Genetic mouse models of parkinsonism: Strengths and limitations

1. NeuroRx. 2005 Jul;2(3):495-503. doi: 10.1602/neurorx.2.3.495.

Genetic mouse models of parkinsonism: strengths and limitations.

Fleming SM(1), Fernagut PO, Chesselet MF.

Author information:
(1)Departments of Neurology and Neurobiology, The David Geffen School of
Medicine, UCLA, Los Angeles, California 90095, USA.

Parkinson’s disease (PD) is a progressive neurodegenerative disorder. Patients
with PD display a combination of motor symptoms including resting tremor,
rigidity, bradykinesia, and postural instability that worsen over time. These
motor symptoms are related to the progressive loss of dopamine neurons in the
substantia nigra pars compacta. PD patients also suffer from nonmotor symptoms
that may precede the cardinal motor symptoms and that are likely related to
pathology in other brain regions. Traditional toxin models of PD have focused on
the nigrostriatal pathway and the loss of dopamine neurons in this region, and
these models have been important in our understanding of PD and in the
development of symptomatic treatments for the disease. However, they are limited
in that they do not reproduce the full pathology and progression seen in PD,
thus creating a need for better models. The recent discovery of specific genes
causing familial forms of PD has contributed to the development of novel genetic
mouse models of PD. This review discusses the validity, benefits, and
limitations of these new models.

DOI: 10.1602/neurorx.2.3.495
PMCID: PMC1144493
PMID: 16389313 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus