Institute of Neuroscience and Medicine (INM‑10), Research Centre Jülich GmbH, Germany.
Department of Anatomy and Cell Biology, School of Medicine, Birjand University of Medical Sciences, Birjand, Iran.
Acta Neurobiol Exp (Wars). 2021;81(4):314-327.
Alzheimer's disease (AD) is a common neurodegenerative disease with a prevalence estimated to reach 115 million by 2050. It is characterized by abnormal extracellular accumulation of amyloid‑beta (Aβ) peptide and intracellular neurofibrillary tangles (NFTs) that result in neuro‑inflammation, synaptic dysfunction, neurotransmitter imbalance, neuronal loss, and dendritic changes. A hypothesis of neurotrophic factor (NTF) involvement in neurodegenerative diseases and their potential as a therapeutic tool has emerged. There are wide information gaps on this topic. However, consistent with this hypothesis, AD may be caused by a deficiency in neurotrophin proteins or receptors expression. In AD brains, an increase in nerve growth factor and a decrease in brain-derived neurotrophic factor in the hippocampus and certain neocortical regions, and a decrease in TrkA in the cortex and nucleus basalis has been observed. Thus, comparative data relating to recent hypotheses addressing NTF content and receptors in experimental animals and human brains, along with their potential roles in the treat ment of AD, are discussed in this review.
阿尔茨海默病（AD）是一种常见的神经退行性疾病，预计到 2050 年其患病率将达到 1.15 亿。其特征是细胞外异常积聚淀粉样β（Aβ）肽和细胞内神经原纤维缠结（NFTs），导致神经炎症、突触功能障碍、神经递质失衡、神经元丧失和树突变化。神经营养因子（NTF）参与神经退行性疾病及其作为治疗工具的潜力的假说已经出现。关于这个主题存在广泛的信息差距。然而，与这一假说一致的是，AD 可能是由于神经营养蛋白或受体表达的缺乏引起的。在 AD 大脑中，已经观察到海马体和某些新皮质区域中神经生长因子增加，脑源性神经营养因子减少，以及皮质和基底核中 TrkA 减少。因此，本综述讨论了与最近的假说有关的实验动物和人脑中 NTF 含量和受体的比较数据，以及它们在 AD 治疗中的潜在作用。
