Objective: The research would like to determine if similar overexpressed genes between CTE and PD may explain the occurrence of parkinsonism in CTE. This was addressed by identifying overexpressed genes common in patients diagnosed with CTE and PD to determine a plausible link between the two conditions that may be associated with aberrant brain activity that leads to their distinct neuropathology.

Background: Chronic traumatic encephalopathy (CTE), a neurodegenerative disease associated with repetitive head impacts that lead to progressive injury, is diagnosed neuropathologically by the accumulation of hyperphosphorylated tau manifesting as neurofibrillary and astrocytic tangles around small vessels and in the depths of the cerebral sulci. The accumulation of tau presents as gross changes in the cortical and subcortical structures. In comparison, Parkinson’s disease (PD) is diagnosed neuropathologically by the presence of Lewy bodies in the substantia nigra and associated brainstem structures. However, the development of PD has been observed in patients that are clinically diagnosed with CTE.[1][2]

Method: Transcripts from the public domain archive of the NCBI SRA were identified for RNA sequence using the search string “Chronic Traumatic Encephalopathy” and “Parkinson”. Available whole RNA sequencing analysis of postmortem brain tissue from patients with CTE, patients with PD, and normal controls were analyzed separately. Comparison between genes of patient groups with CTE and PD identified the presence of overexpressed genes that significantly differed from normal controls but showed similar profile in the CTE and PD groups.[3][4]

Results: Comparison between the two groups showed a significant difference between the expression several genes of diverse function, including genes for transcription factors SOX6 and NCOR1, methyltransferase protein METTL7A, transport protein MVP, and ribonuclease protein RNASE3,  when compared to the controls but no significant difference between the CTE and the PD groups, indicating similar overexpression profile.

Conclusion: The genes that exhibited overexpression in both CTE and PD when compared to controls may be a clue to underlying transcription pathology that propagate the lesions in both conditions. This may provide useful information for future research in understanding the mechanism on why CTE may present with movement disorders and not only cognitive and behavioral changes.

References: [1] Adams JW, Alvarez VE, Mez J, et al. Lewy Body Pathology and Chronic Traumatic Encephalopathy Associated With Contact Sports. J Neuropathol Exp Neurol. 2018;77(9):757-768. [2] McKee AC, Stern RA, Nowinski CJ, et al. The spectrum of disease in chronic traumatic encephalopathy. Brain. 2012;136(Pt 1):43-64. [3] Transcriptome analysis of Chronic traumatic encepahlopathy. NCBI SRA Accession Number: PRJEB13579 https://www.ncbi.nlm.nih.gov/bioproject/392065 [4] mRNA-Seq expression and MS3 proteomics profiling of human post-mortem BA9 brain tissue for Parkinson Disease and neurologically normal individuals. NCBI SRA Accession Number: PRJNA283498 https://www.ncbi.nlm.nih.gov/bioproject/283498

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MDS Abstracts - https://www.mdsabstracts.org/abstract/differential-gene-expression-in-parkinson-disease-and-chronic-traumatic-encephalopathy/