medalphabetМедицинский алфавитMedical alphabet2078-56312949-2807ООО «Альфмед»10.33667/2078-5631-2020-1-10-14medalphabet-1418Research ArticleСтатьиМикробиота и болезнь Паркинсона (обзор)Microbiota and Parkinson's disease (overview)ТютинаР. Р.TyutinaR. R.

аспирант

Кафедра нервных болезней Института профессионального образования

г. Москва

Moscow

ПилиповичА. А.PilipovichA. A.

к. м. н., доцент

Кафедра нервных болезней Института профессионального образования

г. Москва

Moscow

ГолубевВ. Л.GolubevV. L.

д. м. н., проф. кафедры

Кафедра нервных болезней Института профессионального образования

г. Москва

Moscow

ДаниловАл. Б.DanilovAl. B.

д. м. н., проф., зав. кафедрой

Кафедра нервных болезней Института профессионального образования

г. Москва

Moscow

ФГАОУ ВО «Первый Московский государственный медицинский университет имени И. М. Сеченова (Сеченовский университет)» Минздрава РоссииРоссияI. M. Sechenov First Moscow State Medical University (Sechenov University)Russian Federation20201106202001Неврология и психиатрия1014Copyright © Тютина Р.Р., Пилипович А.А., Голубев В.Л., Данилов А.Б., 20202020Тютина Р.Р., Пилипович А.А., Голубев В.Л., Данилов А.Б.Tyutina R.R., Pilipovich A.A., Golubev V.L., Danilov A.B.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.med-alphabet.com/jour/article/view/1418

Болезнь Паркинсона (БП) характеризуется как моторными (гипокинезия, тремор покоя, ригидность, постуральная неустойчивость), так и немоторными симптомами. Известно, что некоторые немоторные проявления, такие как нарушения обоняния, сна, депрессия, желудочно-кишечная дисфункция и другие, могут предшествовать моторным симптомам. Восполнение дефицита дофамина, который, как известно, развивается при БП вследствие гибели дофаминергических нейронов черной субстанции, дает возможность влиять на большинство двигательных и некоторые немоторные симптомы паркинсонизма, однако многие немоторные проявления остаются резистентными к данной терапии. Кроме того, она оказывает лишь симптоматический эффект, а патогенетическое лечение БП на сегодняшний день недоступно, что прежде всего связано с недостаточными знаниями об этиологии и механизмах развития заболевания. В частности, уже установлено, что альфа-синуклеин (патоморфологический маркер БП), начинает откладываться в стенке кишечника, в энтерической нервной системе (ЭНС) задолго до его появления в нейронах черной субстанции. Понимание механизма взаимодействия по оси «кишечник – головной мозг», роли дисфункции кишечной стенки в возникновении и развитии БП может привести к разработке новых направлений в терапии этого заболевания. Сегодня в мире широко изучается роль микробиоты, в частности кишечной микробиоты, в функционировании человеческого организма, различных его систем, в том числе и нервной системы. Рассматривается влияние ее дисбаланса на активацию воспалительных реакций в ЭНС и возможность последующего развития БП. В этом обзоре приводится ряд доказательств, подтверждающих гипотезу, что БП может быть инициирована в кишечнике. Кроме того, рассмотрены возможности влияния на течение БП с помощью пре-, про-, син- и метабиотиков.

Parkinson's disease (PD) is characterized by both motor (hypokinesia, resting tremor, rigidity, postural instability) and non-motor symptoms. It is known that some non-motor manifestations, such as disturbances in smell, sleep, depression, gastrointestinal dysfunction, and others, may precede motor symptoms. Replenishment of dopamine deficiency, which, as known, develops in PD due to the death of dopaminergic neurons of the substantia nigra, makes it possible to influence most motor and some non-motor symptoms of parkinsonism, however many non-motor manifestations remain resistant to this therapy. In addition, it has only a symptomatic effect, and the pathogenetic treatment of PD is currently unavailable, which is primarily due to insufficient knowledge about the etiology and mechanisms of the development of the disease. In particular, it has already been established that alpha synuclein (a pathomorphological marker of PD) begins to be deposited in the intestinal wall, in the enteric nervous system (ENS) long before it appears in neurons of the substantia nigra. Understanding the mechanism of interaction along the axis “intestine – brain”, the role of intestinal wall dysfunction in the onset and development of PD can lead to the development of new directions in the treatment of this disease. Today, the role of microbiota, in particular the intestinal microbiota, in the functioning of the human body, its various systems, including the nervous system, is widely studied in the world. The influence of its imbalance on the activation of inflammatory reactions in the ENS and the possibility of the subsequent development of PD are considered. This review provides some evidence supporting the hypothesis that PD can be initiated in the gut. In addition, the possibilities of influencing the course of BP using pre-, pro-, syn- and metabiotics are considered.

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