The preservation of cognitive longevity and arresting the pandemic of senile dementia engulfing the modern world is arguably the major challenge faced by biomedical research in the 21st century. Age is the leading risk factor for neurodegenerative diseases and vascular dementia, and yet there is a clear distinction between physiological and pathological brain aging; the former proceeds with cognitive abilities mainly preserved, whereas the latter is manifested with rapid cognitive decline. The cellular and molecular mechanisms of brain aging remain disputed, with numerous indications for metabolic and signaling alterations (Mattson and Arumugam, 2018). Chronic neuroinflammation in particular, is frequently considered as a universal attribute of aging (Di Benedetto et al., 2017), with brain aging being but a part of “inflammageing” (Franceschi et al., 2007) embracing the whole organism. This view, however, needs to be corroborated, particularly considering that the concept of neuroinflammation is not clearly defined. Reactive gliosis (astrogliosis or microgliosis, and possibly reactivity of oligodendrocyte precursor cells also known as NG-2 glia) is frequently regarded as the ultimate sign of neuroinflammation and aging is generally believed to be associated with progressive increase in glial reactivity. Experimental evidence for the predominance of reactive glia in the old brain is however controversial; instead, the age-dependent glial morphofunctional decline may present more accurate description of brain aging.