Research Paper Volume 12, Issue 8 pp 7262—7281

Autophagy prevents hippocampal α-synuclein oligomerization and early cognitive dysfunction after anesthesia/surgery in aged rats

Figure 5. Anesthesia and surgery inhibited autophagy, increased α-synuclein oligomer levels, ultimately altering neurotransmitter levels and promoting POCD. (1) (2) Long-term propofol anesthesia (≥ 4 h) or surgery can inhibit autophagy and promote α-synuclein oligomer accumulation in the hippocampus; (3) Hippocampal autophagy inhibition further promotes α-synuclein oligomer accumulation; (4) Hippocampal α-synuclein oligomer accumulation further aggravates the inhibition of autophagy [57, 58]. (5) Hippocampal autophagy inhibition and α-synuclein oligomer accumulation alter neurotransmitter levels, ultimately promoting POCD (7); (6) Neurotransmitter imbalances may further exacerbate α-synuclein oligomer aggregation [46]. (8) Neurobehavior, autophagy-related protein levels and α-synuclein oligomer levels returned to the control levels 18 weeks post-surgery or post-anesthesia. ① Norepinephrine; ② Dopamine; ③ 5-hydroxytryptamine.