Exploring the Involvement of PINK1 in Parkinson’s Disease: A Scanning Tunnelling Microscopy Study of Electron Transfer in Synthetic DNA Samples

Background: Parkinson’s disease (PD) is a neurodegenerative disorder with a complex aetiology involving several genetic and environmental factors. Although no clear evidence of a direct link between the electronic features of DNA and PD has been found, elucidating the role of DNA in cellular function and dysfunction could provide valuable insights into the mechanisms of the disease (e.g. mutations occurring in the phosphatase and tensin homolog [PTEN]-induced kinase 1 [PINK1] DNA of PD). This study aimed to analyse topographic images and measure the electronic conductivity of synthetic normal and mutant PINK1 DNA molecules. Methods: Two 15-mer synthetic oligonucleotides of Oligo1 normal PINK1 (5’-CAG CTG CTG GAA GGC-3’) and Oligo2 mutant PINK1 (5’-CAG CTG CCG GAA GGC-3’) were measured using scanning tunnelling microscopy and spectroscopy. Results: The study’s findings revealed that the mean values of the voltage gap (Vg) between Oligo1 normal and Oligo2 mutant PINK1 DNA molecules at the mutation region A2–C2 are 1.204 ± 0.198 V and 0.676 ± 0.495 V, respectively, indicating differences in the electronic properties between the Oligo1 normal and Oligo2 mutant PINK1 DNA molecules. However, the mean Vg values of Oligo1 normal and Oligo2 mutant PINK1 DNA molecules were found to not significantly differ from each other (P = 0.162 > ? = 0.05). Conclusion: The study found that the voltage gap between normal and mutant PINK1 DNA molecules is not significantly different, suggesting that DNA sequence differences may not directly alter electrical properties. However, PINK1 mutations play a role in early-onset PD due to mitochondrial dysfunction, and future therapies should focus on restoring PINK1-Parkin signalling and mitochondrial health.