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Dysfunction of TGF-β1 signaling in Alzheimer’s disease: perspectives for neuroprotection

机译：TGF-β1信号转导在阿尔茨海默氏病中的作用：神经保护的观点

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Alzheimer’s disease (AD) is a neurodegenerative disorder that affects about 35 million people worldwide. Current drugs for AD only treat the symptoms and do not interfere with the underlying pathogenic mechanisms of the disease. AD is characterized by the presence of β-amyloid (Aβ) plaques, neurofibrillary tangles, and neuronal loss. Identification of the molecular determinants underlying Aβ-induced neurodegeneration is an essential step for the development of disease-modifying drugs. Recently, an impairment of the transforming growth factor-β1 (TGF-β1) signaling pathway has been demonstrated to be specific to the AD brain and, particularly, to the early phase of the disease. TGF-β1 is a neurotrophic factor responsible for the initiation and maintenance of neuronal differentiation and synaptic plasticity. The deficiency of TGF-β1 signaling is associated with Aβ pathology and neurofibrillary tangle formation in AD animal models. Reduced TGF-β1 signaling seems to contribute both to microglial activation and to ectopic cell-cycle re-activation in neurons, two events that contribute to neurodegeneration in the AD brain. The neuroprotective features of TGF-β1 indicate the advantage of rescuing TGF-β1 signaling as a means to slow down the neurodegenerative process in AD.
机译：阿尔茨海默氏病（AD）是一种神经退行性疾病，全球约有3500万人受其影响。当前用于AD的药物仅治疗症状并且不干扰该疾病的潜在致病机制。 AD的特征在于存在β-淀粉样蛋白（Aβ）斑块，神经原纤维缠结和神经元丢失。识别Aβ诱导的神经退行性变的分子决定因素是开发疾病缓解药物的重要步骤。近来，已经证明转化生长因子-β1（TGF-β1）信号传导途径的损伤是AD脑特有的，尤其是疾病的早期。 TGF-β1是神经营养因子，负责启动和维持神经元分化和突触可塑性。在AD动物模型中，TGF-β1信号转导的缺乏与Aβ病理学和神经原纤维缠结的形成有关。降低的TGF-β1信号传导似乎既促进了小胶质细胞的活化，又促进了神经元中异位细胞周期的重新活化，这是导致AD脑神经变性的两个事件。 TGF-β1的神经保护功能表明抢救TGF-β1信号传导的优势是减缓AD中神经退行性过程的一种手段。

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