Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, with epidemiological importance due to the high prevalence of people affected worldwide. Over time, various hypotheses have been raised in the pathophysiology and etiology of the disease and now the study of this disorder, is tackled from a multi-causal perspective, taking into account different etiological factors, among which are: genetics, oxidative stress, intracellular calcium dynamics, vascular effects, inflammation and stress, among others. The following literature review, aims to show studies that correlate stress as a risk factor in AD, recognizing the pathophysiological findings of AD, due to augmentation on glucocorticoids by chronic stress and the subsequent alteration of the hypothalamic-pituitary-adrenal axis. Critical view of these findings according to the literature.
Glucocorticoids
Neurobiología del Estrés Agudo y Crónico: Su Efecto en el Eje Hipotálamo-Hipófisis-Adrenal y la Memoria.
The presently available data about stress and its effects is too broad. That’s why this paper will focus on the effect of stress hormones in some brain areas, like limbic structures and the hypothalamo-pituitary-adrenal axis. In this way we will discuss how repetitive stress can change those areas, mainly by the effect on its two types of nuclear receptors, changing the basal activity of the amygdala, hippocampus and the medial prefrontal cortex, resulting in an increased hypothalamo-pituitaryadrenal axis function and impairing cognitive functions like memory. However, the exact mechanism by which these effects are produced is poorly understood. That is why one of the challenges for future research is to link the cellular changes with its behavioral effects in order to understand how it works in a living organism.
