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Protein LRRK2 may be implicated in sporadic PD. In this study, the specific molecular mechanisms of LRRK2 have been identified and linked to the development of sporadic Parkinson’s. 

Losing control over our bodies seems to be a scary prospect. A neurodegenerative Parkinson’s disease (PD) involves disruption of voluntary movement due to the death of dopaminergic neurons (Nguyen et al. 2019). Dopaminergic neurons die from the toxic effects of misfolded and aggregated protein alpha-synuclein which forms a Lewy body (Menšíková et al. 2022). There are many contributors to alpha-synuclein aggregation. Thus, there are two types of PD: familial and sporadic. Many genes and their mutation were identified as contributors to alpha-synuclein misfolding in familial Parkinson’s. An example of such a gene is LRRK2 (Shihabuddin et al. 2018). LRRK2 is important to neurotransmission, which means passing of the motor signals. Mutations in LRRK2 are among the most common mutations that contribute to PD (Nguyen et al. 2020). However, even if LRRK2 is not mutated (wild type, WT) it was still identified as a risk factor for developing sporadic PD (Panicker et al. 2021). How is WT LRRK2 involved in PD? The specific molecular mechanisms are yet to be studied because there was no appropriate and sensitive measure to do that. In this paper, Di Maio and colleagues have developed a novel method to determine how non-mutated LRRK2 contributes to Parkinson’s pathology (Di Maio et al. 2018). 

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