miR‑660‑5p ameliorates neuronal damage in Alzheimer's disease via targeting APP.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder of the central nervous system. To investigate miR‑660‑5p expression among patients with AD and explore the molecular mechanism underlying its regulation of AD‑related pathological progression. A total of 86 AD patients and 86 healthy controls were enrolled. Serum miR‑660‑5p was detected by real‑time quantitative PCR (RT-qPCR). Inflammatory factors were measured via enzyme‑linked immunosorbent assay (ELISA). SH‑SY5Y cells were treated with aggregated Aβ₁‑₄₂ preparation to establish an in‑vitro AD‑like injury model. Serum miR‑660‑5p was significantly downregulated in AD patients (P < 0.001), positively correlated with Mini‑Mental State Examination (MMSE, r = 0.684) and Montreal Cognitive Assessment (MoCA, r = 0.640) scores, and negatively correlated with serum interleukin‑6 (IL‑6, r = - 0.658) and tumor necrosis factor‑α (TNF‑α, r = - 0.614). Receiver‑operating characteristic (ROC) curve analysis for AD yielded an area under the curve (AUC) of 0.873. Mechanistically, miR‑660‑5p targets and inhibits APP expression to mitigate Aβ‑induced neuronal injury and neuroinflammation. miR-660-5p is downregulated in patients with AD. It mitigates aggregated Aβ₁-₄₂ preparation‑triggered neuronal damage and neuroinflammation in vitro by targeted inhibition of APP expression.