The DOI matches its Crossref record; 109 of the 111 references it cites were found in a registry or an index.
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
Open accessAbstract
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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In the citing paper
“preserves synaptic integrity”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Esposito et al., 2006
In the citing paper
“eliminates the earliest cognitive deficits in a transgenic mouse AD model”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Esposito et al., 2006
In the citing paper
“reduction of mitochondrial superoxide dismutase (MnSOD) levels accelerates AD-like pathology in a transgenic mouse model of AD”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Esposito et al., 2006
In the citing paper
“overexpression of MnSOD decreases Aβ-processing”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Esposito et al., 2006
In the citing paper
“Elevated SOD expression is indicative of the high levels of oxidative stress associated with Aβ plaques in Alzheimer’s disease brains [21,48,80,104].”
From Centella Asiatica Improves Memory and Promotes Antioxidative Signaling in 5XFAD Mice (2019) · cites this paper as [104]
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Mattson, M. P., Gleichmann, M., & Cheng, A. (2008) · Neuron · doi:10.1016/j.neuron.2008.10.010 · Cited by 1,081
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Metadata
- 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)
- 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
- 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
- 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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