Center for Neurologic Diseases, Brigham and Women's Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA, 02115, USA.
Neuron. 2009 Dec 24;64(6):771-3. doi: 10.1016/j.neuron.2009.12.017.
In this issue of Neuron, Lin et al. report that LRRK2 modulates age-related neurodegeneration caused by overexpression of alpha-synuclein in the forebrain of transgenic mice. Overexpression of LRRK2 accelerates the progression of alpha-synuclein-mediated neuropathological changes, whereas deletion of LRRK2 alleviates these alterations. The results reveal an interesting interaction between alpha-synuclein and LRRK2, two gene products linked to dominantly inherited Parkinson's disease.
在本期《神经元》杂志中，Lin 等人报告称，LRRK2 调节了在转基因小鼠前脑中过表达 α-突触核蛋白引起的与年龄相关的神经退行性变。LRRK2 的过表达加速了 α-突触核蛋白介导的神经病理变化的进展，而 LRRK2 的缺失则减轻了这些改变。这些结果揭示了α-突触核蛋白和 LRRK2 之间的有趣相互作用，这两种基因产物与常染色体显性遗传帕金森病有关。
