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Loss of NEIL1 causes defects in olfactory function in mice
Chandrika Canugovi1, Magdalena Misiak2, Morten Scheibye-Knudsen1
1Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Neurobiology of Aging
|December 3, 2014
Summary
Loss of the NEIL1 DNA repair enzyme impairs olfactory function in mice. This finding highlights the critical role of DNA repair in maintaining normal brain function and suggests NEIL1
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Oxidative DNA damage is linked to neurodegenerative diseases like Alzheimer's and Parkinson's.
- The base excision repair pathway combats oxidative DNA damage.
- The role of base excision repair in brain function is under-researched.
Purpose of the Study:
- To investigate the impact of NEIL1 gene loss on olfactory function.
- To explore the necessity of NEIL1 for normal olfaction in mice.
Main Methods:
- Studied olfactory function in NEIL1-deficient (Neil1(-/-)) mice and wild-type controls.
- Utilized three behavioral tests: olfactory sensitivity, performance, and buried food tests.
Main Results:
- NEIL1 deficiency led to significant deficits in olfactory sensitivity, performance, and buried food retrieval.
- NEIL1(-/-) mice performed substantially worse than wild-type mice across all olfactory tests.
Conclusions:
- Complete loss of the NEIL1 gene impairs olfactory function.
- Robust DNA repair is essential for normal brain function, including olfaction.
