vestnik-bio-msuВестник Московского университета. Серия 16. БиологияVestnik Moskovskogo universiteta. Seriya 16. Biologiya0137-0952Lomonosov Moscow State University, School of Biology10.55959/MSU0137-0952-16-78-3-3vestnik-bio-msu-1263Research ArticleМНЕНИЕOPINIONПочему у пресноводной гидры не бывает болезни АльцгеймераWhy freshwater hydra does not get Alzheimer’s diseasehttps://orcid.org/0000-0001-7454-7023ХохловА. Н.KhokhlovA. N.

Хохлов Александр Николаевич – докт. биол. наук, зав. сектором эволюционной цитогеронтологии биологического факультета МГУ.  Тел.: 8-495-939-15-90

119234, Москва, Ленинские горы, д. 1, стр. 12

Evolutionary Cytogerontology Sector, School of Biology

1–12 Leninskie Gory, Moscow, 119234

khokhlov@mail.bio.msu.ruМосковский государственный университет имени М.В. ЛомоносоваРоссияLomonosov Moscow State UniversityRussian Federation202320112023783213220Copyright © Хохлов А.Н., 20232023Хохлов А.Н.Khokhlov A.N.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://vestnik-bio-msu.elpub.ru/jour/article/view/1263

Кратко рассматривается история исследования фундаментальных механизмов патогенеза болезни Альцгеймера (БА). Анализируются концепции, в которых решающая роль в развитии данной болезни приписывалась алюминию или свободным радикалам. Подчеркивается отсутствие на сегодняшний день надежных данных в поддержку этих концепций. Излагается точка зрения автора, согласно которой практически все результаты, свидетельствующие о целесообразности использования антиоксидантов (а также других потенциальных лекарств от БА) для предотвращения и лечения БА, были получены на модельных животных с теми или иными патологиями (например, с сильным окислительным стрессом), которые и способствуют формированию симптомов, сходных с симптомами БА у людей. В этой связи проводятся параллели с экспериментально-геронтологическими работами, направленными на изучение влияния калорийно ограниченного питания на старение и продолжительность жизни. Отмечается, что и в этих исследованиях использовали животных, которые либо не являлись совершенно нормальными, либо находились в неблагоприятных условиях. По мнению автора, отсутствие серьезных успехов в разработке эффективных геропротекторов или препаратов для профилактики/лечения БА связано с игнорированием большинством специалистов принципов классической геронтологии – в частности, определений старения и возрастных болезней, а также корректных подходов к выбору контрольных объектов для своих исследований. Подчеркивается, что человек, к сожалению, не может использовать для борьбы со старением и возрастными болезнями метод пресноводной гидры. Она в определенных условиях непрерывно обновляет все клетки (включая нервные) своего организма и тем самым обеспечивает свое «бессмертие». У человека замена «старых» нейронов может привести к утрате личности/индивидуальности, а «ремонт» этих клеток на сегодняшний день представляется невозможным. В связи с этим автор считает целесообразным проводить исследования старения постмитотических клеток в экспериментах на стационарных клеточных культурах, что может ускорить, в частности, расшифровку механизмов накопления в нейронах бета-амилоида и старческих пигментов типа липофусцина. Отмечается необходимость проведения клинических исследований БА как дополняющих экспериментальные работы, хотя первые и являются гораздо более дорогими и длительными. Только подтверждение в исследованиях на людях эффективности препаратов, разработанных в экспериментах на модельных животных, позволит рекомендовать их для использования в клинике.

The history of research into the basic mechanisms of the pathogenesis of Alzheimer’s disease (AD) is briefly considered. Concepts are analyzed in which a decisive role in the development of this disease was attributed to aluminum or free radicals. The lack of reliable data to date to support these concepts is emphasized. The point of view of the author is presented, according to which almost all the results indicating the feasibility of using antioxidants (as well as other potential drugs for AD) for the prevention and treatment of AD were obtained on 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 are drawn with experimental gerontological research aimed at studying the effect of a calorie-restricted diet on aging and life span. It is noted that in these studies, animals were used that were either not completely normal or were in unfavorable conditions. According to the author, the lack of significant progress in the development of effective geroprotectors or drugs for the prevention/ treatment of AD is due to the fact that most specialists ignore the principles of classical gerontology, in particular, the definitions of aging and age-related diseases, as well as the 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 ones) of its body and thereby ensures its “immortality.” In humans, the replacement of “old” neurons can lead to the loss of personality/individuality, and the “repair” of these cells today seems impossible. In this regard, the author considers it expedient to study the aging of postmitotic cells in experiments on stationary cell cultures, which can accelerate, in particular, the deciphering of the mechanisms of accumulation of beta-amyloid and senile pigments such as lipofuscin in neurons. The need for clinical studies of AD is noted as complementary to experimental work, although the first ones 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 use in the clinical practice.

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The authors declare that there are no conflicts of interest present.