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The NAD+ Precursor Nicotinamide Riboside Rescues Mitochondrial Defects and Neuronal Loss in iPSC derived Cortical Organoid of Alpers' Disease

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F24%3A10479906" target="_blank" >RIV/00216208:11110/24:10479906 - isvavai.cz</a>

  • Result on the web

    <a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=JsD_iY9pCv" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=JsD_iY9pCv</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.7150/ijbs.91624" target="_blank" >10.7150/ijbs.91624</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    The NAD+ Precursor Nicotinamide Riboside Rescues Mitochondrial Defects and Neuronal Loss in iPSC derived Cortical Organoid of Alpers' Disease

  • Original language description

    Alpers&apos; syndrome is an early-onset neurodegenerative disorder usually caused by biallelic pathogenic variants in the gene encoding the catalytic subunit of polymerase-gamma (POLG), which is essential for mitochondrial DNA (mtDNA) replication. The disease is progressive, incurable, and inevitably it leads to death from drug-resistant status epilepticus. The neurological features of Alpers&apos; syndrome are intractable epilepsy and developmental regression, with no effective treatment; the underlying mechanisms are still elusive, partially due to lack of good experimental models. Here, we generated the patient derived induced pluripotent stem cells (iPSCs) from one Alpers&apos; patient carrying the compound heterozygous mutations of A467T (c.1399G&gt;A) and P589L (c.1766C&gt;T), and further differentiated them into cortical organoids and neural stem cells (NSCs) for mechanistic studies of neural dysfunction in Alpers&apos; syndrome. Patient cortical organoids exhibited a phenotype that faithfully replicated the molecular changes found in patient postmortem brain tissue, as evidenced by cortical neuronal loss and depletion of mtDNA and complex I (CI). Patient NSCs showed mitochondrial dysfunction leading to ROS overproduction and downregulation of the NADH pathway. More importantly, the NAD+ precursor nicotinamide riboside (NR) significantly ameliorated mitochondrial defects in patient brain organoids. Our findings demonstrate that the iPSC model and brain organoids are good in vitro models of Alpers&apos; disease; this first-in-its-kind stem cell platform for Alpers&apos; syndrome enables therapeutic exploration and has identified NR as a viable drug candidate for Alpers&apos; disease and, potentially, other mitochondrial diseases with similar causes.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30209 - Paediatrics

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

    2024

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    International Journal of Biological Sciences

  • ISSN

    1449-2288

  • e-ISSN

    1449-2288

  • Volume of the periodical

    20

  • Issue of the periodical within the volume

    4

  • Country of publishing house

    AU - AUSTRALIA

  • Number of pages

    24

  • Pages from-to

    1194-1217

  • UT code for WoS article

    001163043200010

  • EID of the result in the Scopus database

    2-s2.0-85184463063