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阿尔茨海默病:一种神经遗传学联系

摘要

阿尔茨海默病(AD)是一种神经退行性疾病,它逐渐溶解了人类认知的一部分特征。在阿尔茨海默病的神经性病程中,β -淀粉样蛋白斑块的形成对神经元造成损害,导致大脑体积的严重损失。作为AD的结果,被骚扰的个体在智力/官方能力、记忆障碍/不幸和无法约束不得体的行为方面造成了减少。另一种说法是,受折磨的个体不再是他们曾经的那个个体,也就是说,他们的意识形态减弱了。APOE-epsilon4、APP、PSEN1、PSEN2、TREM2等几个性状的变化均与AD频率扩大、运动加快有关。这为认知存在神经遗传关系(NgCC)的观点提供了支持。在过去的研究中,这些NgCC被描绘成人类意识的三个神经遗传学时期。促进是基于质量的神经变性的一个重要样本,它可以发生在第三神经发生阶段。人们相信,随着新的遗传治疗方法的改进,阿尔茨海默病的表现可能会改变。一些高质量的治疗正在进行中,如FGF2、瘦素和NEU1,以改变AD的症状。 On the off chance that these quality treatments are one day fruitful in turning around a percentage of the manifestations of AD, would they be able to in the end be utilized to upgrade human cognizance in people without AD?. Amid the most recent couple of decades a huge writing has advanced, proposing that tactile brokenness, especially smell and taste brokenness, can be early markers for neurodegenerative ailments, for example, Parkinson's and Alzheimer's and neuropsychiatric infections including ADHD and Schizophrenia, all illnesses that include dopaminergic pathology. Smell misfortune and taste brokenness show up in clinical versus non-clinical gatherings, and in longitudinal studies these side effects have been noted years sooner than engine signs in the first degree relatives of people who as of now have the illnesses.

Sunil Kumar Singh, Nisha Dhama, Arif Khan, Gaurav Singh, Sangeeta Yadav

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