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

The result's identifiers

  • Result code in 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>

  • Alternative codes found

    RIV/00064203:_____/21:10442107

  • Result on the web

    <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>

Alternative languages

  • Result language

    angličtina

  • Original language name

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

  • Original language description

    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.

  • Czech name

  • Czech description

Classification

  • Type

    C - Chapter in a specialist book

  • CEP classification

  • OECD FORD branch

    30103 - Neurosciences (including psychophysiology)

Result continuities

  • Project

    <a href="/en/project/TO01000215" target="_blank" >TO01000215: Validation of specific mitophagy biomarkers across Alzheimer's disease continuum</a><br>

  • Continuities

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

Others

  • Publication year

    2021

  • Confidentiality

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

Data specific for result type

  • Book/collection name

    Autophagy in Health and Disease

  • ISBN

    978-0-12-822003-0

  • Number of pages of the result

    13

  • Pages from-to

    287-299

  • Number of pages of the book

    454

  • Publisher name

    Elsevier, Academic Press

  • Place of publication

    London

  • UT code for WoS chapter