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Mechanisms of aluminium neurotoxicity in oxidative stress-induced ...

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INTRODUCTION<br />

mouse models, such as Pitx3-aphakia mouse or Engrailed double knock-out mouse,<br />

were developed on the basis <strong>of</strong> genes crucial for development and survival <strong>of</strong> DAergic<br />

neurons (Nunes et al. 2003, Sgado et al. 2006, D<strong>in</strong>g et al. 2007). Recently, tissue-<br />

specific knock-out mouse models target<strong>in</strong>g the expression <strong>of</strong> genes <strong>of</strong> <strong>in</strong>terest <strong>in</strong> a<br />

region- or neuron-specific manner were created (Gelman et al. 2003, Ekstrand et al.<br />

2004, L<strong>in</strong>deberg et al. 2004, Backet et al. 2005, Zhuang et al. 2005, Backman et al.<br />

2006, Borgkvist et al. 2006, Turiault et al. 2007).<br />

52<br />

As there is no experimental PD model to date that mimics exactly the<br />

pathogenesis and progression happen<strong>in</strong>g <strong>in</strong> PD, one priority at this time is to develop an<br />

experimental model <strong>of</strong> PD that reproduces the cl<strong>in</strong>ical and pathological features <strong>of</strong> PD,<br />

such as progressive loss <strong>of</strong> DAergic neurons <strong>in</strong> the striatum and SN, LB-like <strong>in</strong>clusion<br />

<strong>in</strong> the bra<strong>in</strong>, and L-DOPA-responsive movement disorder.

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