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  1 / 26073 MEDLINE  
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Moriguti, Julio Cesar
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[PMID]:28459000
[Au] Autor:Ramos Bernardes da Silva Filho S; Oliveira Barbosa JH; Rondinoni C; Dos Santos AC; Garrido Salmon CE; da Costa Lima NK; Ferriolli E; Moriguti JC
[Ad] Endereço:Ribeirao Preto Medical School of University of Sao Paulo, Ribeirao Preto, SP, Brazil.
[Ti] Título:Neuro-degeneration profile of Alzheimer's patients: A brain morphometry study.
[So] Source:Neuroimage Clin;15:15-24, 2017.
[Is] ISSN:2213-1582
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Alzheimer's disease (AD) is a primary and progressive neurodegenerative disorder, which is marked by cognitive deterioration and memory impairment. Atrophy of hippocampus and other basal brain regions is one of the most predominant structural imaging findings related to AD. Most studies have evaluated the pre-clinical and initial stages of AD through clinical trials using Magnetic Resonance Imaging. Structural biomarkers for advanced AD stages have not been evaluated yet, being considered only hypothetically. OBJECTIVE: To evaluate the brain morphometry of AD patients at all disease stages, identifying the structural neuro-degeneration profile associated with AD severity. MATERIAL AND METHODS: AD patients aged 60 years or over at different AD stages were recruited and grouped into three groups following the Clinical Dementia Rating (CDR) score: CDR1 (n = 16), CDR2 (n = 15), CDR3 (n = 13). Age paired healthy volunteers (n = 16) were also recruited (control group). Brain images were acquired on a 3T magnetic resonance scanner using a conventional Gradient eco 3D T1-w sequence without contrast injection. Volumetric quantitative data and cortical thickness were obtained by automatic segmentation using the Freesurfer software. Volume of each brain region was normalized by the whole brain volume in order to minimize age and body size effects. Volume and cortical thickness variations among groups were compared. RESULTS: Atrophy was observed in the hippocampus, amygdala, entorhinal cortex, parahippocampal region, temporal pole and temporal lobe of patients suffering from AD at any stage. Cortical thickness was reduced only in the parahippocampal gyrus at all disease stages. Volume and cortical thickness were correlated with the Mini Mental State Examination (MMSE) score in all studied regions, as well as with CDR and disease duration. DISCUSSION AND CONCLUSION: As previously reported, brain regions affected by AD during its initial stages, such as hippocampus, amygdala, entorhinal cortex, and parahippocampal region, were found to be altered even in individuals with severe AD. In addition, individuals, specifically, with CDR 3, have multiple regions with lower volumes than individuals with a CDR 2. These results indicate that rates of atrophy have not plateaued out at CDR 2-3, and in severe patients there are yet neuronal loss and gliosis. These findings can add important information to the more accepted model in the literature that focuses mainly on early stages. Our findings allow a better understanding on the AD pathophysiologic process and follow-up process of drug treatment even at advanced disease stages.
[Mh] Termos MeSH primário: Doença de Alzheimer/diagnóstico por imagem
Mapeamento Encefálico/métodos
Encéfalo/diagnóstico por imagem
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Doença de Alzheimer/patologia
Atrofia/diagnóstico por imagem
Atrofia/patologia
Encéfalo/patologia
Feminino
Seres Humanos
Masculino
Doenças Neurodegenerativas/diagnóstico por imagem
Doenças Neurodegenerativas/patologia
Tamanho do Órgão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1016/j.nicl.2017.04.001


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[PMID]:29269695
[Au] Autor:Hamada K; Takei R; Sakiyama Y; Moriyama H; Hashiguchi A; Takashima H
[Ad] Endereço:Department of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Sciences.
[Ti] Título:[A case of chronic progressive neuro-Behçet disease with extensive cerebral atrophy and elevated CSF IL-6 activity treated with infliximab].
[So] Source:Rinsho Shinkeigaku;58(1):30-34, 2018 Jan 26.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:A 43-year-old man without a previous episode of uveitis presented with slowly progressive neurological symptoms that appeared within the past year such as dysarthria, ataxic gait, and behavioral changes. Brain MRI findings showed atrophic lesions in the brainstem and cerebellum. Because these clinical symptoms and abnormal MRI findings indicated spinocerebellar degeneration as the initial diagnosis, he was admitted to our hospital. On admission, we noticed that he had non-neurological manifestations of Behçet disease, such as stomatitis, genital ulcers, and folliculitis. HLA-B51 was positive. He also showed pleocytosis (29 cells/mm , predominantly mononuclear cells) and elevated cerebrospinal fluid (CSF) IL-6 levels (213 pg/ml), hence he was diagnosed with chronic progressive neuro-Behçet disease (CPNBD). The therapeutic effect of a high-dose intravenous methylprednisolone pulse (1,000 mg/day for 3 days) and methotrexate (maximum dosage, 16 mg/week) was poor against both neurological symptoms and CSF findings. Intravenous infliximab therapy (5 mg/kg, 2 weeks) dramatically decreased CSF IL-6 levels (13 pg/ml) but clinical symptoms remained unchanged. MRI findings of extensive cerebral atrophy and increased CSF IL-6 levels at the pretreatment time point reflected irreversible neurological involvement in CPNBD. For cases with progressive psychiatric symptoms and cerebellar ataxia in the early stage of the disease, skin manifestations should be examined immediately, CSF IL-6 levels measured, and immunosuppressive therapy initiated before CPNBD progresses to brainstem atrophy.
[Mh] Termos MeSH primário: Síndrome de Behçet/diagnóstico
Síndrome de Behçet/tratamento farmacológico
Encéfalo/patologia
Infliximab/administração & dosagem
Interleucina-6/líquido cefalorraquidiano
[Mh] Termos MeSH secundário: Adulto
Atrofia
Síndrome de Behçet/líquido cefalorraquidiano
Síndrome de Behçet/patologia
Biomarcadores/líquido cefalorraquidiano
Doença Crônica
Progressão da Doença
Seres Humanos
Masculino
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Interleukin-6); B72HH48FLU (Infliximab)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-001086


  3 / 26073 MEDLINE  
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[PMID]:28460032
[Au] Autor:Knier B; Leppenetier G; Wetzlmair C; Aly L; Hoshi MM; Pernpeintner V; Biberacher V; Berthele A; Mühlau M; Zimmer C; Hemmer B; Korn T
[Ad] Endereço:Department of Neurology, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany2Department of Experimental Neuroimmunology, Technische Universität München, Munich, Germany.
[Ti] Título:Association of Retinal Architecture, Intrathecal Immunity, and Clinical Course in Multiple Sclerosis.
[So] Source:JAMA Neurol;74(7):847-856, 2017 Jul 01.
[Is] ISSN:2168-6157
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Biomarkers to estimate long-term outcomes in patients with multiple sclerosis (MS) and to assign patients to individual treatment regimens are urgently needed. Objective: To assess whether retinal layer volumes are correlated with immune cell subsets and immunoglobulin indices in the cerebrospinal fluid and whether retinal layer volumes alone or in combination with intrathecal variables are associated with worsening of disease in patients with relapsing-remitting MS. Design, Setting, and Participants: This observational cohort study included 312 patients with relapsing-remitting MS in 2 independent cohorts (72 patients with short disease duration [cohort 1] and 240 patients with longer disease duration [cohort 2]) treated at a single German university hospital from April 15, 2013, through November 11, 2015. Main Outcomes and Measures: The common ganglion cell and inner plexiform layer (GCIPL) and inner nuclear layer (INL) volumes were tested for association with the immunoglobulin indices and the frequencies of immune cells in the cerebrospinal fluid (including B cells, T cells, and natural killer cells) (cohort 1). Volumes of GCIPL alone (cohorts 1 and 2) or GCIPL corrected for intrathecal B-cell frequencies (cohort 1) were tested for their association with worsening disability. Results: A total of 312 patients (212 women [67.9%] and 100 men [32.1%]; median age, 34.0 years [interquartile range (IQR), 28.0-42.0 years]) were available for analysis. In cohort 1 (50 women [69.4%] and 22 men [30.6%]; median age, 31.0 years [IQR, 26.3-38.3 years]), with short disease durations (median, 1.0 months [IQR, 1.0-2.0 months]), low GCIPL volumes were associated with increased intrathecal B-cell frequencies (median, 1.96% [IQR, 1.45%-4.20%]) and intrathecal IgG synthesis (median cerebrospinal fluid/serum IgG index, 0.78 [IQR, 0.53-1.07]). The INL volumes correlated with the frequencies of intrathecal CD56bright natural killer cells (r = 0.28; P = .007). Individuals with low GCIPL volumes (<1.99 mm3) had a 6.4-fold risk for worsening disability during follow-up compared with patients with higher GCIPL values (95% CI, 1.7-24.2; P = .007). This finding was reproduced in cohort 2 (162 women [67.5%] and 78 men [32.5%]; median age, 34.0 years [IQR, 29.0-42.0 years]) consisting of patients with longer disease durations (median, 36.0 months [IQR, 21.0-60.0 months]) (hazard ratio, 2.4; 95% CI, 1.2-4.8; P = .02). In both cohorts, INL volumes correlated with the prospective increase in T2 lesion load and the number of gadolinium-enhancing lesions. Conclusions and Relevance: Retinal layers reflect different aspects of disease activity during MS. Loss of GCIPL is associated with intrathecal B-cell immunity and constitutes an independent risk factor for worsening disability, whereas high INL volumes are associated with activity on magnetic resonance imaging in the brain parenchyma. Thus, retinal optical coherence tomography might be a means to support stratification of patients with MS for different therapeutic regimens.
[Mh] Termos MeSH primário: Líquido Cefalorraquidiano/imunologia
Esclerose Múltipla Recidivante-Remitente/líquido cefalorraquidiano
Esclerose Múltipla Recidivante-Remitente/diagnóstico por imagem
Esclerose Múltipla Recidivante-Remitente/fisiopatologia
Retina/diagnóstico por imagem
Células Ganglionares da Retina/patologia
[Mh] Termos MeSH secundário: Adulto
Atrofia/patologia
Linfócitos B
Biomarcadores
Feminino
Seres Humanos
Células Matadoras Naturais
Imagem por Ressonância Magnética
Masculino
Retina/citologia
Fatores de Risco
Linfócitos T
Tomografia de Coerência Óptica
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1001/jamaneurol.2017.0377


  4 / 26073 MEDLINE  
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[PMID]:29185323
[Au] Autor:Winter R; Kimmel A; Wagner P
[Ti] Título:Maxillo-Mandibular Atrophy: Success Through Interdisciplinary Planning.
[So] Source:Dent Today;35(10):114, 116, 118, 120-1, 2016 Oct.
[Is] ISSN:8750-2186
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Prótese Dentária Fixada por Implante
Mandíbula/patologia
Maxila/patologia
Planejamento de Assistência ao Paciente
Equipe de Assistência ao Paciente
[Mh] Termos MeSH secundário: Atrofia/cirurgia
Seres Humanos
Masculino
Mandíbula/cirurgia
Maxila/cirurgia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:D
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE


  5 / 26073 MEDLINE  
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[PMID]:29328565
[Au] Autor:Jovanovic V; Nikolic L
[Ti] Título:Urrets-Zavalia syndrome after deep anterior lamellar keratoplasty
[So] Source:Vojnosanit Pregl;73(10):973-5, 2016 Oct.
[Is] ISSN:0042-8450
[Cp] País de publicação:Serbia
[La] Idioma:eng
[Ab] Resumo:Introduction: Urrets-Zavalia syndrome is an uncommon complication of the deep anterior lamellar keratoplasty in keratoconus. The manifestations of this syndrome are an irreversible mydriasis, iris atrophy and secondary glaucoma. Case report: Deep anterior lamellar keratoplasty was done for keratoconus with a presumably healed corneal hydrops in a 21-year-old Caucasian man. The graft remained clear, but the surgery was complicated by a fixed, dilated pupil, patches of iris atrophy, ectropium of the iris pigment layer and glaukomflecken in the lens. Conclusion: Although safer than penetrating keratoplasty, the deep anterior lamellar by not trying to secure an unhealed Descemet's membrane with air. Instead, a new Descemet's membrane transplanted within a penetrating graft is a safer choice.
[Mh] Termos MeSH primário: Transplante de Córnea/efeitos adversos
Glaucoma/etiologia
Doenças da Íris/etiologia
Ceratocone/cirurgia
Midríase/etiologia
[Mh] Termos MeSH secundário: Atrofia
Glaucoma/diagnóstico
Seres Humanos
Iris/patologia
Doenças da Íris/diagnóstico
Ceratocone/diagnóstico
Masculino
Midríase/diagnóstico
Síndrome
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.2298/VSP141109088J


  6 / 26073 MEDLINE  
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[PMID]:29304183
[Au] Autor:Rektor I; Svátková A; Vojtísek L; Zikmundová I; Vanícek J; Király A; Szabó N
[Ad] Endereço:Movement Disorders Center; First Department of Neurology, School of Medicine, Masaryk University and St. Anne's University Hospital, Brno, Czech Republic.
[Ti] Título:White matter alterations in Parkinson's disease with normal cognition precede grey matter atrophy.
[So] Source:PLoS One;13(1):e0187939, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: While progressive MRI brain changes characterize advanced Parkinson's disease (PD), little has been discovered about structural alterations in the earliest phase of the disease, i.e. in patients with motor symptoms and with normal cognition. Our study aimed to detect grey matter (GM) and white matter (WM) changes in PD patients without cognitive impairment. METHODS: Twenty PD patients and twenty-one healthy controls (HC) were tested for attention, executive function, working memory, and visuospatial and language domains. High-resolution T1-weighted and 60 directional diffusion-weighted 3T MRI images were acquired. The cortical, deep GM and WM volumes and density, as well as the diffusion properties of WM, were calculated. Analyses were repeated on data flipped to the side of the disease origin. RESULTS: PD patients did not show any significant differences from HC in cognitive functioning or in brain volumes. Decreased GM intensity was found in the left superior parietal lobe in the right (p<0.02) and left (p<0.01) flipped data. The analysis of original, un-flipped data demonstrated elevated axial diffusivity (p<0.01) in the superior and anterior corona radiata, internal capsule, and external capsule in the left hemisphere of PD relative to HC, while higher mean and radial diffusivity were discovered in the right (p<0.02 and p<0.03, respectively) and left (p<0.02 and p<0.02, respectively) in the fronto-temporal WM utilizing flipped data. CONCLUSIONS: PD patients without cognitive impairment and GM atrophy demonstrated widespread alterations of WM microstructure. Thus, WM impairment in PD might be a sensitive sign preceding the neuronal loss in associated GM regions.
[Mh] Termos MeSH primário: Substância Cinzenta/patologia
Doença de Parkinson/patologia
Doença de Parkinson/psicologia
Substância Branca/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Atrofia
Estudos de Casos e Controles
Cognição
Progressão da Doença
Feminino
Substância Cinzenta/diagnóstico por imagem
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Neuroimagem
Testes Neuropsicológicos
Doença de Parkinson/diagnóstico por imagem
Substância Branca/diagnóstico por imagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0187939


  7 / 26073 MEDLINE  
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[PMID]:28468185
[Au] Autor:Park J; Chang M
[Ad] Endereço:*Nune Eye Hospital, Daegu †Department of Ophthalmology, Dongguk University, Ilsan Hospital, Gyounggi, South Korea.
[Ti] Título:Eyelid Fat Atrophy and Depigmentation After an Intralesional Injection of Triamcinolone Acetonide to Treat Chalazion.
[So] Source:J Craniofac Surg;28(3):e198-e199, 2017 May.
[Is] ISSN:1536-3732
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Two patients with depigmentation and fat atrophy after an intralesional injection of triamcinolone acetonide (TA) to treat chalazion are reported. A 2-year-old girl with chalazion in her right lower eyelid received a subconjunctival injection of TA and developed fat atrophy and depigmentation around the injected area. These changes subsided after 7 months. The second patient was a 5-year-old boy who received a triamcinolone injection into a chalazion through the eyelid skin and also developed fat atrophy and depigmentation but these changes improved after 1 year.
[Mh] Termos MeSH primário: Calázio/tratamento farmacológico
Doenças Palpebrais/induzido quimicamente
Pálpebras/patologia
Triancinolona Acetonida/efeitos adversos
[Mh] Termos MeSH secundário: Atrofia/induzido quimicamente
Atrofia/diagnóstico
Calázio/patologia
Pré-Escolar
Doenças Palpebrais/patologia
Pálpebras/efeitos dos fármacos
Feminino
Glucocorticoides/administração & dosagem
Glucocorticoides/efeitos adversos
Seres Humanos
Injeções Intralesionais/efeitos adversos
Masculino
Triancinolona Acetonida/administração & dosagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucocorticoids); F446C597KA (Triamcinolone Acetonide)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180126
[Lr] Data última revisão:
180126
[Sb] Subgrupo de revista:D
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1097/SCS.0000000000003367


  8 / 26073 MEDLINE  
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[PMID]:28459108
[Au] Autor:Kir S; Spiegelman BM
[Ad] Endereço:Department of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
[Ti] Título:CACHEXIA & BROWN FAT: A BURNING ISSUE IN CANCER.
[So] Source:Trends Cancer;2(9):461-463, 2016 Sep.
[Is] ISSN:2405-8033
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cachexia, a progressive weight loss in cancer patients that results from tumor-induced energy wasting, is a serious problem that interferes with response to treatment and affects quality of life. Recent studies suggest that thermogenesis of adipose tissues is involved in energy wasting and also point to a link between the atrophy of fat and muscle. Tumor-derived PTHrP has emerged as a key molecule playing multiple roles in cachexia, from fat "browning" factor to potential therapeutic target.
[Mh] Termos MeSH primário: Tecido Adiposo Marrom/metabolismo
Caquexia/metabolismo
Neoplasias/metabolismo
[Mh] Termos MeSH secundário: Animais
Atrofia
Caquexia/patologia
Seres Humanos
Músculo Esquelético/patologia
Neoplasias/patologia
Termogênese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180125
[Lr] Data última revisão:
180125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1016/j.trecan.2016.07.005


  9 / 26073 MEDLINE  
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[PMID]:29187684
[Au] Autor:Watanabe M; Matsumoto Y; Okamoto K; Okuda B; Mizuta I; Mizuno T
[Ad] Endereço:Department of Neurology, Ehime Prefectural Central Hospital.
[Ti] Título:[A case of hereditary sensory and autonomic neuropathy type 1E with frontal lobe dysfunction as an initial symptom].
[So] Source:Rinsho Shinkeigaku;57(12):753-758, 2017 Dec 27.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:A 49-year-old man had developed gradually personality change, gait disturbance, and hearing loss for five years. On admission, he presented with frontal release signs, stuttering, vertical gaze palsy, sensorineural deafness, muscle rigidity, ataxia, and sensory disturbance with areflexia in the lower extremities. Brain MRI demonstrated atrophy in the cerebellum and midbrain tegmentum as well as cerebral atrophy, predominantly in the frontal lobe. He was tentatively diagnosed as progressive supranuclear palsy on the basis of clinical features and imagings. On nerve conduction study, no sensory nerve action potentials were elicited in the upper and lower extremities. Details of family history revealed a hereditary sensory neuropathy with autosomal dominant inheritance in his relatives. Because genetic analysis showed a rare missense mutation (c.1483T>C, p.Y495H) in DNA methyltransferase 1 gene, we diagnosed him as having hereditary sensory and autonomic neuropathy type 1E (HSAN1E). In addition, p.M232R mutation in prion protein gene was detected. It should be kept in mind that there are some patients with HSAN1E presenting with frontal lobe dysfunction as an initial symptom and with clinical features mimicking progressive supranuclear palsy.
[Mh] Termos MeSH primário: Neuropatias Hereditárias Sensoriais e Autônomas/diagnóstico
Neuropatias Hereditárias Sensoriais e Autônomas/genética
[Mh] Termos MeSH secundário: Atrofia
Encéfalo/patologia
DNA (Citosina-5-)-Metiltransferase 1/genética
Diagnóstico Diferencial
Lobo Frontal
Neuropatias Hereditárias Sensoriais e Autônomas/patologia
Neuropatias Hereditárias Sensoriais e Autônomas/fisiopatologia
Seres Humanos
Masculino
Meia-Idade
Mutação
Proteínas Priônicas/genética
Paralisia Supranuclear Progressiva
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Prion Proteins); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1); EC 2.1.1.37 (DNMT1 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-001043


  10 / 26073 MEDLINE  
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[PMID]:27776262
[Au] Autor:Sterling NW; Du G; Lewis MM; Swavely S; Kong L; Styner M; Huang X
[Ad] Endereço:Department of Neurology, Pennsylvania State University-Milton S. Hershey Medical Center, Hershey, PA, USA.
[Ti] Título:Cortical gray and subcortical white matter associations in Parkinson's disease.
[So] Source:Neurobiol Aging;49:100-108, 2017 Jan.
[Is] ISSN:1558-1497
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cortical atrophy has been documented in both Parkinson's disease (PD) and healthy aging, but its relationship to changes in subcortical white matter is unknown. This was investigated by obtaining T1- and diffusion-weighted images from 76 PD and 70 controls at baseline and 18 and 36 months, from which cortical volumes and underlying subcortical white matter axial diffusivity (AD), radial diffusivity (RD), and fractional anisotropy (FA) were determined. Twelve of 69 cortical subregions had significant group differences, and for these, underlying subcortical white matter was explored. At baseline, higher cortical volumes were significantly correlated with lower underlying subcortical white matter AD, RD, and higher FA (ps ≤ 0.017) in PD. Longitudinally, higher rates of cortical atrophy in PD were associated with increased rates of change in AD RD, and FA values (ps ≤ 0.0013) in 2 subregions explored. The significant gray-white matter associations were not found in controls. Thus, unlike healthy aging, cortical atrophy and subcortical white matter changes may not be independent events in PD.
[Mh] Termos MeSH primário: Córtex Cerebral/patologia
Substância Cinzenta/patologia
Doença de Parkinson/patologia
Substância Branca/patologia
[Mh] Termos MeSH secundário: Idoso
Anisotropia
Atrofia
Córtex Cerebral/diagnóstico por imagem
Imagem de Difusão por Ressonância Magnética
Imagem de Tensor de Difusão
Feminino
Substância Cinzenta/diagnóstico por imagem
Seres Humanos
Masculino
Meia-Idade
Bainha de Mielina
Neuroimagem
Doença de Parkinson/diagnóstico por imagem
Substância Branca/diagnóstico por imagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE



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