Base de dados : MEDLINE
Pesquisa : C10.228.140.380.266.299.500 [Categoria DeCS]
Referências encontradas : 394 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 40 ir para página                         

  1 / 394 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28486594
[Au] Autor:Lansdall CJ; Coyle-Gilchrist ITS; Jones PS; Vázquez Rodríguez P; Wilcox A; Wehmann E; Dick KM; Robbins TW; Rowe JB
[Ad] Endereço:Department of Clinical Neurosciences, University of Cambridge, UK.
[Ti] Título:Apathy and impulsivity in frontotemporal lobar degeneration syndromes.
[So] Source:Brain;140(6):1792-1807, 2017 Jun 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Apathy and impulsivity are common and disabling consequences of frontotemporal lobar degeneration. They cause substantial carer distress, but their aetiology remains elusive. There are critical limitations to previous studies in this area including (i) the assessment of either apathy or impulsivity alone, despite their frequent co-existence; (ii) the assessment of behavioural changes within single diagnostic groups; and (iii) the use of limited sets of tasks or questions that relate to just one aspect of these multifactorial constructs. We proposed an alternative, dimensional approach that spans behavioural and language variants of frontotemporal dementia, progressive supranuclear palsy and corticobasal syndrome. This accommodates the commonalities of apathy and impulsivity across disorders and reveals their cognitive and anatomical bases. The ability to measure the components of apathy and impulsivity and their associated neural correlates across diagnostic groups would provide better novel targets for pharmacological manipulations, and facilitate new treatment strategies and strengthen translational models. We therefore sought to determine the neurocognitive components of apathy and impulsivity in frontotemporal lobar degeneration syndromes. The frequency and characteristics of apathy and impulsivity were determined by neuropsychological and behavioural assessments in 149 patients and 50 controls from the PIck's disease and Progressive supranuclear palsy Prevalence and INcidence study (PiPPIN). We derived dimensions of apathy and impulsivity using principal component analysis and employed these in volumetric analyses of grey and white matter in a subset of 70 patients (progressive supranuclear palsy, n = 22; corticobasal syndrome, n = 13; behavioural variant, n = 14; primary progressive aphasias, n = 21) and 27 control subjects. Apathy and impulsivity were present across diagnostic groups, despite being criteria for behavioural variant frontotemporal dementia alone. Measures of apathy and impulsivity frequently loaded onto the same components reflecting their overlapping relationship. However, measures from objective tasks, patient-rated questionnaires and carer-rated questionnaires loaded onto separate components and revealed distinct neurobiology. Corticospinal tracts correlated with patients' self-ratings. In contrast, carer ratings correlated with atrophy in established networks for goal-directed behaviour, social cognition, motor control and vegetative functions, including frontostriatal circuits, orbital and temporal polar cortex, and the brainstem. Components reflecting response inhibition deficits correlated with focal frontal cortical atrophy. The dimensional approach to complex behavioural changes arising from frontotemporal lobar degeneration provides new insights into apathy and impulsivity, and the need for a joint therapeutic strategy against them. The separation of objective tests from subjective questionnaires, and patient from carer ratings, has important implications for clinical trial design.awx101media15448041163001.
[Mh] Termos MeSH primário: Apatia/fisiologia
Degeneração Lobar Frontotemporal/diagnóstico por imagem
Degeneração Lobar Frontotemporal/fisiopatologia
Substância Cinzenta/diagnóstico por imagem
Comportamento Impulsivo/fisiologia
Substância Branca/diagnóstico por imagem
[Mh] Termos MeSH secundário: Idoso
Afasia Primária Progressiva/diagnóstico por imagem
Afasia Primária Progressiva/fisiopatologia
Feminino
Demência Frontotemporal/diagnóstico por imagem
Demência Frontotemporal/fisiopatologia
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Doença de Pick/diagnóstico por imagem
Doença de Pick/fisiopatologia
Análise de Componente Principal
Paralisia Supranuclear Progressiva/diagnóstico por imagem
Paralisia Supranuclear Progressiva/fisiopatologia
Síndrome
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170510
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx101


  2 / 394 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28413156
[Au] Autor:Combs B; Kanaan NM
[Ad] Endereço:Department of Translational Science and Molecular Medicine, College of Human Medicine, Michigan State University, Grand Rapids, Michigan. Electronic address: benjamin.combs@hc.msu.edu.
[Ti] Título:Exposure of the Amino Terminus of Tau Is a Pathological Event in Multiple Tauopathies.
[So] Source:Am J Pathol;187(6):1222-1229, 2017 Jun.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pathological changes to the tau protein, including conformational changes and aggregation, are major hallmarks of a group of neurodegenerative disorders known as tauopathies. Among the conformational changes are alterations involving the extreme amino terminus of the protein, known as the phosphatase-activating domain (PAD). Aberrant PAD exposure induces a signaling cascade that leads to disruption of axonal transport, a critical function for neuronal survival. Conformational display of PAD is an early marker of pathological tau in Alzheimer disease (AD), but its role in other tauopathies has yet to be firmly established. We used a relatively novel N-terminal, conformation-sensitive antibody, TNT2, to determine whether misfolding in the amino terminus (ie, PAD exposure) occurs in non-AD tauopathies. We found that TNT2 specifically labeled pathological tau in post-mortem human brain tissue from Pick disease, progressive supranuclear palsy, corticobasal degeneration, and chronic traumatic encephalopathy, but did not label nonpathological, parenchymal tau. Tau13, another N-terminal antibody, was not sensitive to pathological N-terminal conformations. Tau13 did not readily distinguish between normal (ie, parenchymal tau) and pathological tau species and showed a range of effectiveness at identifying tau pathologies in the non-AD tauopathies. These findings demonstrate that the conformational display of the PAD in tau represents a common pathological event in many tauopathies.
[Mh] Termos MeSH primário: Tauopatias/genética
Proteínas tau/genética
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Anticorpos Monoclonais
Encéfalo/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Fosforilação
Doença de Pick/genética
Doença de Pick/metabolismo
Doença de Pick/patologia
Conformação Proteica
Dobramento de Proteína
Paralisia Supranuclear Progressiva/genética
Paralisia Supranuclear Progressiva/metabolismo
Paralisia Supranuclear Progressiva/patologia
Tauopatias/metabolismo
Tauopatias/patologia
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (tau Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE


  3 / 394 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28293793
[Au] Autor:Saijo E; Ghetti B; Zanusso G; Oblak A; Furman JL; Diamond MI; Kraus A; Caughey B
[Ad] Endereço:LPVD, Rocky Mountain Laboratories, NIAID, NIH, Hamilton, MT, USA.
[Ti] Título:Ultrasensitive and selective detection of 3-repeat tau seeding activity in Pick disease brain and cerebrospinal fluid.
[So] Source:Acta Neuropathol;133(5):751-765, 2017 May.
[Is] ISSN:1432-0533
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The diagnosis and treatment of diseases involving tau-based pathology such as Alzheimer disease and certain frontotemporal dementias is hampered by the inability to detect pathological forms of tau with sufficient sensitivity, specificity and practicality. In these neurodegenerative diseases, tau accumulates in self-seeding filaments. For example, Pick disease (PiD) is associated with frontotemporal degeneration and accumulation of 3-repeat (3R) tau isoforms in filaments constituting Pick bodies. Exploiting the self-seeding activity of tau deposits, and using a 3R tau fragment as a substrate, we have developed an assay (tau RT-QuIC) that can detect tau seeds in 2 µl aliquots of PiD brain dilutions down to 10 -10 . PiD seeding activities were 100-fold higher in frontal and temporal lobes compared to cerebellar cortex. Strikingly, this test was 10 - to 10 -fold less responsive when seeded with brain containing predominant 4-repeat (4R) tau aggregates from cases of corticobasal degeneration, argyrophilic grain disease, and progressive supranuclear palsy. Alzheimer disease brain, with 3R + 4R tau deposits, also gave much weaker responses than PiD brain. When applied to cerebrospinal fluid samples (5 µl), tau RT-QuIC analyses discriminated PiD from non-PiD cases. These findings demonstrate that abnormal tau aggregates can be detected with high sensitivity and disease-specificity in crude tissue and fluid samples. Accordingly, this tau RT-QuIC assay exemplifies a new approach to diagnosing tauopathies and monitoring therapeutic trials using aggregated tau itself as a biomarker.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Doença de Pick/líquido cefalorraquidiano
Paralisia Supranuclear Progressiva/patologia
Tauopatias/líquido cefalorraquidiano
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Encéfalo/patologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Doença de Pick/diagnóstico
Doença de Pick/patologia
Isoformas de Proteínas/líquido cefalorraquidiano
Paralisia Supranuclear Progressiva/líquido cefalorraquidiano
Paralisia Supranuclear Progressiva/metabolismo
Tauopatias/metabolismo
Tauopatias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MAPT protein, human); 0 (Protein Isoforms); 0 (tau Proteins)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170420
[Lr] Data última revisão:
170420
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.1007/s00401-017-1692-z


  4 / 394 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28133816
[Au] Autor:Spinelli EG; Mandelli ML; Miller ZA; Santos-Santos MA; Wilson SM; Agosta F; Grinberg LT; Huang EJ; Trojanowski JQ; Meyer M; Henry ML; Comi G; Rabinovici G; Rosen HJ; Filippi M; Miller BL; Seeley WW; Gorno-Tempini ML
[Ad] Endereço:Memory and Aging Center, University of California, San Francisco, San Francisco, CA.
[Ti] Título:Typical and atypical pathology in primary progressive aphasia variants.
[So] Source:Ann Neurol;81(3):430-443, 2017 Mar.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To characterize in vivo signatures of pathological diagnosis in a large cohort of patients with primary progressive aphasia (PPA) variants defined by current diagnostic classification. METHODS: Extensive clinical, cognitive, neuroimaging, and neuropathological data were collected from 69 patients with sporadic PPA, divided into 29 semantic (svPPA), 25 nonfluent (nfvPPA), 11 logopenic (lvPPA), and 4 mixed PPA. Patterns of gray matter (GM) and white matter (WM) atrophy at presentation were assessed and tested as predictors of pathological diagnosis using support vector machine (SVM) algorithms. RESULTS: A clinical diagnosis of PPA was associated with frontotemporal lobar degeneration (FTLD) with transactive response DNA-binding protein (TDP) inclusions in 40.5%, FTLD-tau in 40.5%, and Alzheimer disease (AD) pathology in 19% of cases. Each variant was associated with 1 typical pathology; 24 of 29 (83%) svPPA showed FTLD-TDP type C, 22 of 25 (88%) nfvPPA showed FTLD-tau, and all 11 lvPPA had AD. Within FTLD-tau, 4R-tau pathology was commonly associated with nfvPPA, whereas Pick disease was observed in a minority of subjects across all variants except for lvPPA. Compared with pathologically typical cases, svPPA-tau showed significant extrapyramidal signs, greater executive impairment, and severe striatal and frontal GM and WM atrophy. nfvPPA-TDP patients lacked general motor symptoms or significant WM atrophy. Combining GM and WM volumes, SVM analysis showed 92.7% accuracy to distinguish FTLD-tau and FTLD-TDP pathologies across variants. INTERPRETATION: Each PPA clinical variant is associated with a typical and most frequent cognitive, neuroimaging, and neuropathological profile. Specific clinical and early anatomical features may suggest rare and atypical pathological diagnosis in vivo. Ann Neurol 2017;81:430-443.
[Mh] Termos MeSH primário: Doença de Alzheimer
Afasia Primária Progressiva
Degeneração Lobar Frontotemporal
Substância Cinzenta/diagnóstico por imagem
Substância Branca/diagnóstico por imagem
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Doença de Alzheimer/classificação
Doença de Alzheimer/patologia
Doença de Alzheimer/fisiopatologia
Afasia Primária Progressiva/classificação
Afasia Primária Progressiva/patologia
Afasia Primária Progressiva/fisiopatologia
Atrofia/patologia
Feminino
Degeneração Lobar Frontotemporal/classificação
Degeneração Lobar Frontotemporal/patologia
Degeneração Lobar Frontotemporal/fisiopatologia
Seres Humanos
Masculino
Meia-Idade
Doença de Pick/patologia
Doença de Pick/fisiopatologia
Afasia Primária Progressiva não Fluente/patologia
Afasia Primária Progressiva não Fluente/fisiopatologia
Máquina de Vetores de Suporte
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (tau Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170131
[St] Status:MEDLINE
[do] DOI:10.1002/ana.24885


  5 / 394 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27025090
[Au] Autor:Yamamoto K; Ogihara T
[Ti] Título:[Pick's disease].
[So] Source:Nihon Rinsho;74(3):476-81, 2016 Mar.
[Is] ISSN:0047-1852
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Pick's disease is a type of frontotemporal lobar degeneration(FTLD) with circumscribed atrophy in the frontotemporal lobe. The terminology for Pick's disease has evolved over time. Pick's disease was a term formerly used to define a disorder with symptoms caused by frontal and temporal lobe dysfunction. Therefore, the diagnosis was previously based on clinical features and the distribution of brain atrophy. Pick's disease is currently defined by the presence of tau-positive Pick bodies, and thus can be diagnosed only pathologically. The clinical phenotypes of Pick's disease include behavioral variant FTD (bvFTD), progressive nonfluent aphasia (PNFA) and semantic dementia (SD).
[Mh] Termos MeSH primário: Doença de Pick
[Mh] Termos MeSH secundário: Seres Humanos
Doença de Pick/tratamento farmacológico
Doença de Pick/epidemiologia
Doença de Pick/patologia
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160330
[Lr] Data última revisão:
160330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160331
[St] Status:MEDLINE


  6 / 394 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26969837
[Au] Autor:Miki T; Yokota O; Ishizu H; Kuroda S; Oshima E; Terada S; Yamada N
[Ad] Endereço:Department of Psychiatry, Kinoko Espoir Hospital, Okayama, Japan.
[Ti] Título:Behavioral variant of frontotemporal dementia: Fundamental clinical issues associated with prediction of pathological bases.
[So] Source:Neuropathology;36(4):388-404, 2016 Aug.
[Is] ISSN:1440-1789
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Behavioral variant of frontotemporal dementia (bvFTD) is a clinical syndrome characterized mainly by behavioral symptoms due to frontal dysfunction. Major neurodegenerative bases of bvFTD include Pick's disease, frontotemporal lobar degeneration with trans-activation response DNA protein 43-positive inclusions, corticobasal degeneration, and progressive supranuclear palsy. Early disinhibition characterized by socially inappropriate behaviors, loss of manners, and impulsive, rash and careless actions is the most important clinical feature of bvFTD. On the other hand, it was reported that clinical presentations of some Alzheimer's disease cases and patients with psychiatric disorders (e.g., addictive disorders, gambling disorder and kleptomania) often resemble that of bvFTD. Although clinical differentiation of 'true' bvFTD cases with frontotemporal lobar degeneration (FTLD) pathology from mimicking cases without it is not always easy, evaluation of the following features, which were noted in autopsy-confirmed FTLD cases and/or clinical bvFTD cases with circumscribed lobar atrophy, may often provide clues for the diagnosis. (i) The initial symptoms frequently develop at 65 years or younger, and (ii) 'socially inappropriate behaviors' can be frequently interpreted as contextually inappropriate behaviors prompted by environmental visual and auditory stimuli. Taking a detailed history usually reveals various kinds of such behaviors in various situations in everyday life rather than the repetition of a single kind of behavior (e.g., repeated shoplifting). (iii) A correlation between the distribution of cerebral atrophy and neurological and behavioral symptoms is usually observed, and the proportion of FTLD cases with right side-predominant cerebral atrophy may be higher in a psychiatric setting than a neurological setting. Finally, (iv) whether the previous course and the combination of symptoms observed at the first medical visit can be explained by major evolution patterns of clinical syndromes in pathologically confirmed FTLD cases should be considered. These views may provide clues to differentiate FTLD from Alzheimer's disease and to predict a subsequent clinical course and therapeutic interventions needed in the future.
[Mh] Termos MeSH primário: Demência Frontotemporal/diagnóstico
Demência Frontotemporal/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Atrofia
Encéfalo/patologia
Feminino
Demência Frontotemporal/psicologia
Seres Humanos
Masculino
Meia-Idade
Doença de Pick/diagnóstico
Doença de Pick/patologia
Doença de Pick/psicologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170127
[Lr] Data última revisão:
170127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160313
[St] Status:MEDLINE
[do] DOI:10.1111/neup.12290


  7 / 394 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:26866555
[Au] Autor:Maggi P; Bier JC; De Breucker S
[Ad] Endereço:Hôpital Erasme, Université Libre de Bruxelles, Brussels, Belgium maggi.pi@gmail.com.
[Ti] Título:Massive subdural haematoma and dementia: a "yin and yang" paradigm.
[So] Source:Med J Aust;204(3):126-.e1, 2016 Feb 15.
[Is] ISSN:1326-5377
[Cp] País de publicação:Australia
[La] Idioma:eng
[Mh] Termos MeSH primário: Demência/etiologia
Hematoma Subdural/complicações
Hematoma Subdural/diagnóstico por imagem
Yin-Yang
[Mh] Termos MeSH secundário: Idoso de 80 Anos ou mais
Descompressão Cirúrgica/métodos
Hematoma Subdural/etiologia
Hematoma Subdural/cirurgia
Seres Humanos
Masculino
Doença de Pick/complicações
Tomografia Computadorizada por Raios X
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1606
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160212
[St] Status:MEDLINE


  8 / 394 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26583316
[Au] Autor:Irwin DJ; Brettschneider J; McMillan CT; Cooper F; Olm C; Arnold SE; Van Deerlin VM; Seeley WW; Miller BL; Lee EB; Lee VM; Grossman M; Trojanowski JQ
[Ad] Endereço:University of Pennsylvania Frontotemporal Degeneration Center, Department of Neurology, University of Pennsylvania, Philadelphia, PA.
[Ti] Título:Deep clinical and neuropathological phenotyping of Pick disease.
[So] Source:Ann Neurol;79(2):272-87, 2016 Feb.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To characterize sequential patterns of regional neuropathology and clinical symptoms in a well-characterized cohort of 21 patients with autopsy-confirmed Pick disease. METHODS: Detailed neuropathological examination using 70µm and traditional 6µm sections was performed using thioflavin-S staining and immunohistochemistry for phosphorylated tau, 3R and 4R tau isoforms, ubiquitin, and C-terminally truncated tau. Patterns of regional tau deposition were correlated with clinical data. In a subset of cases (n = 5), converging evidence was obtained using antemortem neuroimaging measures of gray and white matter integrity. RESULTS: Four sequential patterns of pathological tau deposition were identified starting in frontotemporal limbic/paralimbic and neocortical regions (phase I). Sequential involvement was seen in subcortical structures, including basal ganglia, locus coeruleus, and raphe nuclei (phase II), followed by primary motor cortex and precerebellar nuclei (phase III) and finally visual cortex in the most severe (phase IV) cases. Behavioral variant frontotemporal dementia was the predominant clinical phenotype (18 of 21), but all patients eventually developed a social comportment disorder. Pathological tau phases reflected the evolution of clinical symptoms and degeneration on serial antemortem neuroimaging, directly correlated with disease duration and inversely correlated with brain weight at autopsy. The majority of neuronal and glial tau inclusions were 3R tau-positive and 4R tau-negative in sporadic cases. There was a relative abundance of mature tau pathology markers in frontotemporal limbic/paralimbic regions compared to neocortical regions. INTERPRETATION: Pick disease tau neuropathology may originate in limbic/paralimbic cortices. The patterns of tau pathology observed here provide novel insights into the natural history and biology of tau-mediated neurodegeneration.
[Mh] Termos MeSH primário: Córtex Cerebral/patologia
Sistema Límbico/patologia
Doença de Pick/patologia
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
Imuno-Histoquímica
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Fenótipo
Doença de Pick/metabolismo
Doença de Pick/fisiopatologia
Coloração e Rotulagem
Tiazóis
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MAPT protein, human); 0 (Thiazoles); 0 (tau Proteins); 2390-54-7 (thioflavin T)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170201
[Lr] Data última revisão:
170201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151120
[St] Status:MEDLINE
[do] DOI:10.1002/ana.24559


  9 / 394 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26538548
[Au] Autor:Irwin DJ; Byrne MD; McMillan CT; Cooper F; Arnold SE; Lee EB; Van Deerlin VM; Xie SX; Lee VM; Grossman M; Trojanowski JQ
[Ad] Endereço:Penn Frontotemporal Degeneration Center, Department of Neurology (DJI, MDB, CTM, FC, MG)
[Ti] Título:Semi-Automated Digital Image Analysis of Pick's Disease and TDP-43 Proteinopathy.
[So] Source:J Histochem Cytochem;64(1):54-66, 2016 01.
[Is] ISSN:1551-5044
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Digital image analysis of histology sections provides reliable, high-throughput methods for neuropathological studies but data is scant in frontotemporal lobar degeneration (FTLD), which has an added challenge of study due to morphologically diverse pathologies. Here, we describe a novel method of semi-automated digital image analysis in FTLD subtypes including: Pick's disease (PiD, n=11) with tau-positive intracellular inclusions and neuropil threads, and TDP-43 pathology type C (FTLD-TDPC, n=10), defined by TDP-43-positive aggregates predominantly in large dystrophic neurites. To do this, we examined three FTLD-associated cortical regions: mid-frontal gyrus (MFG), superior temporal gyrus (STG) and anterior cingulate gyrus (ACG) by immunohistochemistry. We used a color deconvolution process to isolate signal from the chromogen and applied both object detection and intensity thresholding algorithms to quantify pathological burden. We found object-detection algorithms had good agreement with gold-standard manual quantification of tau- and TDP-43-positive inclusions. Our sampling method was reliable across three separate investigators and we obtained similar results in a pilot analysis using open-source software. Regional comparisons using these algorithms finds differences in regional anatomic disease burden between PiD and FTLD-TDP not detected using traditional ordinal scale data, suggesting digital image analysis is a powerful tool for clinicopathological studies in morphologically diverse FTLD syndromes.
[Mh] Termos MeSH primário: Automação
Processamento de Imagem Assistida por Computador/métodos
Imuno-Histoquímica/métodos
Doença de Pick/patologia
Software
Proteinopatias TDP-43/patologia
[Mh] Termos MeSH secundário: Idoso
Algoritmos
Feminino
Seres Humanos
Masculino
Meia-Idade
Doença de Pick/metabolismo
Proteinopatias TDP-43/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1605
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151106
[St] Status:MEDLINE
[do] DOI:10.1369/0022155415614303


  10 / 394 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26382841
[Au] Autor:Irwin DJ
[Ad] Endereço:Department of Neurology, Frontotemporal Degeneration Center (FTDC), University of Pennsylvania Perelman School of Medicine, Hospital of the University of Pennsylvania, 3600 Spruce Street, Philadelphia, PA 19104, United States. Electronic address: dirwin@mail.med.upenn.edu.
[Ti] Título:Tauopathies as clinicopathological entities.
[So] Source:Parkinsonism Relat Disord;22 Suppl 1:S29-33, 2016 Jan.
[Is] ISSN:1873-5126
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tauopathies are a class of neurodegenerative disorders characterized by neuronal and/or glial inclusions composed of the microtubule-binding protein, tau. Several lines of evidence suggest tau aggregation is central to the neurodegenerative process in tauopathies. First, recent animal and cell model studies find abnormally-modified tau alone may be transmitted between adjacent neurons and spread to anatomically connected brain regions to recapitulate human disease. Further, staging efforts in human autopsy cases suggest a sequential distribution of tau aggregation in the central nervous system that could reflect this observed cell-to-cell transmission of pathogenic tau species in animal models. Finally, pathogenic mutations in the MAPT gene encoding tau protein cause hereditary forms of tauopathy. Clinically, tauopathies can present with a range of phenotypes that include both movement- and cognitive/behavioral-disorders (i.e. frontotemporal dementia spectrum disorders) or non-specific amnestic symptoms in advanced age. A major limitation is that current clinical diagnostic criteria for these disorders do not reliably differentiate underlying tauopathy from other neurodegenerative diseases, such as TDP-43 proteinopathies. Thus, current research efforts are focused on improving the ante mortem diagnosis of tauopathies, including pre-clinical stages of disease, as many therapeutic strategies for emerging disease-modifying therapies focus on preventing abnormal folding and spread of tau pathology.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Tauopatias/diagnóstico
Tauopatias/metabolismo
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Animais
Encéfalo/patologia
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Seres Humanos
Doenças Neurodegenerativas/diagnóstico
Doenças Neurodegenerativas/genética
Doenças Neurodegenerativas/metabolismo
Doença de Pick/diagnóstico
Doença de Pick/genética
Doença de Pick/metabolismo
Tauopatias/genética
Proteínas tau/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (TDP-43 protein, human); 0 (tau Proteins)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170101
[Lr] Data última revisão:
170101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150919
[St] Status:MEDLINE



página 1 de 40 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde