TY - JOUR
T1 - Genetic Animal Models of Parkinson's Disease
AU - Dawson, Ted M.
AU - Ko, Han Seok
AU - Dawson, Valina L.
N1 - Funding Information:
This work was supported by the Morris K. Udall Parkinson's Disease Research Center of Excellence NIH/NINDS (NS38377) and NS04826. T.M.D. is the Leonard and Madlyn Abramson Professor in Neurodegenerative Diseases. T.M.D. is a paid consultant to Merck KGAA. The terms of this arrangement are being managed by the Johns Hopkins University in accordance with its conflict of interest policies. We would like to thank Yunjong Lee and Mingyao Ying for critical comments and insights. Due to the nature of this review, we apologize to all of the authors we were not able to cite regarding animal and cellular models of PD.
PY - 2010/6
Y1 - 2010/6
N2 - Parkinson's disease (PD) is a progressive neurodegenerative disorder that is characterized by the degeneration of dopamine (DA) and non-DA neurons, the almost uniform presence of Lewy bodies, and motor deficits. Although the majority of PD is sporadic, specific genetic defects in rare familial cases have provided unique insights into the pathogenesis of PD. Through the creation of animal and cellular models of mutations in LRRK2 and α-synuclein, which are linked to autosomal-dominant PD, and mutations in parkin, DJ-1, and PINK1, which are responsible for autosomal-recessive PD, insight into the molecular mechanisms of this disorder are leading to new ideas about the pathogenesis of PD. In this review, we discuss the animal models for these genetic causes of PD, their limitations, and value. Moreover, we discuss future directions and potential strategies for optimization of the genetic models.
AB - Parkinson's disease (PD) is a progressive neurodegenerative disorder that is characterized by the degeneration of dopamine (DA) and non-DA neurons, the almost uniform presence of Lewy bodies, and motor deficits. Although the majority of PD is sporadic, specific genetic defects in rare familial cases have provided unique insights into the pathogenesis of PD. Through the creation of animal and cellular models of mutations in LRRK2 and α-synuclein, which are linked to autosomal-dominant PD, and mutations in parkin, DJ-1, and PINK1, which are responsible for autosomal-recessive PD, insight into the molecular mechanisms of this disorder are leading to new ideas about the pathogenesis of PD. In this review, we discuss the animal models for these genetic causes of PD, their limitations, and value. Moreover, we discuss future directions and potential strategies for optimization of the genetic models.
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U2 - 10.1016/j.neuron.2010.04.034
DO - 10.1016/j.neuron.2010.04.034
M3 - Review article
C2 - 20547124
AN - SCOPUS:77953666105
SN - 0896-6273
VL - 66
SP - 646
EP - 661
JO - Neuron
JF - Neuron
IS - 5
ER -