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[PMID]:29190651
[Au] Autor:Hohman TJ; Dumitrescu L; Oksol A; Wagener M; Gifford KA; Jefferson AL; Alzheimer's Disease Neuroimaging Initiative
[Ad] Endereço:Vanderbilt Memory and Alzheimer's Center, Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, United States of America.
[Ti] Título:APOE allele frequencies in suspected non-amyloid pathophysiology (SNAP) and the prodromal stages of Alzheimer's Disease.
[So] Source:PLoS One;12(11):e0188501, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Biomarker definitions for preclinical Alzheimer's disease (AD) have identified individuals with neurodegeneration (ND+) without ß-amyloidosis (Aß-) and labeled them with suspected non-AD pathophysiology (SNAP). We evaluated Apolipoprotein E (APOE) ε2 and ε4 allele frequencies across biomarker definitions-Aß-/ND- (n = 268), Aß+/ND- (n = 236), Aß-/ND+ or SNAP (n = 78), Aß+/ND+ (n = 204)-hypothesizing that SNAP would have an APOE profile comparable to Aß-/ND-. Using AD Neuroimaging Initiative data (n = 786, 72±7 years, 48% female), amyloid status (Aß+ or Aß-) was defined by cerebrospinal fluid (CSF) Aß-42 levels, and neurodegeneration status (ND+ or ND-) was defined by hippocampal volume from MRI. Binary logistic regression related biomarker status to APOE ε2 and ε4 allele carrier status, adjusting for age, sex, education, and cognitive diagnosis. Compared to the biomarker negative (Aß-/ND-) participants, higher proportions of ε4 and lower proportions of ε2 carriers were observed among Aß+/ND- (ε4: OR = 6.23, p<0.001; ε2: OR = 0.53, p = 0.03) and Aß+/ND+ participants (ε4: OR = 12.07, p<0.001; ε2: OR = 0.29, p = 0.004). SNAP participants were statistically comparable to biomarker negative participants (p-values>0.30). In supplemental analyses, comparable results were observed when coding SNAP using amyloid imaging and when using CSF tau levels. In contrast to APOE, a polygenic risk score for AD that excluded APOE did not show an association with amyloidosis or neurodegeneration (p-values>0.15), but did show an association with SNAP defined using CSF tau (ß = 0.004, p = 0.02). Thus, in a population with low levels of cerebrovascular disease and a lower prevalence of SNAP than the general population, APOE and known genetic drivers of AD do not appear to contribute to the neurodegeneration observed in SNAP. Additional work in population based samples is needed to better elucidate the genetic contributors to various etiological drivers of SNAP.
[Mh] Termos MeSH primário: Doença de Alzheimer/fisiopatologia
Apolipoproteínas E/genética
Frequência do Gene
Sintomas Prodrômicos
[Mh] Termos MeSH secundário: Idoso
Doença de Alzheimer/diagnóstico por imagem
Doença de Alzheimer/genética
Peptídeos beta-Amiloides/metabolismo
Biomarcadores/metabolismo
Encéfalo/diagnóstico por imagem
Encéfalo/metabolismo
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Apolipoproteins E); 0 (Biomarkers)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188501


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[PMID]:28460069
[Au] Autor:Premi E; Grassi M; van Swieten J; Galimberti D; Graff C; Masellis M; Tartaglia C; Tagliavini F; Rowe JB; Laforce R; Finger E; Frisoni GB; de Mendonça A; Sorbi S; Gazzina S; Cosseddu M; Archetti S; Gasparotti R; Manes M; Alberici A; Cardoso MJ; Bocchetta M; Cash DM; Ourselin S; Padovani A; Rohrer JD; Borroni B; Genetic FTD Initiative (GENFI)
[Ad] Endereço:Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.
[Ti] Título:Cognitive reserve and TMEM106B genotype modulate brain damage in presymptomatic frontotemporal dementia: a GENFI study.
[So] Source:Brain;140(6):1784-1791, 2017 Jun 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Frontotemporal dementia is a heterogeneous neurodegenerative disorder with around a third of cases having autosomal dominant inheritance. There is wide variability in phenotype even within affected families, raising questions about the determinants of the progression of disease and age at onset. It has been recently demonstrated that cognitive reserve, as measured by years of formal schooling, can counteract the ongoing pathological process. The TMEM106B genotype has also been found to be a modifier of the age at disease onset in frontotemporal dementia patients with TDP-43 pathology. This study therefore aimed to elucidate the modulating effect of environment (i.e. cognitive reserve as measured by educational attainment) and genetic background (i.e. TMEM106B polymorphism, rs1990622 T/C) on grey matter volume in a large cohort of presymptomatic subjects bearing frontotemporal dementia-related pathogenic mutations. Two hundred and thirty-one participants from the GENFI study were included: 108 presymptomatic MAPT, GRN, and C9orf72 mutation carriers and 123 non-carriers. For each subject, cortical and subcortical grey matter volumes were generated using a parcellation of the volumetric T1-weighted magnetic resonance imaging brain scan. TMEM106B genotyping was carried out, and years of education recorded. First, we obtained a composite measure of grey matter volume by graph-Laplacian principal component analysis, and then fitted a linear mixed-effect interaction model, considering the role of (i) genetic status; (ii) educational attainment; and (iii) TMEM106B genotype on grey matter volume. The presence of a mutation was associated with a lower grey matter volume (P = 0.002), even in presymptomatic subjects. Education directly affected grey matter volume in all the samples (P = 0.02) with lower education attainment being associated with lower volumes. TMEM106B genotype did not influence grey matter volume directly on its own but in mutation carriers it modulated the slope of the correlation between education and grey matter volume (P = 0.007). Together, these results indicate that brain atrophy in presymptomatic carriers of common frontotemporal dementia mutations is affected by both genetic and environmental factors such that TMEM106B enhances the benefit of cognitive reserve on brain structure. These findings should be considered in evaluating outcomes in future disease-modifying trials, and support the search for protective mechanisms in people at risk of dementia that might facilitate new therapeutic strategies.
[Mh] Termos MeSH primário: Reserva Cognitiva/fisiologia
Escolaridade
Demência Frontotemporal
Substância Cinzenta/diagnóstico por imagem
Proteínas de Membrana/genética
Proteínas do Tecido Nervoso/genética
[Mh] Termos MeSH secundário: Adulto
Atrofia/patologia
Estudos de Coortes
Feminino
Demência Frontotemporal/diagnóstico por imagem
Demência Frontotemporal/genética
Demência Frontotemporal/fisiopatologia
Genótipo
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Polimorfismo Genético
Sintomas Prodrômicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Nerve Tissue Proteins); 0 (TMEM106B protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171127
[Lr] Data última revisão:
171127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx103


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[PMID]:29050382
[Au] Autor:Schöll M; Ossenkoppele R; Strandberg O; Palmqvist S; Jögi J; Ohlsson T; Smith R; Hansson O; Swedish BioFINDER study
[Ad] Endereço:Clinical Memory Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.
[Ti] Título:Distinct 18F-AV-1451 tau PET retention patterns in early- and late-onset Alzheimer's disease.
[So] Source:Brain;140(9):2286-2294, 2017 Sep 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Patients with Alzheimer's disease can present with different clinical phenotypes. Individuals with late-onset Alzheimer's disease (>65 years) typically present with medial temporal lobe neurodegeneration and predominantly amnestic symptomatology, while patients with early-onset Alzheimer's disease (<65 years) exhibit greater neocortical involvement associated with a clinical presentation including dyspraxia, executive dysfunction, or visuospatial impairment. We recruited 20 patients with early-onset Alzheimer's disease, 21 with late-onset Alzheimer's disease, three with prodromal early-onset Alzheimer's disease and 13 with prodromal late-onset Alzheimer's disease, as well as 30 cognitively healthy elderly controls, that had undergone 18F-AV-1451 tau positron emission tomography and structural magnetic resonance imaging to explore whether early- and late-onset Alzheimer's disease exhibit differential regional tau pathology and atrophy patterns. Strong associations of lower age at symptom onset with higher 18F-AV-1451 uptake were observed in several neocortical regions, while higher age did not yield positive associations in neither patient group. Comparing patients with early-onset Alzheimer's disease with controls resulted in significantly higher 18F-AV-1451 retention throughout the neocortex, while comparing healthy controls with late-onset Alzheimer's disease patients yielded a distinct pattern of higher 18F-AV-1451 retention, predominantly confined to temporal lobe regions. When compared against each other, the early-onset Alzheimer's disease group exhibited greater uptake than the late-onset group in prefrontal and premotor, as well as in inferior parietal cortex. These preliminary findings indicate that age may constitute an important contributor to Alzheimer's disease heterogeneity highlighting the potential of tau positron emission tomography to capture phenotypic variation across patients with Alzheimer's disease.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Carbolinas/metabolismo
Sintomas Prodrômicos
Tauopatias/diagnóstico por imagem
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Idade de Início
Idoso
Envelhecimento/metabolismo
Envelhecimento/patologia
Doença de Alzheimer/diagnóstico
Doença de Alzheimer/patologia
Atrofia/patologia
Estudos de Casos e Controles
Córtex Cerebral/metabolismo
Córtex Cerebral/patologia
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Neuroimagem
Tomografia por Emissão de Pósitrons
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole); 0 (Carbolines); 0 (tau Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx171


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[PMID]:28934374
[Au] Autor:Svärd D; Nilsson M; Lampinen B; Lätt J; Sundgren PC; Stomrud E; Minthon L; Hansson O; van Westen D
[Ad] Endereço:Diagnostic Radiology, Lund University, Lund, Sweden.
[Ti] Título:The effect of white matter hyperintensities on statistical analysis of diffusion tensor imaging in cognitively healthy elderly and prodromal Alzheimer's disease.
[So] Source:PLoS One;12(9):e0185239, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diffusion tensor imaging (DTI) has been used to study microstructural white matter alterations in a variety of conditions including normal aging and Alzheimer's disease (AD). White matter hyperintensities (WMH) are common in cognitively healthy elderly as well as in AD and exhibit elevated mean diffusivity (MD) and reduced fractional anisotropy (FA). However, the effect of WMH on statistical analysis of DTI estimates has not been thoroughly studied. In the present study we address this in two ways. First, we investigate the effect of WMH on MD and FA in the dorsal and ventral cingulum, the superior longitudinal fasciculus, and the corticospinal tract, by comparing two matched groups of cognitively healthy elderly (n = 21 + 21) with unequal WMH load. Second, we assess the effects of adjusting for WMH load when comparing MD and FA in prodromal AD subjects (n = 83) to cognitively healthy elderly (n = 132) in the abovementioned white matter tracts. Results showed the WMH in cognitively healthy elderly to have a generally large effect on DTI estimates (Cohen's d = 0.63 to 1.27 for significant differences in MD and -1.06 to -0.69 for FA). These effect sizes were comparable to those of various neurological and psychiatric diseases (Cohen's d = 0.57 to 2.20 for differences in MD and -1.76 to -0.61 for FA). Adjusting for WMH when comparing DTI estimates in prodromal AD subjects to cognitively healthy elderly improved the explanatory power as well as the outcome of the analysis, indicating that some of the differences in MD and FA were largely driven by unequal WMH load between the groups rather than alterations in normal-appearing white matter (NAWM). Thus, our findings suggest that if the purpose of a study is to compare alterations in NAWM between two groups using DTI it may be necessary to adjust the statistical analysis for WMH.
[Mh] Termos MeSH primário: Doença de Alzheimer/diagnóstico por imagem
Doença de Alzheimer/fisiopatologia
Cognição
Imagem de Tensor de Difusão
Processamento de Imagem Assistida por Computador
Sintomas Prodrômicos
Substância Branca/diagnóstico por imagem
[Mh] Termos MeSH secundário: Idoso
Doença de Alzheimer/líquido cefalorraquidiano
Peptídeos beta-Amiloides/líquido cefalorraquidiano
Anisotropia
Estudos de Casos e Controles
Feminino
Seres Humanos
Masculino
Fragmentos de Peptídeos/líquido cefalorraquidiano
Substância Branca/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Peptide Fragments); 0 (amyloid beta-protein (1-40)); 0 (amyloid beta-protein (1-42))
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185239


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[PMID]:28934250
[Au] Autor:Cabanas M; Bassil F; Mons N; Garret M; Cho YH
[Ad] Endereço:Institut de Neurosciences Cognitives et Intégratives d'Aquitaine, CNRS UMR 5287, Pessac, France.
[Ti] Título:Changes in striatal activity and functional connectivity in a mouse model of Huntington's disease.
[So] Source:PLoS One;12(9):e0184580, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hereditary Huntington's disease (HD) is associated with progressive motor, cognitive and psychiatric symptoms. A primary consequence of the HD mutation is the preferential loss of medium spiny projection cells with relative sparing of local interneurons in the striatum. In addition, among GABAergic striatal projection cells, indirect pathway cells expressing D2 dopamine receptors are lost earlier than direct pathway cells expressing D1 receptors. To test in vivo the functional integrity of direct and indirect pathways as well as interneurons in the striatum of male R6/1 transgenic mice, we assessed their c-Fos expression levels induced by a striatal-dependent cognitive task and compared them with age-matched wild-type littermates. We found a significant increase of c-Fos+ nuclei in the dorsomedial striatum, and this only at 2 months, when our HD mouse model is still pre-motor symptomatic, the increase disappearing with symptom manifestation. Contrary to our expectation, the indirect pathway projection neurons did not undergo any severer changes of c-Fos expression regardless of age in R6/1 mice. We also found a decreased activation of interneurons that express parvalbumin in the dorsomedial striatum at both presymptomatic and symptomatic ages. Finally, analysis of c-Fos expression in extended brain regions involved in the cognitive learning used in our study, demonstrates, throughout ages studied, changes in the functional connectivity between regions in the transgenic mice. Further analysis of the cellular and molecular changes underlying the transient striatal hyperactivity in the HD mice may help to understand the mechanisms involved in the disease onset.
[Mh] Termos MeSH primário: Condicionamento Operante/fisiologia
Corpo Estriado/metabolismo
Doença de Huntington/metabolismo
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Animais
Corpo Estriado/patologia
Modelos Animais de Doenças
Progressão da Doença
Doença de Huntington/patologia
Masculino
Camundongos Transgênicos
Atividade Motora/fisiologia
Vias Neurais/metabolismo
Vias Neurais/patologia
Neurônios/patologia
Sintomas Prodrômicos
Proteínas Proto-Oncogênicas c-fos/metabolismo
Distribuição Aleatória
Receptores de Dopamina D1/metabolismo
Receptores de Dopamina D2/metabolismo
Convulsões/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DRD2 protein, rat); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptors, Dopamine D1); 0 (Receptors, Dopamine D2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184580


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[PMID]:28867578
[Au] Autor:Rostami F; Javan M; Moghimi A; Haddad-Mashadrizeh A; Fereidoni M
[Ad] Endereço:Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran.
[Ti] Título:Streptozotocin-induced hippocampal astrogliosis and insulin signaling malfunction as experimental scales for subclinical sporadic Alzheimer model.
[So] Source:Life Sci;188:172-185, 2017 Nov 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Insulin signaling malfunction has recently been suggested as a preliminary event involved in the etiology of Sporadic Alzheimer's disease (SAD). In order to develop insulin resistance-related SAD model, rats were treated with streptozotocin, intracerebroventricularly (icv-STZ). Nevertheless, given the lack of knowledge regarding sub-clinical stages of SAD, the current challenging issue is establishing a practical pre-clinical SAD model. Despite some proposed mechanisms, such as insulin malfunction, neuroinflammation, and gliosis, icv-STZ mechanism of action is not fully understood yet and Streptozotocin-induced rat model of Alzheimer has still major shortcomings. MAIN METHODS: Using three STZ doses (0.5, 1, and 3mg/kg) and three testing time (short-term, medium-term and long-term), we sought the best dose of STZ in order to mimic the characteristic feature of sAD in rats. So, we conducted a series of fifteen-week follow-up cognitive and non-cognitive studies. Besides, IR, tau and ChAT mRNA levels were measured, along with histological analysis of astrocyte, dark neuron numbers, and pyramidal layer thickness, in order to compare the effects of different doses of icv-STZ. KEY FINDINGS: STZ 3mg/kg caused cognitive and insulin signaling disturbance from the very first testing-time. STZ1-injected animals, however, showed an augmented hippocampal astrocyte numbers in a short time; they, also, were diagnosed with disturbed insulin signaling in medium-term post icv-STZ-injection. Moreover, behavioral, molecular and histological impairments induced by 0.5mg/kg icv-STZ were slowly progressing in comparison to high doses of STZ. SIGNIFICANCE: STZ1 and 0.5mg/kg-treated animals are, respectively, suggested as a suitable experimental model of MCI, and sub-clinical stage.
[Mh] Termos MeSH primário: Doença de Alzheimer/diagnóstico
Gliose/patologia
Hipocampo/patologia
Resistência à Insulina
Insulina/metabolismo
Sintomas Prodrômicos
Estreptozocina/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Astrócitos/patologia
Colina O-Acetiltransferase/biossíntese
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Comportamento Exploratório/efeitos dos fármacos
Gliose/induzido quimicamente
Infusões Intraventriculares
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Neurônios/patologia
Ratos
Receptor de Insulina/biossíntese
Recognição (Psicologia)/efeitos dos fármacos
Teste de Desempenho do Rota-Rod
Estreptozocina/administração & dosagem
Fatores de Tempo
Proteínas tau/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (tau Proteins); 5W494URQ81 (Streptozocin); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 2.7.10.1 (Receptor, Insulin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status:MEDLINE


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[PMID]:28679601
[Au] Autor:Sierra M; Martínez-Rodríguez I; Sánchez-Juan P; González-Aramburu I; Jiménez-Alonso M; Sánchez-Rodríguez A; Berciano J; Banzo I; Infante J
[Ad] Endereço:From the Neurology Service (M.S., P.S.-J., I.G.-A., A.S.-R., J.B., J.I.), University Hospital Marqués de Valdecilla and Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), IDIVAL, University of Cantabria (UC); and Nuclear Medicine Department (I.M.-R., M.J.-A., I.B
[Ti] Título:Prospective clinical and DaT-SPECT imaging in premotor G2019S-associated Parkinson disease.
[So] Source:Neurology;89(5):439-444, 2017 Aug 01.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To assess the value of baseline clinical and imaging biomarkers in a cohort of asymptomatic G2019S carriers for predicting conversion to Parkinson disease (PD) at 4 years. METHODS: Thirty-two asymptomatic carriers of G2019S mutation underwent baseline and 4-year evaluation including clinical examination (Unified Parkinson's Disease Rating Scale, part III, olfaction University of Pennsylvania Smell Identification Test [UPSIT]) and dopamine transporter (DaT) SPECT ( I-ioflupane). Visual and semiquantitative analysis of images was performed. The specific striatal binding ratio was calculated (striatal region of interest [ROI] - occipital ROI/occipital ROI). RESULTS: Three carriers, asymptomatic at baseline, had converted to PD at 4-year evaluation. Twenty-three participants were fully evaluated. PD converters had lower striatal DaT binding at baseline than nonconverters ( = 0.002). A baseline scan with a ratio of bilateral striatal uptake below 1 predicted conversion to PD within the 4-year period with high sensitivity and specificity (area under the curve 1; = 0.006). The slope of DaT binding decline between the 2 scans was similar in PD converters and nonconverters. Age-adjusted UPSIT score at baseline and at 4 years was similar in both groups. CONCLUSIONS: Semiquantitative DaT-SPECT could be used to predict early conversion to PD in asymptomatic carriers of the G2019S mutation. Rate of conversion to PD at 4 years in this cohort aged ∼64 years was 12%. The slope of DaT binding decline on DaT-SPECT imaging seems to be similar across different stages of the premotor period.
[Mh] Termos MeSH primário: Corpo Estriado/diagnóstico por imagem
Proteínas da Membrana Plasmática de Transporte de Dopamina/metabolismo
Serina-Treonina Proteína Quinase-2 com Repetições Ricas em Leucina/genética
Doença de Parkinson/diagnóstico por imagem
Doença de Parkinson/genética
Tomografia Computadorizada de Emissão de Fóton Único
[Mh] Termos MeSH secundário: Fatores Etários
Mapeamento Encefálico
Corpo Estriado/metabolismo
Progressão da Doença
Família
Feminino
Heterozigoto
Seres Humanos
Estudos Longitudinais
Masculino
Meia-Idade
Mutação
Nortropanos
Doença de Parkinson/metabolismo
Sintomas Prodrômicos
Estudos Prospectivos
Compostos Radiofarmacêuticos
Índice de Gravidade de Doença
Olfato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dopamine Plasma Membrane Transport Proteins); 0 (Nortropanes); 0 (Radiopharmaceuticals); EC 2.7.11.1 (LRRK2 protein, human); EC 2.7.11.1 (Leucine-Rich Repeat Serine-Threonine Protein Kinase-2); VF232WE742 (ioflupane)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004185


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[PMID]:28679600
[Au] Autor:Kollmer J; Sahm F; Hegenbart U; Purrucker JC; Kimmich C; Schönland SO; Hund E; Heiland S; Hayes JM; Kristen AV; Röcken C; Pham M; Bendszus M; Weiler M
[Ad] Endereço:From the Department of Neuroradiology (J.K., S.H., M.P., M.B.), Amyloidosis Center Heidelberg (J.K., U.H., J.C.P., C.K., S.O.S., E.H., A.V.K., M.W.), Department of Neuropathology (F.S.), Medical Department V (U.H., C.K., S.O.S.), Department of Neurology (J.C.P., E.H., M.W.), Division of Experimental
[Ti] Título:Sural nerve injury in familial amyloid polyneuropathy: MR neurography vs clinicopathologic tools.
[So] Source:Neurology;89(5):475-484, 2017 Aug 01.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To detect and quantify lesions of the small-caliber sural nerve (SN) in symptomatic and asymptomatic transthyretin familial amyloid polyneuropathy (TTR-FAP) by high-resolution magnetic resonance neurography (MRN) in correlation with electrophysiologic and histopathologic findings. METHODS: Twenty-five patients with TTR-FAP, 10 asymptomatic carriers of the mutated transthyretin gene (mut ), and 35 age- and sex-matched healthy controls were prospectively included in this cross-sectional case-control study. All participants underwent 3T MRN with high-structural resolution (fat-saturated, T2-weighted, and double-echo sequences). Total imaging time was ≈45 minutes per patient. Manual SN segmentation was performed from its origin at the sciatic nerve bifurcation to the lower leg with subsequent evaluation of quantitative microstructural and morphometric parameters. Additional time needed for postprocessing was ≈1.5 hours per participant. Detailed neurologic and electrophysiologic examinations were conducted in the TTR group. RESULTS: T2 signal and proton spin density (ρ) reliably differentiated between TTR-FAP (198.0 ± 13.3, 429.6 ± 15.25), mut carriers (137.0 ± 16.9, = 0.0009; 354.7 ± 21.64, = 0.0029), and healthy controls (90.0 ± 3.4, 258.2 ± 9.10; < 0.0001). Marked differences between mut carriers and controls were found for T2 signal ( = 0.0065) and ρ ( < 0.0001). T2 relaxation time was higher in patients with TTR-FAP only ( = 0.015 vs mut carriers, = 0.0432 vs controls). SN caliber was higher in patients with TTR-FAP vs controls and in mut carriers vs controls ( < 0.0001). Amyloid deposits were histopathologically detectable in 10 of 14 SN specimens. CONCLUSIONS: SN injury in TTR-FAP is detectable and quantifiable in vivo by MRN even in asymptomatic mut carriers. Differences in SN T2 signal between controls and asymptomatic mut carriers are derived mainly from an increase of ρ, which overcomes typical limitations of established diagnostic methods as a highly sensitive imaging biomarker for early detection of peripheral nerve lesions. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that MRN accurately identifies asymptomatic mut carriers.
[Mh] Termos MeSH primário: Neuropatias Amiloides Familiares/diagnóstico por imagem
Imagem por Ressonância Magnética
Nervo Sural/diagnóstico por imagem
Nervo Sural/lesões
[Mh] Termos MeSH secundário: Adulto
Idoso
Neuropatias Amiloides Familiares/genética
Neuropatias Amiloides Familiares/patologia
Estudos de Casos e Controles
Estudos Transversais
Avaliação da Deficiência
Diagnóstico Precoce
Feminino
Heterozigoto
Seres Humanos
Processamento de Imagem Assistida por Computador
Masculino
Meia-Idade
Condução Nervosa
Pré-Albumina/genética
Sintomas Prodrômicos
Estudos Prospectivos
Nervo Sural/patologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Prealbumin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004178


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[PMID]:28678992
[Au] Autor:Hafeman DM; Merranko J; Goldstein TR; Axelson D; Goldstein BI; Monk K; Hickey MB; Sakolsky D; Diler R; Iyengar S; Brent DA; Kupfer DJ; Kattan MW; Birmaher B
[Ad] Endereço:Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania.
[Ti] Título:Assessment of a Person-Level Risk Calculator to Predict New-Onset Bipolar Spectrum Disorder in Youth at Familial Risk.
[So] Source:JAMA Psychiatry;74(8):841-847, 2017 Aug 01.
[Is] ISSN:2168-6238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Early identification of individuals at high risk for the onset of bipolar spectrum disorder (BPSD) is key from both a clinical and research perspective. While previous work has identified the presence of a bipolar prodrome, the predictive implications for the individual have not been assessed, to date. Objective: To build a risk calculator to predict the 5-year onset of BPSD in youth at familial risk for BPSD. Design, Setting, and Participants: The Pittsburgh Bipolar Offspring Study is an ongoing community-based longitudinal cohort investigation of offspring of parents with bipolar I or II (and community controls), recruited between November 2001 and July 2007, with a median follow-up period of more than 9 years. Recruitment has ended, but follow-up is ongoing. The present analysis included offspring of parents with bipolar I or II (aged 6-17 years) who had not yet developed BPSD at baseline. Main Outcomes and Measures: This study tested the degree to which a time-to-event model, including measures of mood and anxiety, general psychosocial functioning, age at mood disorder onset in the bipolar parent, and age at each visit, predicted new-onset BPSD. To fully use longitudinal data, the study assessed each visit separately, clustering within individuals. Discrimination was measured using the time-dependent area under the curve (AUC), predicting 5-year risk; internal validation was performed using 1000 bootstrapped resamples. Calibration was assessed by comparing observed vs predicted probability of new-onset BPSD. Results: There were 412 at-risk offspring (202 [49.0%] female), with a mean (SD) visit age of 12.0 (3.5) years and a mean (SD) age at new-onset BPSD of 14.2 (4.5) years. Among them, 54 (13.1%) developed BPSD during follow-up (18 with BD I or II); these participants contributed a total of 1058 visits, 67 (6.3%) of which preceded new-onset BPSD within the next 5 years. Using internal validation to account for overfitting, the model provided good discrimination between converting vs nonconverting visits (AUC, 0.76; bootstrapped 95% CI, 0.71-0.82). Important univariate predictors of outcome (AUC range, 0.66-0.70) were dimensional measures of mania, depression, anxiety, and mood lability; psychosocial functioning; and parental age at mood disorder. Conclusions and Relevance: This risk calculator provides a practical tool for assessing the probability that a youth at familial risk for BPSD will develop new-onset BPSD within the next 5 years. Such a tool may be used by clinicians to inform frequency of monitoring and treatment options and for research studies to better identify potential participants at ultra high risk of conversion.
[Mh] Termos MeSH primário: Transtorno Bipolar/diagnóstico
Diagnóstico Precoce
Saúde da Família
[Mh] Termos MeSH secundário: Adolescente
Idade de Início
Criança
Feminino
Seres Humanos
Estudos Longitudinais
Masculino
Modelos Psicológicos
Sintomas Prodrômicos
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE
[do] DOI:10.1001/jamapsychiatry.2017.1763


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[PMID]:28659431
[Au] Autor:Lafaille-Magnan ME; Poirier J; Etienne P; Tremblay-Mercier J; Frenette J; Rosa-Neto P; Breitner JCS; PREVENT-AD Research Group
[Ad] Endereço:From the Centre for Studies on Prevention of AD (M.-E.L.-M., J.P., P.E., J.T.-M., J.F., P.R.-N., J.C.S.B.) and McGill Centre for Studies in Aging (P.R.-N.), Douglas Mental Health University Institute, McGill University, Faculty of Medicine, Montreal, Quebec, Canada. Marie-Elyse.Lafaille-Magnan@mail.
[Ti] Título:Odor identification as a biomarker of preclinical AD in older adults at risk.
[So] Source:Neurology;89(4):327-335, 2017 Jul 25.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To assess odor identification (OI) as an indicator of presymptomatic Alzheimer disease (AD) pathogenesis in cognitively normal aging individuals at increased risk of AD dementia. METHODS: In 274 members of the PREVENT-AD cohort of healthy aging persons with a parental or multiple-sibling history of AD dementia, we assessed the cross-sectional association of OI with potential indicators of presymptomatic AD. Some 101 participants donated CSF, thus enabling assessment of AD pathology with the biomarkers total tau (t-tau), phospho-tau (P -tau), and their ratios with ß-amyloid (Aß ). Adjusted analyses considered age, cognition, ε4 status, education, and sex as covariates. We measured OI using the University of Pennsylvania Smell Identification Test and cognitive performance using the Repeatable Battery for Assessment of Neuropsychological Status. Standard kits provided assays of the AD biomarkers. Analyses used robust-fit linear regression models. RESULTS: Reduced OI was associated with lower cognitive score and older age, as well as increased ratios of CSF t-tau and P -tau to Aß (all < 0.02). However, the observed associations of OI with age and cognition were unapparent in adjusted models that restricted observations to CSF donors and included AD biomarkers. OI showed little association with CSF Aß alone except in ε4 carriers having lowest-quartile Aß levels. CONCLUSIONS: These findings from healthy high-risk older individuals suggest that OI reflects degree of preclinical AD pathology, while its relationships with age and cognition result from the association of these latter variables with such pathology. Diminished OI may be a practical and affordable biomarker of AD pathology.
[Mh] Termos MeSH primário: Doença de Alzheimer/diagnóstico
Percepção Olfatória
Reconhecimento Fisiológico de Modelo
Recognição (Psicologia)
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Envelhecimento/fisiologia
Envelhecimento/psicologia
Doença de Alzheimer/líquido cefalorraquidiano
Doença de Alzheimer/genética
Doença de Alzheimer/fisiopatologia
Peptídeos beta-Amiloides/líquido cefalorraquidiano
Apolipoproteína E4/genética
Biomarcadores/líquido cefalorraquidiano
Cognição
Estudos de Coortes
Estudos Transversais
Feminino
Seres Humanos
Masculino
Meia-Idade
Fragmentos de Peptídeos/líquido cefalorraquidiano
Fosforilação
Sintomas Prodrômicos
Risco
Proteínas tau/líquido cefalorraquidiano
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Apolipoprotein E4); 0 (Biomarkers); 0 (MAPT protein, human); 0 (Peptide Fragments); 0 (amyloid beta-protein (1-42)); 0 (tau Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170630
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004159



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