Base de dados : MEDLINE
Pesquisa : H01.158.610.184 [Categoria DeCS]
Referências encontradas : 60 [refinar]
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[PMID]:28594894
[Au] Autor:Xu Z; Asahchop EL; Branton WG; Gelman BB; Power C; Hobman TC
[Ad] Endereço:Department of Cell Biology, University of Alberta, Edmonton, Alberta, Canada.
[Ti] Título:MicroRNAs upregulated during HIV infection target peroxisome biogenesis factors: Implications for virus biology, disease mechanisms and neuropathology.
[So] Source:PLoS Pathog;13(6):e1006360, 2017 Jun.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:HIV-associated neurocognitive disorders (HAND) represent a spectrum neurological syndrome that affects up to 25% of patients with HIV/AIDS. Multiple pathogenic mechanisms contribute to the development of HAND symptoms including chronic neuroinflammation and neurodegeneration. Among the factors linked to development of HAND is altered expression of host cell microRNAs (miRNAs) in brain. Here, we examined brain miRNA profiles among HIV/AIDS patients with and without HAND. Our analyses revealed differential expression of 17 miRNAs in brain tissue from HAND patients. A subset of the upregulated miRNAs (miR-500a-5p, miR-34c-3p, miR-93-3p and miR-381-3p), are predicted to target peroxisome biogenesis factors (PEX2, PEX7, PEX11B and PEX13). Expression of these miRNAs in transfected cells significantly decreased levels of peroxisomal proteins and concomitantly decreased peroxisome numbers or affected their morphology. The levels of miR-500a-5p, miR-34c-3p, miR-93-3p and miR-381-3p were not only elevated in the brains of HAND patients, but were also upregulated during HIV infection of primary macrophages. Moreover, concomitant loss of peroxisomal proteins was observed in HIV-infected macrophages as well as in brain tissue from HIV-infected patients. HIV-induced loss of peroxisomes was abrogated by blocking the functions of the upregulated miRNAs. Overall, these findings point to previously unrecognized miRNA expression patterns in the brains of HIV patients. Targeting peroxisomes by up-regulating miRNAs that repress peroxisome biogenesis factors may represent a novel mechanism by which HIV-1 subverts innate immune responses and/or causes neurocognitive dysfunction.
[Mh] Termos MeSH primário: Infecções por HIV/genética
HIV-1/fisiologia
MicroRNAs/metabolismo
Transtornos Neurocognitivos/virologia
Peroxissomos/metabolismo
[Mh] Termos MeSH secundário: Encéfalo/metabolismo
Encéfalo/virologia
Infecções por HIV/metabolismo
Infecções por HIV/patologia
Infecções por HIV/virologia
HIV-1/genética
Seres Humanos
MicroRNAs/genética
Transtornos Neurocognitivos/genética
Transtornos Neurocognitivos/metabolismo
Transtornos Neurocognitivos/patologia
Neuropatologia
Peroxissomos/genética
Peroxissomos/virologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006360


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[PMID]:28395088
[Au] Autor:Laquerriere A; Maillard C; Cavallin M; Chapon F; Marguet F; Molin A; Sigaudy S; Blouet M; Benoist G; Fernandez C; Poirier K; Chelly J; Thomas S; Bahi-Buisson N
[Ad] Endereço:Department of Pathology, Normandy Centre for Genomic and Personalized Medicine, Normandie University, Rouen University Hospital, NeoVasc Team, UNIROUEN, Inserm U1245, Rouen, France.
[Ti] Título:Neuropathological Hallmarks of Brain Malformations in Extreme Phenotypes Related to DYNC1H1 Mutations.
[So] Source:J Neuropathol Exp Neurol;76(3):195-205, 2017 03 01.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dyneins play a critical role in a wide variety of cellular functions such as the movement of organelles and numerous aspects of mitosis, making it central player in neocortical neurogenesis and migration. Recently, cytoplasmic dynein-1, heavy chain-1 (DYNC1H1) mutations have been found to cause a wide spectrum of brain cortical malformations. We report on the detailed neuropathological features of brain lesions from 2 fetuses aged 36 and 22 weeks of gestation (WG), respectively, carrying de novo DYNC1H1 mutations, p.Arg2720Lys and p.Val3951Ala and presenting the most severe phenotype reported to date. Analysis using the Dictyostelium discoideum dynein motor crystal structure showed that the mutations are both predicted to have deleterious consequences on the function of the motor domain. Both fetuses showed a similar macroscopic and histological brain malformative complex associating bilateral fronto-parietal polymicrogyria (PMG), dysgenesis of the corpus callosum and of the cortico-spinal tracts, along with brainstem and cerebellar abnormalities. Both exhibited extremely severe disrupted cortical lamination. Immunohistochemical studies provided the evidence for defects in cell proliferation and postmitotic neuroblast ability to exit from the subventricular zone resulting in a failure of radial migration toward the cortical plate, thus providing new insights for the understanding of the pathophysiology in these cortical malformations.
[Mh] Termos MeSH primário: Encéfalo/anormalidades
Encéfalo/patologia
Dineínas do Citoplasma/genética
Mutação/genética
Fenótipo
[Mh] Termos MeSH secundário: Adulto
Técnicas de Cultura de Células
Feminino
Feto
Seres Humanos
Neuropatologia
Gravidez
Estrutura Secundária de Proteína
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DYNC1H1 protein, human); EC 3.6.4.2 (Cytoplasmic Dyneins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlw124


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[PMID]:28395084
[Au] Autor:Bruner JM; Louis DN; McLendon R; Rosenblum MK; Archambault WT; Most S; Tihan T
[Ad] Endereço:MD Anderson Cancer Center, Houston, Texas, USA.
[Ti] Título:The Utility of Expert Diagnosis in Surgical Neuropathology: Analysis of Consultations Reviewed at 5 National Comprehensive Cancer Network Institutions.
[So] Source:J Neuropathol Exp Neurol;76(3):189-194, 2017 03 01.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to characterize the type and degree of discrepancies between non-expert and expert diagnoses of CNS tumors to identify the value of consultations in surgical neuropathology. Neuropathology experts from 5 National Comprehensive Cancer Network (NCCN) member institutions participated in the review of 1281 consultations selected based on inclusion criteria. The consultation cases were re-reviewed at the NCCN headquarters to determine concordance with the original diagnoses. Among all consultations, 249 (19.4%) were submitted for expert diagnoses without final diagnoses from the submitting institution. Within the remaining 1032 patients, the serious/major discrepancy rate was 4.8%, and less serious and minor discrepancies were seen in 19.4% of the cases. The discrepancy rate was higher among patients who were referred to NCCN institutions for consultation compared to those who were referred for treatment only. The discrepancy rates, patient demographics, type of consultations and submitting institutions varied among participating NCCN institutions. Expert consultations identified a subset of cases with significant diagnostic discrepancies, and constituted the initial diagnoses in some cases. These data indicate that expert consultations in glial tumors and all types of pediatric CNS tumors can improve accurate diagnosis and enable appropriate management.
[Mh] Termos MeSH primário: Institutos de Câncer/normas
Neoplasias do Sistema Nervoso Central/patologia
Neuropatologia/normas
Patologistas/normas
Patologistas/utilização
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlw122


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[PMID]:28304301
[Au] Autor:Alosco ML; Duskin J; Besser LM; Martin B; Chaisson CE; Gunstad J; Kowall NW; McKee AC; Stern RA; Tripodis Y
[Ad] Endereço:Boston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, MA, USA.
[Ti] Título:Modeling the Relationships Among Late-Life Body Mass Index, Cerebrovascular Disease, and Alzheimer's Disease Neuropathology in an Autopsy Sample of 1,421 Subjects from the National Alzheimer's Coordinating Center Data Set.
[So] Source:J Alzheimers Dis;57(3):953-968, 2017.
[Is] ISSN:1875-8908
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The relationship between late-life body mass index (BMI) and Alzheimer's disease (AD) is poorly understood due to the lack of research in samples with autopsy-confirmed AD neuropathology (ADNP). The role of cerebrovascular disease (CVD) in the interplay between late-life BMI and ADNP is unclear. We conducted a retrospective longitudinal investigation and used joint modeling of linear mixed effects to investigate causal relationships among repeated antemortem BMI measurements, CVD (quantified neuropathologically), and ADNP in an autopsy sample of subjects across the AD clinical continuum. The sample included 1,421 subjects from the National Alzheimer's Coordinating Center's Uniform Data Set and Neuropathology Data Set with diagnoses of normal cognition (NC; n = 234), mild cognitive impairment (MCI; n = 201), or AD dementia (n = 986). ADNP was defined as moderate to frequent neuritic plaques and Braak stageIII-VI. Ischemic Injury Scale (IIS) operationalized CVD. Joint modeling examined relationships among BMI, IIS, and ADNP in the overall sample and stratified by initial visit Clinical Dementia Rating score. Subject-specific random intercept for BMI was the predictor for ADNP due to minimal BMI change (p = 0.3028). Analyses controlling for demographic variables and APOE É›4 showed lower late-life BMI predicted increased odds of ADNP in the overall sample (p < 0.001), and in subjects with CDR of 0 (p = 0.0021) and 0.5 (p = 0.0012), but not ≥1.0 (p = 0.2012). Although higher IIS predicted greater odds of ADNP (p < 0.0001), BMI did not predict IIS (p = 0.2814). The current findings confirm lower late-life BMI confers increased odds for ADNP. Lower late-life BMI may be a preclinical indicator of underlying ADNP.
[Mh] Termos MeSH primário: Doença de Alzheimer/patologia
Índice de Massa Corporal
Transtornos Cerebrovasculares/patologia
Neuropatologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Autopsia
Conjuntos de Dados como Assunto
Feminino
Seres Humanos
Masculino
National Institute on Aging (U.S.)/estatística & dados numéricos
Testes Neuropsicológicos
Estudos Retrospectivos
Estados Unidos/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE
[do] DOI:10.3233/JAD-161205


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[PMID]:28234572
[Au] Autor:Neill SG; Saxe DF; Rossi MR; Schniederjan MJ; Brat DJ
[Ti] Título:Genomic Analysis in the Practice of Surgical Neuropathology: The Emory Experience.
[So] Source:Arch Pathol Lab Med;141(3):355-365, 2017 Mar.
[Is] ISSN:1543-2165
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The evaluation of central nervous system tumors increasingly relies on molecular genetic methods to aid in classification, offer prognostic information, and predict response to therapy. Available assays make it possible to assess genetic losses, amplifications, translocations, mutations, or the expression levels of specific gene transcripts or proteins. Current molecular diagnostics frequently use a panel-based approach and whole genome analysis, and generally rely either on DNA sequencing or on hybridization-based methodologies, such as those used in cytogenomic microarrays. In some cases, immunohistochemistry can be used as a surrogate for genetic analysis when the mutation of interest consistently results in overexpression or underexpression of a known protein product. In surgical neuropathology practice, the diagnostic workup of diffuse gliomas, medulloblastomas, low-grade circumscribed gliomas, as well as other diseases, now routinely incorporates the results of genomic studies. Here we summarize our institution's current approach to diagnostic surgical neuropathology, using these contemporary molecular diagnostic applications.
[Mh] Termos MeSH primário: Neoplasias do Sistema Nervoso Central/genética
Perfilação da Expressão Gênica/métodos
Neuropatologia/métodos
Patologia Cirúrgica/métodos
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/genética
Seres Humanos
Neurocirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers, Tumor)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170309
[Lr] Data última revisão:
170309
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE
[do] DOI:10.5858/arpa.2016-0276-SAI


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[PMID]:28162776
[Au] Autor:Costa E Silva JA; Steffen RE
[Ad] Endereço:PUC-RJ Medical School; Brazilian Brain Institute.
[Ti] Título:The future of psychiatry: brain devices.
[So] Source:Metabolism;69S:S8-S12, 2017 Apr.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent advances in deep brain stimulators and brain-machine interfaces have greatly expanded the possibilities of neuroprosthetics and neuromodulation. Together with advances in neuroengineering, nanotechnology, molecular biology and material sciences, it is now possible to address fundamental questions in neuroscience in new, more powerful ways. It is now possible to apply these new technologies in ways that range from augmenting and restoring function to neuromodulation modalities that treat neuropsychiatric disorders. Recent developments in neuromodulation methods offer significant advantages and potential clinical benefits for a variety of disorders. Here we describe the current state of the art in neuromodulation methods, and some advances in brain-machine interfaces, describing the advantages and limitations of the clinical applications of each method. The future applications of these new methods and how they will shape the future of psychiatry and medicine, along with safety and ethical implications, are also discussed.
[Mh] Termos MeSH primário: Neuropatologia/métodos
Neuropsiquiatria/métodos
Neurociências/métodos
Psiquiatria/métodos
Transtornos Psicóticos/terapia
Terapias em Estudo/instrumentação
[Mh] Termos MeSH secundário: Estimulação Acústica/efeitos adversos
Estimulação Acústica/métodos
Estimulação Acústica/tendências
Animais
Engenharia Biomédica/métodos
Engenharia Biomédica/tendências
Interfaces Cérebro-Computador/efeitos adversos
Interfaces Cérebro-Computador/tendências
Estimulação Encefálica Profunda/efeitos adversos
Estimulação Encefálica Profunda/instrumentação
Estimulação Encefálica Profunda/tendências
Seres Humanos
Neuropatologia/tendências
Neuropsiquiatria/tendências
Neurociências/tendências
Psiquiatria/tendências
Transtornos Psicóticos/patologia
Transtornos Psicóticos/fisiopatologia
Terapias em Estudo/efeitos adversos
Terapias em Estudo/tendências
Estimulação Magnética Transcraniana/efeitos adversos
Estimulação Magnética Transcraniana/tendências
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE


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[PMID]:28159330
[Au] Autor:Nicolaidis S
[Ad] Endereço:Retired from Collège de France and CNRS, 84 Boulevard du Maréchal Joffre, 92340 Bourg-la-Reine, France. Electronic address: Snicolaidis33@gmail.com.
[Ti] Título:Neurosurgery of the future: Deep brain stimulations and manipulations.
[So] Source:Metabolism;69S:S16-S20, 2017 Apr.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Important advances are afoot in the field of neurosurgery-particularly in the realms of deep brain stimulation (DBS), deep brain manipulation (DBM), and the newly introduced refinement "closed-loop" deep brain stimulation (CLDBS). Use of closed-loop technology will make both DBS and DBM more precise as procedures and will broaden their indications. CLDBS utilizes as feedback a variety of sources of electrophysiological and neurochemical afferent information about the function of the brain structures to be treated or studied. The efferent actions will be either electric, i.e. the classic excitatory or inhibitory ones, or micro-injection of such things as neural proteins and transmitters, neural grafts, implants of pluripotent stem cells or mesenchymal stem cells, and some variants of gene therapy. The pathologies to be treated, beside Parkinson's disease and movement disorders, include repair of neural tissues, neurodegenerative pathologies, psychiatric and behavioral dysfunctions, i.e. schizophrenia in its various guises, bipolar disorders, obesity, anorexia, drug addiction, and alcoholism. The possibility of using these new modalities to treat a number of cognitive dysfunctions is also under consideration. Because the DBS-CLDBS technology brings about a cross-fertilization between scientific investigation and surgical practice, it will also contribute to an enhanced understanding of brain function.
[Mh] Termos MeSH primário: Estimulação Encefálica Profunda
Transtornos Mentais/terapia
Doenças do Sistema Nervoso/terapia
Neuropatologia/métodos
Neurocirurgia/métodos
Terapias em Estudo
[Mh] Termos MeSH secundário: Animais
Pesquisa Biomédica/métodos
Pesquisa Biomédica/tendências
Conectoma
Estimulação Encefálica Profunda/efeitos adversos
Estimulação Encefálica Profunda/instrumentação
Estimulação Encefálica Profunda/tendências
Seres Humanos
Comunicação Interdisciplinar
Transtornos Mentais/patologia
Transtornos Mentais/fisiopatologia
Transtornos Mentais/cirurgia
Sistema Nervoso/patologia
Sistema Nervoso/fisiopatologia
Doenças do Sistema Nervoso/patologia
Doenças do Sistema Nervoso/fisiopatologia
Doenças do Sistema Nervoso/cirurgia
Neuropatologia/tendências
Neurocirurgia/instrumentação
Neurocirurgia/tendências
Esquizofrenia/patologia
Esquizofrenia/fisiopatologia
Esquizofrenia/cirurgia
Esquizofrenia/terapia
Terapias em Estudo/efeitos adversos
Terapias em Estudo/instrumentação
Terapias em Estudo/tendências
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170205
[St] Status:MEDLINE


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[PMID]:28139215
[Au] Autor:Wurtman RJ
[Ad] Endereço:Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Electronic address: dick@mit.edu.
[Ti] Título:Connectomics and other novel methods for examining neural systems.
[So] Source:Metabolism;69S:S13-S15, 2017 Apr.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Novel approaches for studying the brain and relating its activities to mental phenomena have come into use during the past decade (Bargmann, 2015). These include both new laboratory methods - involving, among others, generation of isolated cells which retain neuronal characteristics in vivo; the selective stimulation of neurons by light in vivo; and direct electrical stimulation of specific brain regions to restore a system's balance of excitation and inhibition - and a new organizing principle, "connectomics", which recognizes that networks, and not simply a key nucleus or region, underlie most brain functions and malfunctions. Its application has already improved our comprehension of how the brain normally functions and our ability to help patients with such poorly treated neurologic and psychiatric diseases as Alzheimer's disease.
[Mh] Termos MeSH primário: Pesquisa Biomédica/métodos
Conectoma
Doenças do Sistema Nervoso/fisiopatologia
Fenômenos Fisiológicos do Sistema Nervoso
Neuropatologia/métodos
Neurociências/métodos
[Mh] Termos MeSH secundário: Doença de Alzheimer/patologia
Doença de Alzheimer/fisiopatologia
Doença de Alzheimer/terapia
Animais
Pesquisa Biomédica/tendências
Conectoma/tendências
Seres Humanos
Rede Nervosa/citologia
Rede Nervosa/patologia
Rede Nervosa/fisiologia
Rede Nervosa/fisiopatologia
Doenças do Sistema Nervoso/patologia
Doenças do Sistema Nervoso/terapia
Vias Neurais/patologia
Vias Neurais/fisiologia
Vias Neurais/fisiopatologia
Neurônios/citologia
Neurônios/patologia
Neurônios/fisiologia
Neuropatologia/tendências
Neurociências/tendências
Sinapses/patologia
Sinapses/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170201
[St] Status:MEDLINE


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[PMID]:28082297
[Au] Autor:Boyle PA; Yang J; Yu L; Leurgans SE; Capuano AW; Schneider JA; Wilson RS; Bennett DA
[Ad] Endereço:Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA.
[Ti] Título:Varied effects of age-related neuropathologies on the trajectory of late life cognitive decline.
[So] Source:Brain;140(3):804-812, 2017 Mar 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The objective of this study was to examine whether the effects of age-related neuropathologies on cognition change over time. Participants were 1096 deceased persons from two clinical-pathologic studies. All were without dementia at baseline, completed a detailed battery of cognitive tests annually over up to 21 years, died, and underwent detailed neuropathologic examinations to identify Alzheimer's disease pathology, vascular pathologies (i.e. macro- and microscopic infarcts, atherosclerosis, arteriolar sclerosis, and cerebral amyloid angiopathy), Lewy bodies, transactive response DNA-binding protein 43 (TDP-43) pathology, and hippocampal sclerosis. A time-varying effects model was used to flexibly characterize the trajectory of global cognition and assess whether the effects of demographics and each neuropathologic index on cognition changed over time. Results indicated that the mean trajectory of global cognition was characterized by gradual cognitive decline beginning ∼15 years before death and accelerated decline in the last few years. With the exception of microinfarcts and arteriolar sclerosis, all neuropathologies were associated with the cognitive trajectory. However, the nature of their associations varied. Alzheimer's disease pathology, macroscopic infarcts, Lewy bodies, TDP-43 pathology, and hippocampal sclerosis were associated with progressive cognitive decline, with their deleterious effects increasing over time. By contrast, atherosclerosis and cerebral amyloid angiopathy pathology were associated with a lower level of cognition but their effects were relatively stable over time. These results suggest that age-related neuropathologies are differentially related to late life cognitive trajectories. Whereas some contribute to progressive cognitive deterioration, others lower the level of cognition but exert relatively stable effects over time.
[Mh] Termos MeSH primário: Envelhecimento/patologia
Encéfalo/patologia
Transtornos Cognitivos/patologia
Neuropatologia/métodos
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
Estudos Longitudinais
Masculino
Testes Neuropsicológicos
Estatística como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170930
[Lr] Data última revisão:
170930
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.1093/brain/aww341


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[PMID]:27084356
[Au] Autor:Simic G; Babic Leko M; Wray S; Harrington CR; Delalle I; Jovanov-Milosevic N; Bazadona D; Buée L; de Silva R; Di Giovanni G; Wischik CM; Hof PR
[Ad] Endereço:Department of Neuroscience, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Zagreb, Croatia. Electronic address: gsimic@hiim.hr.
[Ti] Título:Monoaminergic neuropathology in Alzheimer's disease.
[So] Source:Prog Neurobiol;151:101-138, 2017 Apr.
[Is] ISSN:1873-5118
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:None of the proposed mechanisms of Alzheimer's disease (AD) fully explains the distribution patterns of the neuropathological changes at the cellular and regional levels, and their clinical correlates. One aspect of this problem lies in the complex genetic, epigenetic, and environmental landscape of AD: early-onset AD is often familial with autosomal dominant inheritance, while the vast majority of AD cases are late-onset, with the ε4 variant of the gene encoding apolipoprotein E (APOE) known to confer a 5-20 fold increased risk with partial penetrance. Mechanisms by which genetic variants and environmental factors influence the development of AD pathological changes, especially neurofibrillary degeneration, are not yet known. Here we review current knowledge of the involvement of the monoaminergic systems in AD. The changes in the serotonergic, noradrenergic, dopaminergic, histaminergic, and melatonergic systems in AD are briefly described. We also summarize the possibilities for monoamine-based treatment in AD. Besides neuropathologic AD criteria that include the noradrenergic locus coeruleus (LC), special emphasis is given to the serotonergic dorsal raphe nucleus (DRN). Both of these brainstem nuclei are among the first to be affected by tau protein abnormalities in the course of sporadic AD, causing behavioral and cognitive symptoms of variable severity. The possibility that most of the tangle-bearing neurons of the LC and DRN may release amyloid ß as well as soluble monomeric or oligomeric tau protein trans-synaptically by their diffuse projections to the cerebral cortex emphasizes their selective vulnerability and warrants further investigations of the monoaminergic systems in AD.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Doença de Alzheimer/patologia
Monoaminas Biogênicas/metabolismo
Neuropatologia
[Mh] Termos MeSH secundário: Doença de Alzheimer/diagnóstico
Doença de Alzheimer/genética
Animais
Seres Humanos
Fosforilação
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biogenic Monoamines); 0 (tau Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160417
[St] Status:MEDLINE



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