RESUMO
In post-mortem brain specimens from patients dying with a clinical diagnosis of Huntington's disease (HD) immunohistochemistry showed a substantial loss from the neostriatum of neurons containing the calcium-binding protein calbindin 28K. These calbindin neurons, and the straital compartment in which they are sited, are particularly damaged in HD, suggesting that a failure of calcium buffering or homeostasis may contribute to cell death in HD.
Assuntos
Química Encefálica , Proteínas de Ligação ao Cálcio/análise , Corpo Estriado/análise , Doença de Huntington/patologia , Neurônios/análise , Adulto , Idoso , Corpo Estriado/patologia , Feminino , Humanos , Imuno-Histoquímica , Masculino , Pessoa de Meia-Idade , Neurônios/patologia , Substância Negra/análise , Substância Negra/patologiaRESUMO
Substance P, neurokinin A, neuropeptide K, and neurokinin B were measured in both control (neurologically normal) and Huntington's disease brains obtained post mortem. All four peptides were significantly reduced in the substantia nigra of Huntington's disease patients compared with the control group. No differences were observed in frontal or temporal cortex except that neuropeptide K was significantly reduced in the frontal cortex of Huntington's disease cases. Correlation of the cell loss observed in the striatum and the tachykinin depletions detected in the substantia nigra in the Huntington's disease brains showed that the degree of cell loss agreed well with the extent of tachykinin depletion. Results of double-staining immunocytochemistry were consistent with the coexistence of substance P and neurokinin A in the substantia nigra of control brains and showed a marked depletion of immunoreactivity to both in Huntington's disease brains.
Assuntos
Encéfalo/metabolismo , Doença de Huntington/metabolismo , Neuropeptídeos/metabolismo , Animais , Encéfalo/patologia , Humanos , Doença de Huntington/patologia , Imuno-Histoquímica , Masculino , Neurocinina A , Neurocinina B , Radioimunoensaio , Ratos , Ratos Endogâmicos , Substância P/metabolismo , TaquicininasAssuntos
Corpo Estriado/patologia , Doença de Huntington/genética , Atrofia , Humanos , Masculino , Pessoa de Meia-Idade , RiscoRESUMO
Herpes-simplex virus type (HSV-1) nucleic-acid sequences were detected by in-situ hybridisation in thin sections of brains from mice which had been inoculated 24 weeks previously with HSV-1. These mice were not ill, and infectious virus could not be recovered from them. HSV-1 sequences were also present in brain smears from 3 of 4 elderly patients who had died with chronic psychiatric illness and neuropathological changes but not in smears from 2 patients who had had acute psychotic episodes and minimum abnormal histology. Adenovirus type 7 nucleic-acid sequences were not detected in these human specimens.
Assuntos
Encéfalo/microbiologia , DNA Viral/isolamento & purificação , Genes Virais , Simplexvirus/genética , Adenovírus Humanos/genética , Idoso , Animais , Autorradiografia , Encefalite por Arbovirus/microbiologia , Feminino , Imunofluorescência , Humanos , Marcação por Isótopo , Masculino , Camundongos , Microscopia Eletrônica , Pessoa de Meia-Idade , Hibridização de Ácido Nucleico , Simplexvirus/isolamento & purificação , TrítioAssuntos
Córtex Cerebral/enzimologia , Transtornos Neurocognitivos/enzimologia , Adulto , Idoso , Atrofia/enzimologia , Atrofia/patologia , Córtex Cerebral/patologia , DNA/metabolismo , Demência/enzimologia , Doenças Desmielinizantes/enzimologia , Doenças Desmielinizantes/patologia , Enzimas/metabolismo , Feminino , Humanos , Hipóxia Encefálica/enzimologia , Masculino , Pessoa de Meia-Idade , Degeneração Neural , Transtornos Neurocognitivos/patologia , Neurônios/enzimologia , Neurônios/ultraestrutura , Proteínas S100/metabolismoRESUMO
Choline acetyltransferase activity (presynaptic cholinergic system) and high affinity binding of cholinergic antagonists (postsynaptic cholinergic system) were measured in brain tissue removed after death from both mentally normal and demented old people. Muscarinic receptor binding sites in frontal cortex decreased with advancing years only in old people without appreciable morphological evidence of senile degeration. Preliminary data for temporal lobe suggested that also in Pick's disease the density of receptor binding sites is reduced. The markers are not significantly reduced in cases of mixed senile and vascular dementia. However, in non-vascular senile dementia of the Alzheimer type, there were indications that the presynaptic marker is selectively depleted. Therefore, centrally acting anticholinesterases might be beneficial, particularly in the early stages of the disease.
