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Influence of DNA repair deficiency in the development and progression of Alzheimer's Disease in mouse model

Grant number: 13/11052-1
Support Opportunities:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): August 12, 2013
Effective date (End): July 11, 2014
Field of knowledge:Biological Sciences - Genetics - Mutagenesis
Principal Investigator:Elza Tiemi Sakamoto Hojo
Grantee:Giovana da Silva Leandro
Supervisor: Vilhelm A. Bohr
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Research place: National Institutes of Health, Baltimore (NIH), United States  
Associated to the scholarship:12/07879-5 - Evaluation of the efficiency of DNA repair mechanisms and gene expression in lymphocytes from patients with Alzheimer's Disease, BP.DR


Oxidative stress seems to be strictly correlated with the development and progression of neurodegenerative diseases and also with the aging process itself. It has been reported that oxidative stress plays a role in the development of Alzheimer's disease (AD), which is a neurodegenerative disease with large impact on public health. Since base excision repair (BER) seems to be the main mechanism for the repair of oxidative damage, comparisons between functional alterations in BER pathways and dysfunctions of AD can be an interesting approach to study risk factors for AD. The present proposal aims to analyze mitochondrial and nuclei DNA lesions in the brain of AD mouse model in comparison with polymerase ² deficient mice (deficiency in BER mechanisms), using the Long PCR amplification technique. Moreover, our purpose is to measure BER activity in protein extracts from various brain regions, and to undertake a behavioral analysis by comparing AD mouse models and mouse models deficient for Polymerase ². Besides, it will be performed comparisons between gene expression profiles of mouse brain and peripheral blood mononuclear cells; these cells may represent important targets in terms of biomarkers for AD. Studies on this approach are important to establish a relationship between deficiency in DNA repair and the AD disease. The results may be important to improve the knowledge in the area, and also to provide novel information which can be useful for diagnosis, prognosis and treatment of AD. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
SYKORA, P.; KANNO, S.; AKBARI, M.; KULIKOWICZ, T.; BAPTISTE, B. A.; LEANDRO, G. S.; LU, H.; TIAN, J.; MAY, A.; BECKER, K. A.; et al. DNA Polymerase Beta Participates in Mitochondrial DNA Repair. MOLECULAR AND CELLULAR BIOLOGY, v. 37, n. 16, . (13/11052-1)
SYKORA, PETER; MISIAK, MAGDALENA; WANG, YUE; GHOSH, SOMNATH; LEANDRO, GIOVANA S.; LIU, DONG; TIAN, JANE; BAPTISTE, BEVERLY A.; CONG, WEI-NA; BRENERMAN, BORIS M.; et al. DNA polymerase beta deficiency leads to neurodegeneration and exacerbates Alzheimer disease phenotypes. Nucleic Acids Research, v. 43, n. 2, p. 943-959, . (13/11052-1)

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