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Leucine-rich repeat kinase 2 (LRRK2) is a ROCO family member which its mutation is closely related with Parkinson's disease, and LRRK2 is widely involved into the regulation of autophagy, vesicle transport and neuronal proliferation. However, the roles of LRRK2 during mammalian oocyte maturation are still largely unclear. In present study, we disturbed the activity of LRRK2 and showed its essential roles in porcine oocytes.

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Leucine-rich repeat kinase 2 (LRRK2) inhibition is a promising disease-modifying therapy for LRRK2-associated Parkinson's disease (L2PD) and idiopathic PD (iPD). However, pharmaco-dynamic readouts and progression biomarkers for clinical trials aiming for disease modification are insufficient since no endogenous marker reflecting enhanced kinase activity of the most common LRRK2 G2019S mutation has been reported yet in L2PD patients. Employing phospho-/proteomic analyses we assessed the impact that LRRK2 activating mutations had in peripheral blood mononuclear cells (PBMCs) from a LRRK2 clinical cohort from Spain (n=174).

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