Astrocyte and microglial aging

Astrocytes have long been regarded as space filler cells, or at best providing trophic support for neurons. Recent evidence has shown that even in eugeric aging there is activation of both astrocytes and microglia, including decreases in the total length of processes emanating from the cell body. This is duplicated in several chronic inflammatory conditions including in HIV-associated neurocognitive disorders. The loss of the total length of characteristic processes emanating from the cell soma will be directly linked to synaptic dysfunction, and increased proinflammatory cytokines. Further, there is increasing evidence that long-term exposure to these cytokines (including tumor necrosis factor and interleukins) during chronic neuroinflammatory conditions or eugeric aging induces astrocytes and microglia to enter a senescent state as evidenced by increased expression of senescence markers and decreased release of ATP. Thus, senescence is likely to be a result of mitochondrial dysfunction providing a potential target for therapeutics.