“…These changes include accumulation of mutations, telomere attrition, and epigenetic alterations, resulting in genomic instability and thus priming for neuronal damage and loss, reduced neurotransmitter levels, enhanced neuroinflammation, increased susceptibility to cerebral ROS, and decreased cerebral vascular compliance. All of these adverse processes are associated with increased risk of age-related neurological diseases, such as stroke, epilepsy, Parkinson’s disease, and dementia/cognitive decline [ 58 ]. Immunosenescence and inflammaging, as the most recognized effects of aging [ 59 ], might promote neuroinflammatory processes along with cerebral oxidative stress, via altered microglia activation (immune cells of the brain), which are central to neurotoxicity through the release of neurotoxic cytokines, such as TNFα, IL-1β, and INF-γ, as well as different ROS such as ONOO − and O 2 •− [ 60 , 61 ].…”