Loss of NEIL1 causes defects in olfactory function in mice

Chandrika Canugovi, Magdalena Misiak, Morten Scheibye-Knudsen, Deborah L. Croteau, Mark P. Mattson, Vilhelm A. Bohr

Research output: Contribution to journalArticle

Abstract

Oxidative DNA damage accumulation has been implicated in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. The base excision repair pathway is a primary responder to oxidative DNA damage. Effects of loss of base excision repair on normal brain function is a relatively nascent area of research that needs further exploration for better understanding of related brain diseases. Recently, we found that loss of a versatile DNA glycosylase endonuclease 8-like 1 (NEIL1) causes deficits in spatial memory retention using the Morris water maze test. Furthermore, we found that there is a significant loss of NEIL1 enzyme levels and its activity in postmortem Alzheimer's disease brains. Based on the Allen Brain Atlas in situ hybridization data, the expression levels of Neil1 messenger RNA are higher in the olfactory bulb compared with other areas of the brain. Olfaction in mice is a central brain function that involves many central nervous system pathways. Here, we studied the effect of complete loss of Neil1 gene on olfactory function. We explored olfactory function in mice with 3 different behavioral tests namely, olfactory sensitivity, performance, and buried food tests. Neil1-/- mice performed poorly compared with wild-type mice in all 3 tests. Our data indicate that loss of Neil1 causes olfactory function deficits supporting our previous findings and that normal brain function requires robust DNA repair.

Original languageEnglish (US)
Pages (from-to)1007-1012
Number of pages6
JournalNeurobiology of Aging
Volume36
Issue number2
DOIs
StatePublished - Feb 1 2015
Externally publishedYes

Fingerprint

Brain
DNA Repair
DNA Damage
Alzheimer Disease
DNA Glycosylases
Smell
Atlases
Olfactory Bulb
Deoxyribonuclease I
Brain Diseases
Neurodegenerative Diseases
In Situ Hybridization
Parkinson Disease
Central Nervous System
Food
Messenger RNA
Water
Enzymes
Research
Genes

Keywords

  • Aging, smell
  • Base excision repair
  • DNA repair
  • Glycosylase
  • NEIL1
  • Olfactory sense
  • Oxidative DNA damage
  • Oxidative stress

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)
  • Aging
  • Developmental Biology
  • Geriatrics and Gerontology

Cite this

Canugovi, C., Misiak, M., Scheibye-Knudsen, M., Croteau, D. L., Mattson, M. P., & Bohr, V. A. (2015). Loss of NEIL1 causes defects in olfactory function in mice. Neurobiology of Aging, 36(2), 1007-1012. https://doi.org/10.1016/j.neurobiolaging.2014.09.026

Loss of NEIL1 causes defects in olfactory function in mice. / Canugovi, Chandrika; Misiak, Magdalena; Scheibye-Knudsen, Morten; Croteau, Deborah L.; Mattson, Mark P.; Bohr, Vilhelm A.

In: Neurobiology of Aging, Vol. 36, No. 2, 01.02.2015, p. 1007-1012.

Research output: Contribution to journalArticle

Canugovi, C, Misiak, M, Scheibye-Knudsen, M, Croteau, DL, Mattson, MP & Bohr, VA 2015, 'Loss of NEIL1 causes defects in olfactory function in mice', Neurobiology of Aging, vol. 36, no. 2, pp. 1007-1012. https://doi.org/10.1016/j.neurobiolaging.2014.09.026
Canugovi C, Misiak M, Scheibye-Knudsen M, Croteau DL, Mattson MP, Bohr VA. Loss of NEIL1 causes defects in olfactory function in mice. Neurobiology of Aging. 2015 Feb 1;36(2):1007-1012. https://doi.org/10.1016/j.neurobiolaging.2014.09.026
Canugovi, Chandrika ; Misiak, Magdalena ; Scheibye-Knudsen, Morten ; Croteau, Deborah L. ; Mattson, Mark P. ; Bohr, Vilhelm A. / Loss of NEIL1 causes defects in olfactory function in mice. In: Neurobiology of Aging. 2015 ; Vol. 36, No. 2. pp. 1007-1012.
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