Astrogliosis
Mostrando 1-12 de 34 artigos, teses e dissertações.
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1. Memory impairments and increased GFAP expression in hippocampal astrocytes following hypercaloric diet in rats
RESUMO Objetivo: A inflamação hipotalâmica e a superexpressão da proteína glial fibrilar ácida (GFAP) em astrócitos são bem descritas em animais obesos, assim como déficits cognitivos e de memória. Como o hipocampo desempenha importante papel na consolidação de informações, esta investigação teve como objetivo observar a função da memória
Arq. Neuro-Psiquiatr.. Publicado em: 23/09/2019
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2. Efeito da inibição da enzima JAK2 sobre a morte neuronal, astrogliose e neurogênese no estriado de camundongos adultos após injeção unilateral de ácido quinolínico / Effect of JAK2 enzyme inhibition on neuronal death, astrogliosis and neurogenesis in the striatum of adult mice after unilateral injection of quinolinic acid
A injeção de ácido quinolínico (AQ), um agonista glutamatérgico do receptor N-metil-D-aspartato, no estriado de roedores induz morte seletiva de neurônios espinhosos médios, gliose reativa e neurogênese na zona subventricular, acompanhada da migração dos neurônios recém-gerados para o estriado lesado. Tais achados são também descritos na doenç
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 22/06/2011
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3. Influence of the MHC I expression modulation on reactive astrogliosis and synaptic plasticity / Influencia da modulação da expressão do MHC I sobre a astroglicose reativa e plasticidade sinaptica
O complexo de histocompatibilidade principal de classe I (MHC I) é uma molécula originalmente do Sistema Imunológico. A presença desses elementos no Sistema Nervoso Central (SNC) parece estar relacionada a diferentes funções, apresentando papel importante no refinamento sináptico durante o desenvolvimento do SNC e sendo fundamental no processo de elim
Publicado em: 2009
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4. Signal changes on MRI and increases in reactive microgliosis, astrogliosis, and iron in the putamen of two patients with multiple system atrophy.
A correlation of clinical, MRI, and neuropathological data is reported in two patients with multiple system atrophy (MSA). On MRI, patient 1 showed striatal atrophy, reduction of T2 relaxation times within most of the putamen, and a band of hyperintense signal changes in the lateral putamen. In patient 2, MRI disclosed only shortening of the T2 signal in the
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5. Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain
Neurofibromatosis type 1 (NF1) is a prevalent genetic disorder that affects growth properties of neural-crest-derived cell populations. In addition, approximately one-half of NF1 patients exhibit learning disabilities. To characterize NF1 function both in vitro and in vivo, we circumvent the embryonic lethality of NF1 null mouse embryos by generating a condi
Cold Spring Harbor Laboratory Press.
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6. Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease.
Interleukin 1, an immune response-generated cytokine that stimulates astrocyte proliferation and reactivity (astrogliosis), was present in up to 30 times as many glial cells in tissue sections of brain from patients with Down syndrome and Alzheimer disease compared with age-matched control subjects. Most interleukin 1-immunoreactive glia in Down syndrome and
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7. Glioblastoma expression of vitronectin and the alpha v beta 3 integrin. Adhesion mechanism for transformed glial cells.
Glioblastoma multiforme, the most malignant astroglial-derived tumor, grows as an adherent mass and locally invades normal brain. An examination of adult cerebral glioblastoma biopsy material for the expression of adhesive proteins that might potentiate adhesion and invasion demonstrated tumor cell-associated vitronectin (5/5). In contrast, vitronectin was n
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8. Progressive cerebral poliodystrophy – Alpers' disease: Disorganized giant neuronal mitochondria on electron microscopy
Three siblings who suffered from progressive mental retardation, seizures, and rigidity showed degeneration of the cerebral cortex. This was manifested by severe to complete neuronal loss with astrogliosis and microgliosis. In one child a brain biopsy was performed at the age of 3 months. The only lesion found was large disorganized perinuclear mitochondria
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9. A nontransgenic mouse model shows inducible amyloid-β (Aβ) peptide deposition and elucidates the role of apolipoprotein E in the amyloid cascade
The amyloid-β (Aβ) peptide, a major pathological hallmark of Alzheimer's disease (AD), undergoes a cascade of interactions resulting in the formation of soluble aggregates and their conversion in the brain to insoluble deposits and mature senile plaques. Furthermore, the apoE4 isoform of apolipoprotein E (apoE), which is the major genetic risk factor of AD
National Academy of Sciences.
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10. Inactivation of liver X receptor β leads to adult-onset motor neuron degeneration in male mice
Male mice with inactivated liver X receptor (LXR) β suffer from adult-onset motor neuron degeneration. By 7 months of age, motor coordination is impaired, and this condition is associated with lipid accumulation and loss of motor neurons in the spinal cord, together with axonal atrophy and astrogliosis. Several of these features are reminiscent of the neuro
National Academy of Sciences.
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11. Forebrain degeneration and ventricle enlargement caused by double knockout of Alzheimer's presenilin-1 and presenilin-2
Early-onset familial Alzheimer's disease is the most aggressive form of Alzheimer's, striking patients as early as their 30s; those patients typically carry mutations in presenilin-1 and presenilin-2. To investigate the coordinated functions of presenilin in the adult brain, we generated double knockout mice, in which both presenilins were deleted in the for
National Academy of Sciences.
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12. Scrapie-associated prion protein accumulates in astrocytes during scrapie infection.
In the course of scrapie, a transmissible spongiform encephalopathy caused by an unconventional agent, a normal cellular protein is converted to an abnormal form that copurifies with infectivity and aggregates to form deposits of amyloid. We have used immunocytochemistry and methods that enhance detection of amyloidogenic proteins to investigate the types of