In order to understand the normal function of LRRK2, JHU faculty have generated a targeted mutation in the murine homolog of LRRK2. LRRK2 mice are viable, fertile and show no gross pathologic abnormalities.There are no significant difference in body weight, general appearance and viability of surviving LRRK2 deficient mice. Gross histological examination of different organs and the brain reveals normal morphology of the LRRK2 null mice. Detailed examination of the LRRK2 mice reveals that that have defects in vesicular trafficking. These mice will be valuable for studying the role of LRRK2 in normal brain function and behavior as well as LRRK2 potential role in Neurodegenerative diseases.
Technical Details:
Mutations in Leucine repeat rich kinase 2 (LRRK2) are associated with familial Parkinson’s disease. These LRRK2 knockout mice can be used to characterize the normal physiological function of LRRK2 in the brain. Since LRRK2 is a kinase, knockout mice can be used to identify potential LRRK2 phosphorylation substrates.
Looking for Partners:
If a molecular footprint can be identified in the LRRK2 mouse, then the molecular footprint could be used as a diagnostic biomarker for PD as well as monitoring the rate of progression of PD and response to potential neuroprotective or neurorestorative therapies.
