
Estatísticas não Paramétricas
Tiazóis/farmacocinética
Trítio/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole); 0 (Amyloid beta-Peptides); 0 (Aniline Compounds); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Thiazoles); 10028-17-8 (Tritium); 9061-61-4 (Nerve Growth Factor); EC 2.3.1.6 (Choline O-Acetyltransferase)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140218
[St] Status:MEDLINE


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[PMID]:24807277
[Au] Autor:Aoki Y; Mochizuki Y; Isozaki E; Bando M; Oyanagi K; Mizutani T
[Ad] Endereço:Department of Neurology, Tokyo Metropolitan Neurological Hospital.
[Ti] Título:[Autopsy case of frontotemporal lobar degeneration with motor neuron disease associated with numerous diffuse plaques, pretangles and neuropil threads].
[So] Source:Rinsho Shinkeigaku;54(4):325-9, 2014.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:We report an autopsy case of dementia associated with amyotrophic lateral sclerosis (ALS) in a 73-year-old female. She developed memory impairment at the age of 68 years. Atrophy of her hand muscles was noted at the age of 71 years. She was not aware of her memory impairment or muscle weakness, and was loquacious and euphoric. She was clinically diagnosed as having Alzheimer disease (AD) complicated by ALS with dementia/frontotemporal lobar degeneration with motor neuron disease (ALS-D/FTLD-MND). A neuropathological study confirmed the presence of features of sporadic ALS. Furthermore, severe neuronal loss involving the subiculum and the rostral portion of the medial side of the temporal pole cortex was detected, and TAR DNA-binding protein-43-positive-neuronal cytoplasmic inclusions were identified in the granule cells of the dentate gyrus. These findings were compatible with the pathological features of ALS-D/FTLD-MND. Although many pretangles, neuropil threads and senile plaques were revealed in the degenerated areas, there were few neurofibrillary tangles and typical plaques (Braak stage III, C). Further discussion is required to determine whether AD with ALS-D/FTLD-MND is different from typical AD. This case might be helpful for diagnosing similar cases in the future.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/patologia
Encéfalo/patologia
Degeneração Lobar Frontotemporal/patologia
Doença dos Neurônios Motores/patologia
Emaranhados Neurofibrilares/patologia
Filamentos do Neurópilo/patologia
Placa Amiloide/patologia
[Mh] Termos MeSH secundário: Idoso
Doença de Alzheimer/complicações
Doença de Alzheimer/diagnóstico
Doença de Alzheimer/patologia
Esclerose Amiotrófica Lateral/complicações
Esclerose Amiotrófica Lateral/diagnóstico
Autopsia
Biomarcadores/análise
Proteínas de Ligação a DNA/análise
Giro Denteado/citologia
Giro Denteado/metabolismo
Feminino
Degeneração Lobar Frontotemporal/complicações
Degeneração Lobar Frontotemporal/diagnóstico
Seres Humanos
Corpos de Inclusão/metabolismo
Doença dos Neurônios Motores/complicações
Doença dos Neurônios Motores/diagnóstico
Placa Amiloide/complicações
[Pt] Tipo de publicação:CASE REPORTS; ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (DNA-Binding Proteins)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:160826
[Lr] Data última revisão:
160826
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140509
[St] Status:MEDLINE


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[PMID]:23773070
[Au] Autor:LeBlanc AC
[Ad] Endereço:Bloomfield Center for Research in Aging, Lady Davis Institute for Medical Research, Sir Mortimer B Davis Jewish General Hospital, Montréal, QC, Canada. andrea.leblanc@mcgill.ca
[Ti] Título:Caspase-6 as a novel early target in the treatment of Alzheimer's disease.
[So] Source:Eur J Neurosci;37(12):2005-18, 2013 Jun.
[Is] ISSN:1460-9568
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:A recent paradigm shift appears to be underway on what scientists believe to be the cause of Alzheimer's disease (AD). The amyloid hypothesis has dominated the field of basic research for the last 25 years, and although these massive efforts have culminated in efficient removal of amyloid from the brains of patients, the absence of beneficial effects for the patient have been greatly disappointing. This has created a shift in the focus on amyloid to a much greater focus on Tau protein, in the hope that preventing tangle formation may inhibit or delay the progression of AD. Although there are promising developments in this area of research, diversifying our efforts to identify novel early targets by understanding the upstream molecular mechanisms that lead to, or occur with, neurofibrillary tangle and plaque formation may provide more efficient therapies against AD. Among many areas in development, an emphasis on the role of caspase-6 (Casp6) activity in early neurodegenerative mechanisms brings hope of a novel target against AD. Casp6 activity is intimately associated with the pathologies that define AD, correlates well with lower cognitive performance in aged individuals, and is involved in axonal degeneration in several cellular and in vivo animal models. This is a review of the evidence showing the relevance of Casp6 activation as an early event that could be inhibited to prevent the progression of AD.
[Mh] Termos MeSH primário: Doença de Alzheimer/enzimologia
Peptídeos beta-Amiloides/metabolismo
Caspase 6/metabolismo
Degeneração Neural/enzimologia
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Doença de Alzheimer/patologia
Doença de Alzheimer/terapia
Precursor de Proteína beta-Amiloide/metabolismo
Animais
Inibidores de Caspase/uso terapêutico
Seres Humanos
Camundongos
Degeneração Neural/patologia
Emaranhados Neurofibrilares/enzimologia
Filamentos do Neurópilo/enzimologia
Fosforilação/fisiologia
Placa Amiloide/enzimologia
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Amyloid beta-Protein Precursor); 0 (Caspase Inhibitors); 0 (tau Proteins); EC 3.4.22.- (Caspase 6)
[Em] Mês de entrada:1312
[Cu] Atualização por classe:130618
[Lr] Data última revisão:
130618
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130619
[St] Status:MEDLINE
[do] DOI:10.1111/ejn.12250


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[PMID]:22465174
[Au] Autor:Braak H; Del Tredici K
[Ad] Endereço:Clinical Neuroanatomy Section, Department of Neurology, Center for Biomedical Research, Ulm University, Germany. heiko.braak@uni-ulm.de
[Ti] Título:Alzheimer's disease: pathogenesis and prevention.
[So] Source:Alzheimers Dement;8(3):227-33, 2012 May.
[Is] ISSN:1552-5279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tau lesions (pretangles, neuropil threads, neurofibrillary tangles) in select neuronal types are essential to the pathogenesis of Alzheimer's disease. Pretangle formation marks the beginning of the pathological process and is of particular interest because it is temporally closer to the prevailing conditions that induce the pathological process underlying Alzheimer's disease in contrast to late-stage disease. However, not all pretangles convert into neurofibrillary tangles. We propose that the development of tau lesions in Alzheimer's disease is traceable to differences between early- versus late-maturing oligodendrocytes and to the exceptionally protracted myelination of late-developing portions of the human brain. Conclusions drawn from these considerations should encourage development of new preventative and disease-modifying strategies.
[Mh] Termos MeSH primário: Doença de Alzheimer/etiologia
Doença de Alzheimer/prevenção & controle
Encéfalo/patologia
[Mh] Termos MeSH secundário: Fatores Etários
Doença de Alzheimer/patologia
Animais
Seres Humanos
Filamentos do Neurópilo/patologia
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (tau Proteins)
[Em] Mês de entrada:1208
[Cu] Atualização por classe:120501
[Lr] Data última revisão:
120501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120403
[St] Status:MEDLINE
[do] DOI:10.1016/j.jalz.2012.01.011


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[PMID]:22363686
[Au] Autor:Muscedere ML; Traniello JF
[Ad] Endereço:Department of Biology, Boston University, Boston, Massachusetts, United States of America. mario@bu.edu
[Ti] Título:Division of labor in the hyperdiverse ant genus Pheidole is associated with distinct subcaste- and age-related patterns of worker brain organization.
[So] Source:PLoS One;7(2):e31618, 2012.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The evolutionary success of ants and other social insects is considered to be intrinsically linked to division of labor among workers. The role of the brains of individual ants in generating division of labor, however, is poorly understood, as is the degree to which interspecific variation in worker social phenotypes is underscored by functional neurobiological differentiation. Here we demonstrate that dimorphic minor and major workers of different ages from three ecotypical species of the hyperdiverse ant genus Pheidole have distinct patterns of neuropil size variation. Brain subregions involved in sensory input (optic and antennal lobes), sensory integration, learning and memory (mushroom bodies), and motor functions (central body and subesophageal ganglion) vary significantly in relative size, reflecting differential investment in neuropils that likely regulate subcaste- and age-correlated task performance. Worker groups differ in brain size and display patterns of altered isometric and allometric subregion scaling that affect brain architecture independently of brain size variation. In particular, mushroom body size was positively correlated with task plasticity in the context of both age- and subcaste-related polyethism, providing strong, novel support that greater investment in this neuropil increases behavioral flexibility. Our findings reveal striking levels of developmental plasticity and evolutionary flexibility in Pheidole worker neuroanatomy, supporting the hypothesis that mosaic alterations of brain composition contribute to adaptive colony structure and interspecific variation in social organization.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Formigas/anatomia & histologia
Formigas/crescimento & desenvolvimento
Encéfalo/anatomia & histologia
Encéfalo/fisiologia
Hierarquia Social
[Mh] Termos MeSH secundário: Animais
Comportamento Animal
Tamanho Corporal
Análise Discriminante
Estágios do Ciclo de Vida
Mosaicismo
Análise Multivariada
Filamentos do Neurópilo/metabolismo
Tamanho do Órgão
Fenótipo
Especificidade da Espécie
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Em] Mês de entrada:1206
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120225
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0031618


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[PMID]:21175864
[Au] Autor:Mori F; Tanji K; Kakita A; Takahashi H; Wakabayashi K
[Ad] Endereço:Department of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki Department of Pathology, Resource Branch for Brain Disease Research CBBR, Brain Research Institute, University of Niigata, Niigata, Japan. neuropal@cc.hirosaki-u.ac.jp
[Ti] Título:Enhancement of native and phosphorylated TDP-43 immunoreactivity by proteinase K treatment following autoclave heating.
[So] Source:Neuropathology;31(4):401-4, 2011 Aug.
[Is] ISSN:1440-1789
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:TDP-43 is a major disease protein in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with TDP-43 (FTLD-TDP). To evaluate the effectiveness of proteinase K (PK) treatment in antigen retrieval for native and phosphorylated TDP-43 protein, we examined the temporal cortex and spinal cord from patients with sporadic ALS and FTLD-TDP and control subjects. PK treatment following heat retrieval enhanced the immunoreactivity for native TDP-43 in controls as well as for native and phosphorylated TDP-43 in ALS and FTLD-TDP. A significant number of TDP-43-positive neuropil threads were demonstrated in lesions, in which routine immunohistochemistry revealed that the predominant inclusions are cytoplasmic. This retrieval method is the best of immunohistochemical techniques for demonstrating TDP-43 pathology, especially in the neuropil.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/diagnóstico
Proteínas de Ligação a DNA/metabolismo
Endopeptidase K
Degeneração Lobar Frontotemporal/diagnóstico
Imuno-Histoquímica/métodos
[Mh] Termos MeSH secundário: Idoso
Esclerose Amiotrófica Lateral/metabolismo
Encéfalo/metabolismo
Encéfalo/patologia
Degeneração Lobar Frontotemporal/metabolismo
Seres Humanos
Corpos de Inclusão/metabolismo
Meia-Idade
Filamentos do Neurópilo/metabolismo
Fosforilação
Medula Espinal/metabolismo
Medula Espinal/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA-Binding Proteins); EC 3.4.21.64 (Endopeptidase K)
[Em] Mês de entrada:1112
[Cu] Atualização por classe:160826
[Lr] Data última revisão:
160826
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:101224
[St] Status:MEDLINE
[do] DOI:10.1111/j.1440-1789.2010.01184.x


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[PMID]:20345790
[Au] Autor:Uryu K; Haddix T; Robinson J; Nakashima-Yasuda H; Lee VM; Trojanowski JQ
[Ad] Endereço:Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-4283, USA.
[Ti] Título:Burden of neurodegenerative diseases in a cohort of medical examiner subjects.
[So] Source:J Forensic Sci;55(3):642-5, 2010 May.
[Is] ISSN:1556-4029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Here we report studies of the burden of neurodegenerative neuropathologies in a cohort of Medical Examiner (ME) subjects from the County of Santa Clara (California) to determine if this unique population of decedents manifested evidence of neurodegeneration that might underlie causes of death seen in an ME practice. We found that 13% of the brains from ME cases showed significant tau pathology, including 55% of those 65 years old and older and 63% of those 70 years old and older. The histochemical and immunohistochemical findings were consistent with Alzheimer's disease (AD) in 7 subjects and frontotemporal lobar degeneration (FTLD) tauopathy type in six cases. There were no cases of Parkinson's disease, dementia with Lewy Bodies or other neurodegenerative conditions. Our study suggests that decedents >65 years of age in an ME practice are afflicted by common causes of dementia such as AD and FTLD which could contribute wholly or in part to their causes of death.
[Mh] Termos MeSH primário: Doença de Alzheimer/patologia
Encéfalo/patologia
Degeneração Lobar Frontotemporal/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Atrofia
Encéfalo/metabolismo
Edema Encefálico/patologia
Estudos de Coortes
Médicos Legistas
Feminino
Patologia Legal
Pessoas em Situação de Rua
Seres Humanos
Higiene
Imuno-Histoquímica
Masculino
Desnutrição/epidemiologia
Meia-Idade
Emaranhados Neurofibrilares/metabolismo
Emaranhados Neurofibrilares/patologia
Filamentos do Neurópilo/patologia
Placa Amiloide/patologia
Coloração e Rotulagem
Tauopatias/patologia
Tiazóis/metabolismo
Adulto Jovem
alfa-Sinucleína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Thiazoles); 0 (alpha-Synuclein); 2390-54-7 (thioflavin T)
[Em] Mês de entrada:1009
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100330
[St] Status:MEDLINE
[do] DOI:10.1111/j.1556-4029.2010.01347.x



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