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Published on: March 16, 2016
Apocynin administration does not improve behavioral and neuropathological deficits in a transgenic mouse model of
Magali Dumont1, Cliona Stack, Ceyhan Elipenhali
1Weill Cornell Medical College, Department of Neurology and Neuroscience, 525 East 68th Street, New York, NY 10065, USA. mad2138@med.cornell.edu
Abstract:
In addition to mitochondria, NADPH oxidase (NOX) is a source of oxidative stress, which can induce oxidative damage in Alzheimer's disease (AD). For this reason, several groups have investigated the effect of its inhibition. In AD mice, NADPH oxidase 2 (NOX2) deficiency improved behavior and cerebrovascular function, and reduced oxidative stress. In our study, we administered the NOX inhibitor apocynin to Tg19959 mice, and found that it did not improve cognitive and synaptic deficits, and did not decrease amyloid deposition, microgliosis and hyperphosphorylated tau. However, apocynin reduced carbonyl levels in the cerebral cortex but not the hippocampus, which may have not been sufficient to ameliorate symptoms. Also, the reduction of NOX-mediated oxidative stress may not be sufficient to prevent AD, since other sources of reactive oxygen species such as mitochondria may be more important.
Insights
In Alzheimer's disease (AD), inhibiting NADPH oxidase (NOX) with apocynin did not improve cognitive deficits or AD pathology. Other oxidative stress sources like mitochondria may be more critical for AD progression.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Oxidative stress from NADPH oxidase (NOX) contributes to Alzheimer's disease (AD) pathology.
- Previous studies showed NOX inhibition benefits in AD mouse models.
Purpose of the Study:
- To investigate the therapeutic potential of the NOX inhibitor apocynin in a mouse model of Alzheimer's disease.
Main Methods:
- Administration of apocynin to Tg19959 mice, an AD model.
- Assessment of cognitive function, synaptic deficits, amyloid deposition, microgliosis, hyperphosphorylated tau, and oxidative stress markers (carbonyl levels).
Main Results:
- Apocynin treatment did not improve cognitive and synaptic deficits in Tg19959 mice.
- Apocynin failed to reduce amyloid deposition, microgliosis, or hyperphosphorylated tau.
- Apocynin decreased carbonyl levels in the cerebral cortex but not the hippocampus.
Conclusions:
- Inhibition of NOX-derived oxidative stress alone may not be sufficient to ameliorate Alzheimer's disease symptoms.
- Mitochondria and other reactive oxygen species sources might play a more significant role in AD pathogenesis.
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