Why Freshwater Hydra Does Not Get Alzheimer’s Disease

Q3 Agricultural and Biological Sciences Moscow University Biological Sciences Bulletin Pub Date : 2024-03-01 DOI:10.3103/s0096392523700104
A. N. Khokhlov
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Abstract

The history of research into the fundamental mechanisms of the pathogenesis of Alzheimer’s disease (AD) is briefly reviewed. Concepts in which a decisive role in the development of this disease was attributed to aluminum or free radicals are analyzed. The lack of reliable data to date to support these concepts is highlighted. The author’s point of view is stated, according to which almost all the results indicating the advisability of using antioxidants (as well as other potential drugs for AD) for the prevention and treatment of AD were obtained in model animals with certain pathologies (for example, with severe oxidative stress), which contribute to the formation of symptoms similar to those of AD in humans. In this regard, parallels with experimental gerontological work aimed at studying the effect of calorie-restricted nutrition on aging and life span are drawn. It is noted that these studies also used animals that were either not completely normal or were in unfavorable conditions. According to the author, the lack of serious success in the development of effective geroprotectors or drugs for the prevention/treatment of AD is due to the ignorance by most specialists of the principles of classical gerontology, in particular, the definitions of aging and age-related diseases, as well as correct approaches to the selection of control objects for their studies. It is emphasized that humans, unfortunately, cannot use the freshwater hydra method to combat aging and age-related diseases. Under certain conditions, it continuously renews all cells (including nerve cells) of its body and thereby ensures its “immortality.” In humans, replacing “old” neurons can lead to loss of personality/individuality, and “repairing” these cells seems impossible today. In this regard, the author considers it advisable to conduct studies of the aging of postmitotic cells in experiments on stationary cell cultures, which can accelerate, in particular, elucidation of the mechanisms of accumulation of beta-amyloid and senile pigments, such as lipofuscin, in neurons. The need to conduct clinical studies of AD as complementary to experimental work is noted, although the former are much more expensive and time-consuming. Only confirmation in human studies of the effectiveness of drugs developed in experiments on model animals will allow them to be recommended for clinical use.

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淡水水螅为何不会患老年痴呆症
摘要 本文简要回顾了阿尔茨海默病(AD)发病基本机制的研究历史。其中分析了铝或自由基在该病发展中起决定性作用的概念。重点指出了迄今为止缺乏支持这些概念的可靠数据。作者阐述了自己的观点,即几乎所有表明使用抗氧化剂(以及其他可能用于治疗注意力缺失症的药物)预防和治疗注意力缺失症的可取性的结果,都是在患有某些病症(例如,严重氧化应激)的模型动物身上获得的,这些病症会导致形成与人类注意力缺失症类似的症状。在这方面,与旨在研究限制卡路里营养对衰老和寿命影响的老年学实验工作有相似之处。值得注意的是,这些研究使用的动物要么不完全正常,要么处于不利条件下。作者认为,在开发有效的老年保护剂或预防/治疗注意力缺失症的药物方面之所以没有取得重大成功,是因为大多数专家不了解经典老年学的原理,特别是对衰老和老年相关疾病的定义,以及选择研究对照对象的正确方法。需要强调的是,遗憾的是,人类无法使用淡水水螅的方法来对抗衰老和老年疾病。在特定条件下,淡水九头蛇会不断更新其身体的所有细胞(包括神经细胞),从而确保其 "永生"。对于人类来说,更换 "老 "的神经细胞会导致人格/个性的丧失,而 "修复 "这些细胞在今天看来是不可能的。在这方面,作者认为最好在静止细胞培养实验中对有丝分裂后细胞的衰老进行研究,这尤其能加速阐明神经元中β-淀粉样蛋白和脂褐素等老年色素的积累机制。我们注意到,有必要开展 AD 临床研究,作为实验工作的补充,尽管前者更为昂贵和耗时。只有在人体研究中确认在模式动物实验中开发的药物的有效性,才能建议将其用于临床。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Moscow University Biological Sciences Bulletin
Moscow University Biological Sciences Bulletin Agricultural and Biological Sciences-Agricultural and Biological Sciences (all)
CiteScore
1.00
自引率
0.00%
发文量
18
期刊介绍: Moscow University Biological Sciences Bulletin  is forum for research in all important areas of modern biology. It publishes original work on qualitative, analytical and experimental aspects of research. The scope of articles to be considered includes plant biology, zoology, ecology, evolutionary biology, biophysics, genetics, genomics, proteomics, molecular biology, cell biology, biochemistry, endocrinology, immunology, physiology, pharmacology, neuroscience, gerontology, developmental biology, bioinformatics, bioengineering, virology, and microbiology.
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