A study published in the Biological Psychiatry, Elsevier indicated that various neuropathology illnesses might be caused by "somatic" gene changes in brain cells.

The exomes, or sections of genes that encode proteins, were sequenced using deep whole-exome sequencing in the current study. In order to compare the sequences in the two tissues, the researchers sequenced postmortem samples from the brain, liver, heart, or spleen of 27 individuals with schizophrenia and 31 participants who served as controls. In brain samples from individuals with schizophrenia (SCZ), the team discovered an average of 4.9 somatic single-nucleotide variations (SNV), or mutations, and 5.6 somatic SNVs in brain samples from control patients.

The scientists then identified the proteins that recently discovered somatic mutations would influence. Surprisingly, GRIN2B, a protein, was found to be severely damaged, and two SCZ patients had somatic mutations in the GRIN2B gene. The NMDA-type glutamate receptors, essential for brain signaling, contain the protein GRIN2B. The pathogenesis of SCZ has long been thought to be influenced by defective glutamate receptors, and GRIN2B is one of the most studied genes in schizophrenia. 

This work experimentally demonstrated the biological impact of somatic mutations that resulted in neuronal abnormalities linked to SCZ. It shows that brain somatic mutations may be a substantial hidden factor behind developing SCZ and provides new information on the molecular genetic architecture of SCZ.

(Source: https://theprint.in/health/rare-mutations-may-have-big-impact-on-schizophrenia-pathology/1214678/)