Semaglutide and the pathogenesis of progressive neurodegenerative disease: the central role of mitochondria

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064165%3A_____%2F25%3A10504132" target="_blank" >RIV/00064165:_____/25:10504132 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11110/25:10504132

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=M_BaoGs09g" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=M_BaoGs09g</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.yfrne.2025.101217" target="_blank" >10.1016/j.yfrne.2025.101217</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Semaglutide and the pathogenesis of progressive neurodegenerative disease: the central role of mitochondria

Popis výsledku v původním jazyce

While mitochondria provide critical energy resources, mitochondrial dysfunction can lead to both metabolic and neurodegenerative disorders. Primary mitochondrial disorders (e.g., Leigh syndrome) are uniformly associated with profound neurodegeneration. Recent studies have also implicated mitochondrial dysfunction as a central feature of progressive neurodegenerative diseases, notably Alzheimer&apos;s disease, Parkinson&apos;s disease, Amyotrophic Lateral Sclerosis, and Huntington&apos;s Disease. In addition to its profound impact on metabolic disease, the glucagon-like peptide-1 receptor agonist, semaglutide, has significant neuroprotective features and may limit the progression of one or more of these disorders. These observations might be explained at least in part by the impact of this drug on mitochondrial function and energy production. Collectively, these observations highlight disrupted energy homeostasis as a critical feature of neurodegenerative disease and suggest novel targets for the development of much-needed new neuropharmaceutical strategies.

Název v anglickém jazyce

Semaglutide and the pathogenesis of progressive neurodegenerative disease: the central role of mitochondria

Popis výsledku anglicky

While mitochondria provide critical energy resources, mitochondrial dysfunction can lead to both metabolic and neurodegenerative disorders. Primary mitochondrial disorders (e.g., Leigh syndrome) are uniformly associated with profound neurodegeneration. Recent studies have also implicated mitochondrial dysfunction as a central feature of progressive neurodegenerative diseases, notably Alzheimer&apos;s disease, Parkinson&apos;s disease, Amyotrophic Lateral Sclerosis, and Huntington&apos;s Disease. In addition to its profound impact on metabolic disease, the glucagon-like peptide-1 receptor agonist, semaglutide, has significant neuroprotective features and may limit the progression of one or more of these disorders. These observations might be explained at least in part by the impact of this drug on mitochondrial function and energy production. Collectively, these observations highlight disrupted energy homeostasis as a critical feature of neurodegenerative disease and suggest novel targets for the development of much-needed new neuropharmaceutical strategies.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30215 - Psychiatry

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Frontiers in Neuroendocrinology

ISSN

0091-3022

e-ISSN

1095-6808

Svazek periodika

79

Číslo periodika v rámci svazku

October

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

7

Strana od-do

101217

Kód UT WoS článku

001590527600001

EID výsledku v databázi Scopus

2-s2.0-105017571070