Biology Department, College of Sciences and Arts Muhayil Assir, King Khalid University, Abha 61421, Saudi Arabia.
Department of Neurochemistry, Inge Grundke-Iqbal Research Floor, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA.
Biomolecules. 2022 Oct 2;12(10):1409. doi: 10.3390/biom12101409.
Alzheimer's disease (AD) is a progressive neurodegenerative disease with an insidious onset and multifactorial nature. A deficit in neurogenesis and synaptic plasticity are considered the early pathological features associated with neurofibrillary tau and amyloid β pathologies and neuroinflammation. The imbalance of neurotrophic factors with an increase in FGF-2 level and a decrease in brain derived neurotrophic factor (BDNF) and neurotrophin 4 (NT-4) in the hippocampus, frontal cortex and parietal cortex and disruption of the brain micro-environment are other characteristics of AD. Neurotrophic factors are crucial in neuronal differentiation, maturation, and survival. Several attempts to use neurotrophic factors to treat AD were made, but these trials were halted due to their blood-brain barrier (BBB) impermeability, short-half-life, and severe side effects. In the present review we mainly focus on the major etiopathology features of AD and the use of a small neurotrophic and neurogenic peptide mimetic compound; P021 that was discovered in our laboratory and was found to overcome the difficulties faced in the administration of the whole neurotrophic factor proteins. We describe pre-clinical studies on P021 and its potential as a therapeutic drug for AD and related neurodegenerative disorders. Our study is limited because it focuses only on P021 and the relevant literature; a more thorough investigation is required to review studies on various therapeutic approaches and potential drugs that are emerging in the AD field.
阿尔茨海默病(AD)是一种进行性神经退行性疾病,发病隐匿,病因复杂。神经发生和突触可塑性的不足被认为是与神经纤维缠结和淀粉样β病理学以及神经炎症相关的早期病理特征。神经递质失衡,成纤维细胞生长因子-2(FGF-2)水平升高,海马体、额叶皮层和顶叶皮层中的脑源性神经营养因子(BDNF)和神经营养素 4(NT-4)减少,以及大脑微环境的破坏是 AD 的另一些特征。神经递质对于神经元的分化、成熟和存活至关重要。曾有几次尝试使用神经递质来治疗 AD,但由于其血脑屏障(BBB)通透性差、半衰期短和严重的副作用,这些试验都被停止了。在本综述中,我们主要关注 AD 的主要发病机制特征以及使用一种在我们实验室发现的小神经递质和神经生成肽模拟化合物 P021。该化合物被发现可以克服整个神经递质蛋白给药所面临的困难。我们描述了 P021 的临床前研究及其作为 AD 和相关神经退行性疾病治疗药物的潜力。我们的研究是有限的,因为它只关注 P021 和相关文献;需要更全面的研究来审查 AD 领域中各种治疗方法和新兴潜在药物的研究。