FIGURE 1.

Impact of SNCs and Neuroinflammation on Neuronal degeneration and Alzheimer´s disease. Healthy and young cells, including microglia (Alzheimer’s Disease International, 2020) and astrocytes, release pro- and anti-inflammatory mediators, growth factors (Prince et al., 2015) and bioenergetic pathway mediators (Dubois et al., 2016), which contribute to the maintenance of brain homeostasis, neuronal survival and cognitive functions (Onyango et al., 2016). In conjunction with the integrity of the blood-brain barrier (World-Health-Organization, 2021), characterized by a specific receptor ratio that ensures selectivity to molecules and cells. However, senescent microglia (Alzheimer’s Disease International, 2020) and senescent astrocytes (Dubois et al., 2016) maintain a chronically higher than basal level of activation, cell cycle arrest, remain hyper activated to different stimuli with low resolution of the inflammatory response (Prince et al., 2015). These senescent cells acquire a senescence-associated secretory phenotype (SASP), characterized by the constant release of pro-inflammatory mediators, which directly affect the activation of neurodegenerative cascades, cognitive impairment and death. In addition, the senescence of elements of the blood-brain barrier (World-Health-Organization, 2021), and the decrease or alteration in the proportion of specific receptors that ensure selectivity to molecules and cells, contribute to perpetuate brain deterioration and the development of AD (Onyango et al., 2016).