Throughout the course of evolution, the human genome has integrated genetic material from ancient retroviral infections, which now constitute approximately 8% of its total DNA. Significant portion of these endogenous retroviruses (ERVs) are non-functional due to mutations and deletions. However, some of the more recently acquired families, such as HERV-K (HML-2), retain intact genes that are capable of producing viral proteins. ERVs play roles in various physiological processes that are beneficial or crucial for the host, including the development of the placenta, protection of neurons, and differentiation of cells in the early stages of embryonic development. Various studies have mentioned that ERVs, which are suppressed by epigenetic methods during the aging process, can become activated and potentially accelerate aging and neuroinflammation. To test the hypothesis that ERVs become activated in the brain with aging, potentially triggering brain aging and neuroinflammation, the forantal cortex samples of 7 young, 7 middle-aged, and 5 old rats were collected. SETDB1 expression, which suppresses ERVs, and inflammation-related IL-6 and GFAP mRNA expressions were examined in real-time PCR. GAPDH was used as a reference gene. While no expected significant results were found for Synctin-B, GFAP and SETDB1, it was found that the expression of IL-6 in old rats compared to young rats showed a statistically significant increase with p = 0.039. We also aim to strengthen our hyopthesis with additional validations by analyzing the expression of LINE-1, IAP, Syncytin-A and Nf-KB.