According to the oxidation-inflammation theory of aging, chronic oxidative stress and inflammatory stress situations (with
higher levels of oxidant and inflammatory compounds and lower antioxidant and anti-inflammatory defenses) are the basis of the agerelated
impairment of organism functions, including those of the nervous and immune systems, as well as of the neuroimmune communication,
which explains the altered homeostasis and the resulting increase of morbidity and mortality. Overproduction of oxidant compounds
can induce an inflammatory response, since oxidants are inflammation effectors. Thus, oxidation and inflammation are interlinked
processes and have many feedback loops. However, the nature of their potential interactions, mainly in the brain and immune
cells, and their key involvement in aging remain unclear. Moreover, in the context of the neuroimmune communication, it has been described
that an oxidative-inflammatory situation occurs in subjects with anxiety, and this situation contributes to an immunosenescence,
alteration of survival responses and shorter life span. As an example of this, a model of premature aging in mice, in which animals show
a poor response to stress and high levels of anxiety, an oxidative stress in their immune cells and tissues, as well as a premature immunosenescence
and a shorter life expectancy, will be commented in the present review. This model supports the hypothesis that anxiety can
be a situation of chronic oxidative stress and inflammation, especially in brain and immune cells, and this accelerates the rate of aging.
Oxidative stress, inflammation, oxi-inflamm-aging, inmunosenescence, anxiety, neuroendocrine immune axis, premature aging.
Department of Physiology (Animal Physiology II), Faculty of Biological Sciences, Madrid Complutense University, José Antonio Novais, 2, 28040 Madrid, Spain.