No abstract

No abstract

Resumo Os neurônios são células que, através de estímulos diversos, fazem comunicações com outros neurônios transmitindo, através da sinapse, a troca de informações. Essas informações são a essência do ser humano, distingue a personalidade, a maneira de agir e a maneira que o corpo toma através dos anos. Até os 20 anos de idade podemos ter aproximadamente 1,2 quilogramas de massa cerebral, após essa idade, há uma perda progressiva ao longo do envelhecimento. A plasticidade neural pode ser definida como novas maneiras e novas ligações que os neurônios passam a ter. Com o passar dos anos, já na terceira idade, a não estimulação do cérebro pode fazer com que as conexões se tornem fracas e se enfraqueçam, porém, alguns estudos apontam que o cérebro de um indivíduo de terceira idade, após algum trauma, retém a capacidade de plasticidade neural. O estímulo neural nessa idade, com atividades que motivam o cognitivo, é imprescindível, pois novas aprendizagens, novos desafios e momentos de lazer podem aumentar a plasticidade neural, dessa maneira, criando uma plasticidade compensatória.Trata-se de uma pesquisa de revisão bibliográfica, sobre os fatores que abordam a plasticidade neural em idosos, O tema engloba os fatores que influenciam no bem-estar dos idosos, que afetam diretamente na qualidade de vida, e podemos constatar que a plasticidade neural é possível nos indivíduos na terceira idade, como alguns dos estudos apresentados nos levam a crer.

Evaluating the histopathological and morphometric changes caused by Leishmania (Leishmania) infantum chagasi infection either in the presence or absence of B‐1 cells. Wild‐type Balb/c and XID mice were used. Half of XID mice received B‐1 cells adoptive transfer (XID + B1). Five animals from each group were infected (Balb/c I, XID I and XID + B1 I), totalizing six groups (n = 5). After 45 days of infection, the ileum was collected for histological processing and analysis. After infection, the XID animals showed an increase in the thickness of the intestinal layers, in the depth and width of the crypt and in the villi width. However, the Balb/c I group showed a reduction in almost all these parameters, whereas the villi width was increased. The villi height decreased in the infected XID animals; however, it was increased in the XID + B1 I group. Leishmania (L) infantum chagasiinfection caused a decrease in the number of Paneth cells; however, their area was increased. Finally, goblet cells and enterocytes presented different change profiles among groups. This study showed that the parasite infection causes structural and histopathological alterations in the intestine. These changes might be influenced by the absence of B‐1 cells.

Leishmania (Viannia) braziliensis is one of the main causes of cutaneous leishmaniasis in the Americas. This species presents genetic polymorphism that can cause destructive lesions in oral, nasal, and oropharyngeal tracts. In a previous study, the parasite caused several histopathological changes to hamster ileums. Our study evaluates immune response components, morphological changes, and effects on neurons in the ileums of hamsters infected by three different strains of L. (V.) braziliensis in two infection periods. For the experiment, we separated hamsters into four groups: a control group and three infected groups. Infected hamsters were euthanized 90- or 120-days post infection. We used three strains of L. (V.) braziliensis: the reference MHOM/BR/1975/M2903 and two strains isolated from patients who had different responses to Glucantime® treatment (MHOM/BR/2003/2314 and MHOM/BR/2000/1655). After laparotomy, ileums were collected for histological processing, biochemical analysis, and evaluation of neurons in the myenteric and submucosal plexuses of the enteric nervous system (ENS). The results demonstrated the increase of blood leukocytes after the infection. Optical microscopy analysis showed histopathological changes with inflammatory infiltrates, edemas, ganglionitis, and Leishmania amastigotes in the ileums of infected hamsters. We observed changes in the organ histoarchitecture of infected hamsters when compared to control groups, such as thicker muscular and submucosa layers, deeper and wider crypts, and taller and broader villi. The number of intraepithelial lymphocytes and TGF-β-immunoreactive cells increased in all infected groups when compared to the control groups. Mast cells increased with longer infection periods. The infection also caused remodeling of intestinal collagen and morphometry of myenteric and submucosal plexus neurons; but this effect was dependent on infection duration. Our results show that L. (V.) braziliensis infection caused time-dependent alterations in hamster ileums. This was demonstrated by the reduction of inflammatory cells and the increase of tissue regeneration factors at 120 days of infection. The infected groups demonstrated different profiles in organ histoarchitecture, migration of immune cells, and morphometry of ENS neurons. These findings suggest that the small intestine (or at least the ileum) is a target organ for L. (V.) braziliensis infection, as the infection caused changes that were dependent on duration and strain.