GNG5, a member of the G-protein family, is involved in multiple biological processes. It plays a role in cell-cell communication as part of G-protein-coupled receptor (GPCR) signaling pathways, which are crucial for various physiological functions such as neurotransmission, immune response, and cell growth regulation [3,5].

In gliomas, GNG5 is overexpressed compared to normal samples and is associated with clinicopathologic characteristics. It is frequent in the Mesenchymal subtype and lowly expressed in the Proneural subtype of glioblastomas. Glioma patients with GNG5 overexpression have shorter survival time, and it is an independent prognostic indicator of overall survival. Functional experiments in vitro and in vivo show that GNG5 can participate in glioma cell proliferation and migration [1,3].

In Alzheimer's disease, GNG5 expression is upregulated in the hippocampal-entorhinal region of pathological cases compared with normal controls. It is positively correlated with Aβ pathology and significantly promotes Aβ pathology and Aβ42 production both in vivo and in vitro [2].

During cortical development in mice and human cerebral organoids, GNG5, highly expressed in progenitors and downregulated in neurons, is critical for controlling the number of apical and basal progenitors and neuronal migration [4].

In conclusion, GNG5 is a significant gene involved in cell-cell communication via GPCR-related pathways. Its dysregulation is associated with gliomas, Alzheimer's disease, and abnormal cortical development. Studies, including those using in vivo models like mice and cerebral organoids, have been crucial in uncovering these functions, highlighting its potential as a biomarker and therapeutic target in related diseases.