Cited by 254Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchMitochondrial Function and Pathology

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Reduction in mitochondrial superoxide dismutase modulates Alzheimer’s disease-like pathology and accelerates the onset of behavioral changes in human amyloid precursor protein transgenic mice

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Esposito, Luke, Raber, Jacob, Kekonius, Lisa, Yan, Fengrong, Yu, Giu-Qiu, Bien-Ly, Nga, Puoliväli, Jukka, Scearce-Levie, Kimberly, Masliah, Eliezer, Mucke, Lennart·2006·The Journal of Neuroscience

DOI 10.1523/jneurosci.0482-06.2006PMC PMC6674260

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Abstract

Alzheimer's disease (AD) is associated with accumulations of amyloid-beta (Abeta) peptides, oxidative damage, mitochondrial dysfunction, neurodegeneration, and dementia. The mitochondrial antioxidant manganese superoxide dismutase-2 (Sod2) might protect against these alterations. To test this hypothesis, we inactivated one Sod2 allele (Sod2(+/-)) in human amyloid precursor protein (hAPP) transgenic mice, reducing Sod2 activity to approximately 50% of that in Sod2 wild-type (Sod2(+/+)) mice. A reduction in Sod2 activity did not obviously impair mice without hAPP/Abeta expression. In hAPP mice, however, it accelerated the onset of behavioral alterations and of deficits in prepulse inhibition of acoustic startle, a measure of sensorimotor gating. In these mice, it also worsened hAPP/Abeta-dependent depletion of microtubule-associated protein 2, a marker of neuronal dendrites. Sod2 reduction decreased amyloid plaques in the brain parenchyma but promoted the development of cerebrovascular amyloidosis, gliosis, and plaque-independent neuritic dystrophy. Sod2 reduction also increased the DNA binding activity of the transcription factor nuclear factor kappaB. These results suggest that Sod2 protects the aging brain against hAPP/Abeta-induced impairments. Whereas reductions in Sod2 would be expected to trigger or exacerbate neuronal and vascular pathology in AD, increasing Sod2 activity might be of therapeutic benefit.

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See all 254

Authors: Esposito, L., Raber, J., Kekonius, L., Yan, F., Yu, G.-Q., Bien-Ly, N., Puoliväli, J., Scearce-Levie, K., Masliah, E., & Mucke, L.
Affiliations: University of California, San Francisco (US)
University of California San Diego (US)
Gladstone Institutes (US)
ORCID: Esposito, Luke
Raber, Jacob
Scearce-Levie, Kimberly
Masliah, Eliezer
Mucke, Lennart
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2006-05-10
Volume: 26
Issue: 19
Pages: 5167-5179
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.0482-06.2006
PMC: PMC6674260
OpenAlex: W2109187744
Cited by: 254
References: 111
Citations by year: 2026: 5 · 2025: 6 · 2024: 9 · 2023: 12 · 2022: 14 · 2021: 16 · 2020: 18 · 2019: 8 · 2018: 11 · 2017: 13 · 2016: 13 · 2015: 16 · 2014: 16 · 2013: 10 · 2012: 12
FWCI: 10.60
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 184 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (AG‐022074, AG011385)
National Institute on Aging (AG011385, AG022074, P01AG022074)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords: Alzheimer's disease, manganese superoxide dismutase, amyloid precursor protein transgenic mice, amyloid-beta, mitochondrial dysfunction, oxidative stress, prepulse inhibition, sensorimotor gating, MAP2, dendritic degeneration, gliosis, neuritic dystrophy, nuclear factor-kappaB, behavioral deficits, neuroprotection
MeSH terms: Superoxide Dismutase 2, Alzheimer Disease, Animals, Mental Disorders, Enzyme Activation, Humans, Mice, Transgenic, Mitochondria, Receptors, Cell Surface, Superoxide Dismutase, Amyloid beta-Protein Precursor, Mice, Protease Nexins

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Reduction in mitochondrial superoxide dismutase modulates Alzheimer’s disease-like pathology and accelerates the onset of behavioral changes in human amyloid precursor protein transgenic mice

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