The mechanism of miR-665 targeting GNB3 in aluminum-induced neuronal apoptosis.

Background: Aluminum exerts neurotoxic effects through various mechanisms, mainly manifested as impaired learning and memory function.

Methods: Forty SD rats were divided into 0, 10, 20, and 40 mM maltol aluminum [Al(mal)] groups. Cell experiments are divided into 0, 100, 200, and 400 μM Al(mal) dose group and control, Al(mal), Al(mal)+inhibitor NC, Al(mal)+miR-665 inhibitor intervention group.

Increased mA modification of BDNF mRNA via FTO promotes neuronal apoptosis following aluminum-induced oxidative stress.

N6-methyladenosine (mA) RNA modification is a new epigenetic molecular mechanism involved in various biological or pathological processes. Exposure to aluminum (Al) has been considered to promote neuronal apoptosis resulting in cognitive dysfunction, yet whether mA modification participates in the underlying mechanism remains largely unknown. Here, rats exposed to aluminum-maltolate [Al(mal)] for 90 days showed impaired learning and memory function and elevated apoptosis, which were related to the increased mA level and decreased fat mass and obesity-associated protein (FTO, an mA demethylase) in the hippocampus.