Bri3, also known as ITM2C, is a gene encoding a type II transmembrane glycoprotein relevant in neuronal systems [5]. It has multiple functions and is involved in several biological pathways. Bri3 plays a role in the regulation of cell death, amyloid-related processes, and neuronal differentiation [1,2,3,4]. It may also be associated with lipid metabolism based on its presence in genes related to adipose, brain, and liver biology [6].

In L929 cells, disruption of Bri3 expression by expressing antisense RNA promoted over 1000-fold resistance to TNF-induced cell death, indicating its important role in this process [1]. In the context of amyloid-related diseases like Alzheimer's disease (AD), Bri3 interacts with amyloid precursor protein (APP) and serves as an endogenous negative regulator of Abeta production. Reducing endogenous Bri3 levels by RNA interference increased Abeta secretion [4]. In PC12 cells, Bri3 associates with the microtubule-destabilizing protein SCG10, stabilizes the microtubule network, and attenuates NGF-induced neurite outgrowth [3].

In conclusion, Bri3 is crucial in processes such as TNF-induced cell death, amyloid-related regulation, and neuronal differentiation. Its study, especially through loss-of-function experiments like those with Bri3 antisense RNA, has provided insights into its role in these biological processes. In the field of AD research, understanding Bri3's function could potentially offer new approaches to therapy and prevention [1,3,4].