Departments of Neurology and Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Ann N Y Acad Sci. 2010 Jan;1184:87-105. doi: 10.1111/j.1749-6632.2009.05117.x.
Tuberous sclerosis complex (TSC) is an autosomal dominant disorder that results from mutations in the TSC1 or TSC2 genes and is associated with hamartoma formation in multiple organ systems. The neurological manifestations of TSC are particularly challenging and include infantile spasms, intractable epilepsy, cognitive disabilities, and autism. Progress over the past 15 years has demonstrated that the TSC1 or TSC2 encoded proteins modulate cell function via the mTOR signaling cascade and serve as keystones in regulating cell growth and proliferation. The mTOR pathway provides an intersection for an intricate network of protein cascades that respond to cellular nutrition, energy levels, and growth-factor stimulation. In the brain, TSC1 and TSC2 have been implicated in cell body size, dendritic arborization, axonal outgrowth and targeting, neuronal migration, cortical lamination, and spine formation. Antagonism of the mTOR pathway with rapamycin and related compounds may provide new therapeutic options for TSC patients.
结节性硬化症(TSC)是一种常染色体显性遗传疾病,由 TSC1 或 TSC2 基因突变引起,并与多个器官系统的错构瘤形成有关。TSC 的神经表现尤其具有挑战性,包括婴儿痉挛、难治性癫痫、认知障碍和自闭症。过去 15 年来的进展表明,TSC1 或 TSC2 编码的蛋白通过 mTOR 信号级联调节细胞功能,并作为调节细胞生长和增殖的关键因子。mTOR 途径为响应细胞营养、能量水平和生长因子刺激的复杂蛋白级联网络提供了一个交点。在大脑中,TSC1 和 TSC2 参与了胞体大小、树突分支、轴突生长和靶向、神经元迁移、皮质分层和棘突形成。用雷帕霉素和相关化合物拮抗 mTOR 途径可能为 TSC 患者提供新的治疗选择。