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<XML><RECORDS>
<RECORD>
	<REFERENCE_TYPE>31</REFERENCE_TYPE>
	<AUTHORS>
		<AUTHOR>Li, Yanping</AUTHOR>
		<AUTHOR>Liu, Wencheng</AUTHOR>
		<AUTHOR>Oo, Tinmarla F</AUTHOR>
		<AUTHOR>Wang, Lei</AUTHOR>
		<AUTHOR>Tang, Yi</AUTHOR>
		<AUTHOR>Jackson-Lewis, Vernice</AUTHOR>
		<AUTHOR>Zhou, Chun</AUTHOR>
		<AUTHOR>Geghman, Kindiya</AUTHOR>
		<AUTHOR>Bogdanov, Mikhail</AUTHOR>
		<AUTHOR>Przedborski, Serge</AUTHOR>
		<AUTHOR>Beal, M Flint</AUTHOR>
		<AUTHOR>Burke, Robert E</AUTHOR>
		<AUTHOR>Li, Chenjian</AUTHOR>
	</AUTHORS>
	<YEAR>2009</YEAR>
	<TITLE>Mutant LRRK2(R1441G) BAC transgenic mice recapitulate cardinal features of Parkinson's disease.</TITLE>
	<SECONDARY_TITLE>Nature neuroscience</SECONDARY_TITLE>
	<DATE>2009 Jun 7</DATE>
	<ALTERNATE_TITLE>Nat. Neurosci.</ALTERNATE_TITLE>
	<CUSTOM1>http://www.ncbi.nlm.nih.gov/pubmed/19503083?dopt=Abstract</CUSTOM1>
	<ABSTRACT>Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson's disease. We created a LRRK2 transgenic mouse model that recapitulates cardinal features of the disease: an age-dependent and levodopa-responsive slowness of movement associated with diminished dopamine release and axonal pathology of nigrostriatal dopaminergic projection. These mice provide a valid model of Parkinson's disease and are a resource for the investigation of pathogenesis and therapeutics.</ABSTRACT>
</RECORD>
</RECORDS></XML>