Targeting mitochondrial dysfunction in Alzheimer's disease: New findings and perspectives

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064165%3A_____%2F25%3A10503572" target="_blank" >RIV/00064165:_____/25:10503572 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11110/25:10503572

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=VWJL4LJ4XJ" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=VWJL4LJ4XJ</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.pnpbp.2025.111491" target="_blank" >10.1016/j.pnpbp.2025.111491</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Targeting mitochondrial dysfunction in Alzheimer's disease: New findings and perspectives

Popis výsledku v původním jazyce

Alterations in mitochondrial energy metabolism, impaired processes of mitochondrial dynamics and mitophagy have recently been identified as important contributors to the pathophysiology of Alzheimer&apos;s disease (AD). Genetic predispositions and defects in mitochondrial metabolism, particularly within the electron transport chain of the oxidative phosphorylation system, have been linked to the pathology of intracellular and extracellular amyloid-beta (A(3) and tau protein. This review summarizes the current molecular background of AD and explains the relationships between genetic factors, impaired energy metabolism, and the formation of pathological proteins. It highlights altered mitochondrial dynamics, impaired mitochondrial signaling, mitophagy, neuroinflammation, and apoptosis. Based on these findings, the review discusses mitochondrial biomarkers and novel molecules targeting mitochondrial dysfunction in the pathophysiology of AD.

Název v anglickém jazyce

Targeting mitochondrial dysfunction in Alzheimer's disease: New findings and perspectives

Popis výsledku anglicky

Alterations in mitochondrial energy metabolism, impaired processes of mitochondrial dynamics and mitophagy have recently been identified as important contributors to the pathophysiology of Alzheimer&apos;s disease (AD). Genetic predispositions and defects in mitochondrial metabolism, particularly within the electron transport chain of the oxidative phosphorylation system, have been linked to the pathology of intracellular and extracellular amyloid-beta (A(3) and tau protein. This review summarizes the current molecular background of AD and explains the relationships between genetic factors, impaired energy metabolism, and the formation of pathological proteins. It highlights altered mitochondrial dynamics, impaired mitochondrial signaling, mitophagy, neuroinflammation, and apoptosis. Based on these findings, the review discusses mitochondrial biomarkers and novel molecules targeting mitochondrial dysfunction in the pathophysiology of AD.

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

Progress in Neuro-Psychopharmacology &amp; Biological Psychiatry

ISSN

0278-5846

e-ISSN

1878-4216

Svazek periodika

142

Číslo periodika v rámci svazku

October

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

19

Strana od-do

111491

Kód UT WoS článku

001574067300004

EID výsledku v databázi Scopus

2-s2.0-105015873383