ABSTRACT
Objective To assess the cognitive function, prevalence, and risk factors associated with cognitive decline and dementia in people above 65 years of age in Santa Cruz Island, Galápagos, Ecuador. Methods This is a cross-sectional observational study that was carried out in adults over 65 years of age in Santa Cruz Island, Galápagos, Ecuador. The mini-mental state examination (MMSE) and ascertain dementia eight-item informant questionnaire (AD8)-validated Ecuador Spanish versions were used to assess cognition. Results There were a total of 80 participants, 55 (67%) women and 25 (31.2%) men. The majority of participants were Mestizos (85.3%), with the remainder classified as White (4.8%), Afro-Ecuadorians (2.4%), or Indigenous (3.6%). The prevalence of cognitive impairment is 30.0%-43.7%. The MMSE results showed that older age and lack of education are risk factors for cognitive decline (p < 0.01). There was high correlation between MMSE and AD8 scores. The AD8 showed that older age, widowhood, and living in Santa Rosa were risk factors for cognitive decline (p < 0.01). According to the AD8, the group with the highest education (six years or more) had the lowest risk of cognitive decline and dementia (p < 0.01). Conclusions The main risk factors for cognitive decline and dementia in individuals above 65 years old in Santa Cruz Island, Galápagos, Ecuador are increased age, lack of education, and widowhood. The prevalence of cognitive impairment is similar to previous studies in Ecuador.
ABSTRACT
Parasitic enteric nematodes induce a type 2 immune response characterized by increased production of Th2 cytokines, IL-4 and IL-13, and recruitment of alternatively activated macrophages (M2) to the site of infection. Nematode infection is associated with changes in epithelial permeability and inhibition of sodium-linked glucose absorption, but the role of M2 in these effects is unknown. Clodronate-containing liposomes were administered prior to and during nematode infection to deplete macrophages and prevent the development of M2 in response to infection with Nippostrongylus brasiliensis. The inhibition of epithelial glucose absorption that is associated with nematode infection involved a macrophage-dependent reduction in SGLT1 activity, with no change in receptor expression, and a macrophage-independent down-regulation of GLUT2 expression. The reduced transport of glucose into the enterocyte is compensated partially by an up-regulation of the constitutive GLUT1 transporter consistent with stress-induced activation of HIF-1α. Thus, nematode infection results in a "lean" epithelial phenotype that features decreased SGLT1 activity, decreased expression of GLUT2 and an emergent dependence on GLUT1 for glucose uptake into the enterocyte. Macrophages do not play a role in enteric nematode infection-induced changes in epithelial barrier function. There is a greater contribution, however, of paracellular absorption of glucose to supply the energy demands of host resistance. These data provide further evidence of the ability of macrophages to alter glucose metabolism of neighboring cells.
