Objective: The aim of this research is to compare the overexpressed genes in patients with Parkinson’s Disease (PD) and patients with Bipolar Disorder (BD) versus normal controls to determine if parallel overexpression in certain genes may indicate the possible association at the level of gene function.

Background: Research illustrating the association between PD and BD in genome-wide association studies and single nucleotide polymorphism report have shown that the two diseases are associated. Although certain genes have been described to occur in both PD and BD, there is no discussion on the established function of these genes and the possible common mechanisms between PD and BD that is linked to such increase in gene expression. [1] [2]

Method: The samples utilized were taken from the public domain archive of the NCBI SRA. RNA sequence transcripts were detected using the search string “Bipolar Disorder” and “Parkinson”. Only whole RNA sequencing analysis of postmortem brain tissues from patients with BD, patients with PD, and normal controls were analyzed. The gene expression frequency of the patient groups with BD and PD were used to identify highly expressed genes that significantly differed from normal controls but showed similar profile in the two patient groups. The genes compared were limited to only those that have a 0.1+/- difference in expression. Only the known genes that were described to be associated with inflammation, repair, tissue injury, and remodeling were compared.

Results: Among the common genes that were expressed in both cases more than the normal controls, IMPA2 was the only gene that had an established associated with BD. However, certain genes that have been described to increase in high oxidative stress processes (VNN), innate immunity and damage control (CPAMD8, FGFBP2), apoptosis (MAP3K10), tissue differentiation (GPRC5A, LIF, PCDI), tissue remodeling (CHI3L1), and response to hypoxia (EPAS1) showed comparably similar overexpression profiles, which were not seen in normal controls.

Conclusion: The increase in expression in genes associated with tissue injury, remodeling, and repair may be an indicator of an underlying pathobiologic mechanism that may explain the occurrence of PD in patients with a history of mood disorder. [3] This information may be useful in planning future studies to identify the risk of developing PD in cases diagnosed with BD or major depressive disorder.

References: [1] Schulze T, Akula N, Breuer R, Steele J, et al. Molecular genetic overlap in bipolar disorder, schizophrenia, and major depressive disorder. The World Journal of Biological Psychiatry, 2014; 15;3, 200-208. [2] Buervenich S, Xiang F, Sydow O, Jönsson EG, et al. Identification of four novel polymorphisms in the calcitonin/α‐CGRP (CALCA) gene and an investigation of their possible associations with Parkinson disease, schizophrenia, and manic depression. Hum. Mutat.,2001; 17: 435-436. [3] Gustafsson H, Nordström A, Nordström P. Depression and subsequent risk of Parkinson disease: A nationwide cohort study. Neurology. 2015;84(24):2422-9.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/comparison-of-gene-expression-in-parkinsons-disease-and-bipolar-disorder/