Autophagic processes in early- and late-onset Alzheimer's disease

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F21%3A10442107" target="_blank" >RIV/00216208:11130/21:10442107 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00064203:_____/21:10442107

Výsledek na webu

<a href="https://doi.org/10.1016/B978-0-12-822003-0.00012-7" target="_blank" >https://doi.org/10.1016/B978-0-12-822003-0.00012-7</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/B978-0-12-822003-0.00012-7" target="_blank" >10.1016/B978-0-12-822003-0.00012-7</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Autophagic processes in early- and late-onset Alzheimer's disease

Popis výsledku v původním jazyce

Autophagy plays a fundamental role in maintaining intracellular homeostasis and cell survival by degrading damaged and unnecessary subcellular components via the lysosome. Impaired autophagy is evident in otherwise &quot;normal&quot; elderly individuals and patients with neurodegenerative diseases, such as Alzheimer&apos;s disease (AD). As the most common type of dementia, AD is an age-associated disease with memory loss as the primary clinical feature as well as extracellular Aβ plaques and intracellular Tau tangles as disease-defining pathological features. Recent studies in animal models of AD, AD patient-derived stem cells, and AD postmortem brain tissues suggest that compromised mitophagy/autophagy plays a causative role in AD progression. Supporting this hypothesis, pharmacological approaches to induce mitophagy/autophagy-e.g., the use of the small natural molecule oxidized nicotinamide adenine dinucleotide (NAD+)-slow AD progression in animal models. This chapter reviews the extant literature on autophagy in AD and covers recent progress on the molecular mechanisms of NAD+-dependent mitophagy/autophagy regulation and mechanisms underlying the anti-AD potential of NAD+. Further studies to define the NAD+-mitophagy/autophagy axis may shed light on novel therapeutics to treat AD and potentially provide insights into other neurodegenerative diseases.

Název v anglickém jazyce

Autophagic processes in early- and late-onset Alzheimer's disease

Popis výsledku anglicky

Autophagy plays a fundamental role in maintaining intracellular homeostasis and cell survival by degrading damaged and unnecessary subcellular components via the lysosome. Impaired autophagy is evident in otherwise &quot;normal&quot; elderly individuals and patients with neurodegenerative diseases, such as Alzheimer&apos;s disease (AD). As the most common type of dementia, AD is an age-associated disease with memory loss as the primary clinical feature as well as extracellular Aβ plaques and intracellular Tau tangles as disease-defining pathological features. Recent studies in animal models of AD, AD patient-derived stem cells, and AD postmortem brain tissues suggest that compromised mitophagy/autophagy plays a causative role in AD progression. Supporting this hypothesis, pharmacological approaches to induce mitophagy/autophagy-e.g., the use of the small natural molecule oxidized nicotinamide adenine dinucleotide (NAD+)-slow AD progression in animal models. This chapter reviews the extant literature on autophagy in AD and covers recent progress on the molecular mechanisms of NAD+-dependent mitophagy/autophagy regulation and mechanisms underlying the anti-AD potential of NAD+. Further studies to define the NAD+-mitophagy/autophagy axis may shed light on novel therapeutics to treat AD and potentially provide insights into other neurodegenerative diseases.

Druh

C - Kapitola v odborné knize

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

<a href="/cs/project/TO01000215" target="_blank" >TO01000215: Validace specifických biomarkerů mitofagie v kontinuu Alzheimerovy nemoci</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2021

Kód důvěrnosti údajů

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

Název knihy nebo sborníku

Autophagy in Health and Disease

ISBN

978-0-12-822003-0

Počet stran výsledku

13

Strana od-do

287-299

Počet stran knihy

454

Název nakladatele

Elsevier, Academic Press

Místo vydání

London

Kód UT WoS kapitoly

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