A misbalance in Ca²⁺ homeostasis seems to be related to the development of Alzheimer’s disease (AD). Indeed, neuronal Ca²⁺ balance may affect the levels of proteins associated with AD, such as amyloid-beta (Ab) and tau¹.

Calcium homeostasis modulator 1 (CALHM1) is a cerebral Ca²⁺ channel component responsible for controlling intracellular Ca²⁺ levels and Ab metabolism^2,3. CALHM1 is a three transmembrane glycoprotein, mostly localized to the endoplasmic reticulum although it can be detected at the plasma membrane. A functional channel is formed by multiple subunits which has some structural similarities to the NMDA receptor. It is expressed in all brain regions¹.

In cultured cells, overexpression of CALHM1 increases intracellular Ca²⁺ levels and reduces Ab accumulation, thereby reinforcing its implication in the development of AD. Indeed, a polymorphism in the gene was found to affect the onset of AD².