Subsequent research reported that the transfer of Aβ-specific Th17 cells into amyloid precursor protein/presenilin1 (APP/PS1) transgenic AD mice worsened clinical symptoms, including memory impairment, systemic inflammation, and amyloid deposition, while reducing anti-inflammatory regulatory T cell frequencies and diminishing the immunosuppressive response (Machhi et al. 2021). The gene discussed is APP; the disease is memory impairment.