Hostname: page-component-586b7cd67f-g8jcs Total loading time: 0 Render date: 2024-11-20T15:33:06.107Z Has data issue: false hasContentIssue false
  • English
  • Français

Lack of association of neprilysin gene polymorphisms with Alzheimer's disease in a southern Chinese community

Published online by Cambridge University Press:  02 March 2009

Yan Fu ,
Ai Feng Li ,
Jia Jun Shi ,
Mou Ni Tang ,
Yang Bo Guo  and
Zhen Huan Zhao
Yan Fu*
Affiliation:
Guangzhou Psychiatric Hospital, Guangzhou, Guangdong, China
Ai Feng Li
Affiliation:
Guangzhou Psychiatric Hospital, Guangzhou, Guangdong, China
Jia Jun Shi
Affiliation:
Department of Psychiatry, University of Chicago, Chicago, Illinois, USA
Mou Ni Tang
Affiliation:
Guangzhou Psychiatric Hospital, Guangzhou, Guangdong, China
Yang Bo Guo
Affiliation:
Guangzhou Psychiatric Hospital, Guangzhou, Guangdong, China
Zhen Huan Zhao
Affiliation:
Guangzhou Psychiatric Hospital, Guangzhou, Guangdong, China
*
Correspondence should be addressed to: Yan Fu, Guangzhou Psychiatric Hospital, Guangzhou, Guangdong, China. Phone: +852 906 26680; Fax: +852 263 65090. Email: [email protected].
Get access Rights & Permissions [Opens in a new window]

Abstract

Background: Increasing evidence suggests that neprilysin (NEP) may be the major degrading enzyme of amyloid beta (Aβ) in the brain and the NEP gene has been proposed as a candidate gene for Alzheimer's disease (AD). Association results between the NEP gene and AD are still preliminary. This study investigates the effect of the polymorphisms of −204G/C and 159C/T in the NEP gene on the development of sporadic Alzheimer's disease (SAD) in a southern Chinese community.

Method: 236 sporadic late-onset AD patients were recruited from Guangzhou Psychiatric Hospital in southern China, and 332 healthy elderly controls were enrolled from three old age homes in suburban Guangzhou. NEP and ApoE genotype were determined by PCR–RFLP.

Results: No differences in genotypic and allelic frequencies of −204G/C and 159C/T polymorphisms in NEP were found between AD and control group (for −204G/C genotype: χ2 = 2.34, P > 0.05; for allele: χ2 = 2.31, P > 0.05; for 159C/T genotype: χ2 = 1.34, P > 0.05; for allele: χ2 = 0.88, P > 0.05). Neither was any difference found in genotypic and allelic frequency when stratified by sex or by ApoE ε4 allele (P > 0.05).

Conclusions: Our results suggest that −204G/C and 159C/T polymorphisms of the NEP gene may not be associated with SAD. Moreover, both sex and ApoE ε4 allele do not affect the distribution of NEP gene polymorphisms.

Keywords

NEPapolipoprotein EAlzheimer's diseasegene polymorphism
Type
Research Article
Information
International Psychogeriatrics , Volume 21 , Issue 2 , April 2009 , pp. 354 - 358
Copyright
Copyright © International Psychogeriatric Association 2009

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Carpentier, M., Robitaille, Y., DesGroseillers, L., Boileau, G. and Marcinkiewicz, M. (2002). Declining expression of neprilysin in Alzheimer disease vasculature: possible involvement in cerebral amyloid angiopathy. Journal of Neuropathology and Experimental Neurology, 61, 849–856.Google Scholar
Clarimon, J. et al. (2003). Possible increased risk for Alzheimer's disease associated with neprilysin gene. Journal of Neural Transmission, 110, 651–657.CrossRefGoogle ScholarPubMed
Goate, A. et al. (1991). Segregation of amissense mutation in the amyloid precursor protein gene with familial Alzheimer's disease. Nature, 349, 704–706.CrossRefGoogle Scholar
Haouas, H., Morello, D., Lavenu, A., Billard, M., Jasmin, C. and Boucheix, C. (1995). Characterization of the 5' region of the CD10/neutral endopeptidase 24.11 gene. Biochemical and Biophysical Research Communications, 207, 933–942.Google Scholar
Helisalmi, S. et al. (2004). Polymorphisms in neprilysin gene affect the risk of Alzheimer's disease in Finnish patients. Journal of Neurology, Neurosurgery and Psychiatry, 75, 1746–1748.CrossRefGoogle ScholarPubMed
Hixson, J. E. and Vernier, D. T. (1990). Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with Hha. Journal of Lipid Research, 31, 545–548.Google Scholar
Iwata, N. et al. (2001). Metabolic regulation of brain Abeta by neprilysin. Science 25, 1550–1552.CrossRefGoogle Scholar
Jiajun, S. et al. (2005). Mutation screening and association study of the neprilysin gene in sporadic Alzheimer's disease in Chinese persons. Journal of Gerontology: Biological Sciences, 60A, 301–306.Google Scholar
Mohajeri, M. H., Kuehnle, K., Li, H., Poirier, R., Tracy, J. and Nitsch, R. M. (2004). Anti-amyloid activity of neprilysin in plaque-bearing mouse models of Alzheimer's disease. FEBS Letters, 26, 16–21.CrossRefGoogle Scholar
Poduslo, S. E. et al. (1999). A familial case of Alzheimer's disease without tau pathology may be linked with chromosome 3 markers. Human Genetics, 105, 32–37.CrossRefGoogle ScholarPubMed
Reilly, C. E. (2001). Neprilysin content is reduced in Alzheimer brain areas. Journal of Neurology, 248, 159–160.Google ScholarPubMed
Rogaev, E. I. et al. (1995). Familial Alzheimer's disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer's disease type 3 gene. Nature, 376, 775–778.CrossRefGoogle Scholar
Sakai, A. et al. (2004). Association of the neprilysin gene with susceptibility to late-onset Alzheimer's disease. Dementia and Geriatric Cognitive Disorder, 17, 164–169.CrossRefGoogle ScholarPubMed
Sherrington, R. et al. (1995). Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease. Nature, 375, 754–760.Google Scholar
Sodeyama, N., Mizusawa, H., Yamada, M., Itoh, Y., Otomo, E. and Matsushita, M. (2001). Lack of association of neprilysin polymorphism with Alzheimer's disease and Alzheimer's disease-type neuropathological changes. Journal of Neurology, Neurosurgery and Psychiatry, 71, 817–818.Google Scholar
Tanzi, R. E., Kovacs, D. M., Kim, T. W., Moir, R. D., Guenette, S. Y. and Wasco, W. (1996). The gene defects responsible for familial Alzheimer's disease. Neurobiology of Disease, 3, 159–168.Google Scholar
Yasojima, K., Akiyama, H., McGeer, E. G. and McGeer, P. L. (2001). Reduced neprilysin in high plaque areas of Alzheimer brain: a possible relationship to deficient degradation of beta-amyloid peptide. Neuroscience Letters, 297, 97–100.CrossRefGoogle Scholar