Abstract: The old definition of the central nervous system as an “immune privilege” site is now considered obsolete, as it has been demonstrated that there is a complex interaction between immune cells and other brain cells, which creates an environment-controlled surveillance with different immune niches that are now beginning to be understood. Thus, brain aging is characterized by a series of immunological, vascular, and metabolic changes that erode defense mechanisms and neuronal homeostasis of the neural circuits. Among the most notable is inflammaging, defined as a basal state of low-grade chronic inflammation that progressively sets in and affects synaptic function, neuronal plasticity, and cell viability. This proinflammatory environment is accompanied by dysregulation of resident immune cells, especially in microglia and brain macrophages, which progressively transition from a homeostatic phenotype to a regulatory-immunosuppressive state (Segura-Collar et al., 2025). The progressive loss of integrity of the blood-brain barrier is a key event in this process, as it allows the entry and persistence of peripheral immune cells with the ability to adapt to the brain microenvironment, thereby accelerating the onset and chronicity of neurodegenerative and neoplastic diseases (Segura-Collar et al., 2022).