Cited by 25Alzheimer's disease research and treatmentsMitochondrial Function and PathologyNerve injury and regeneration

Nerve growth factor attenuates oxidant‐induced β‐amyloid neurotoxicity in sporadic Alzheimer’s disease cybrids

Onyango, Isaac G., Ahn, Jin‐Young, Tuttle, Jeremy B., Bennett Jr, James P., Swerdlow, Russell H.·2010·Journal of Neurochemistry

Abstract

Although mitochondrial dysfunction has been linked to Alzheimer's disease (AD), it is not fully understood how this dysfunction may induce neuronal death. In this study, we show that transmitochondrial hybrid cells (cybrids) expressing mitochondrial genes from patients with sporadic AD (SAD) have substantial alterations in basal upstream tyrosine kinase signaling and downstream serine-threonine kinase signaling that are mediated by intracellular free radicals. This is associated with reduced tropomyocin receptor kinase (TrkA) and p75 neurotrophin receptor receptor expression that profoundly alters nerve growth factor signaling, increases generation of Aβ and decreases viability. Many of these observed effects in SAD cybrids would be predicted to increase risk of premature neuronal death and reduce resistance to stressors and add further support for the pathogenic role of mtDNA expression in the pathogenesis of SAD.

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Crossref · 10.1111/j.1471-4159.2010.06871.x

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66 of 66 references verified0 citation errors · 0 not checkable

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Authors
Onyango, I. G., Ahn, J., Tuttle, J. B., Bennett Jr, J. P., & Swerdlow, R. H.
Affiliations
  • University of Kansas Medical Center (US)
  • Seoul Medical Center (KR)
  • University of Virginia (US)
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2010-09
Volume
114
Issue
6
Pages
1605-1618
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
OpenAlex
W1640499549
Cited by
25
References
66
Citations by year
2023: 3 · 2022: 1 · 2021: 1 · 2020: 3 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 3 · 2014: 1 · 2013: 2
FWCI
1.08
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
Keywords
nerve growth factor, amyloid-beta, sporadic Alzheimer's disease, cybrids, mitochondrial dysfunction, mitochondrial DNA, TrkA, p75 neurotrophin receptor, tyrosine kinase signaling, free radicals, neuronal cell death, neurotoxicity
MeSH terms
Acetylcysteine, Aged, Alzheimer Disease, Cell Survival, Cells, Cultured, DNA, Mitochondrial, Female, Glutathione, Humans, Hybrid Cells, Male, Mitochondria, Nerve Growth Factors, Neurons, Peptide Fragments, Phosphorylation, Tyrosine, Signal Transduction, Amyloid beta-Peptides, NF-kappa B, Reactive Oxygen Species, Receptors, Nerve Growth Factor, Receptor, trkA, Mitogen-Activated Protein Kinases, Proto-Oncogene Proteins c-akt

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