Mutations of TP53 Gene and Oxidative Stress in Alzheimer’s Disease Patients

Autor:	Wojciech Kozubski, Izabela Postrach, Jolanta Dorszewska, Anna Oczkowska, Jolanta Florczak-Wyspianska, Paweł P. Jagodziński, Michal Prendecki, Agata Rozycka, Mateusz Dezor
Rok vydání:	2014
Předmět:	Silent mutation medicine.medical_specialty Mutation endocrine system diseases DNA damage General Medicine Biology Bioinformatics medicine.disease_cause Pathogenesis chemistry.chemical_compound Exon Endocrinology chemistry Internal medicine medicine Deoxyguanosine neoplasms Gene Oxidative stress
Zdroj:	Advances in Alzheimer's Disease. :24-32
ISSN:	2169-2467 2169-2459
DOI:	10.4236/aad.2014.31004
Popis:	Alzheimer’s disease (AD) leads to the generation of β-amyloid (Aβ), which may damage DNA and thus lead to apoptosis induction by the p53 pathway. Dysfunction of the p53 protein may then be connected with the development of AD. Studies were conducted on 28 AD patients and 30 non-AD controls. Analysis of TP53 mutations in exon 7 was performed on DNA isolated from whole blood and biochemical parameters in the peripheral lymphocytes of these individuals. Our study showed a silent mutation TP53 C708T (21%) [p TP53 C748A (4%) only in the AD patients. Moreover, in AD patients with the TP53 C748A mutation, the level of 8-oxo-2’- deoxyguanosine (8-oxo2dG) was more than 5 times higher than the average level in this study group. In AD patients with the wild-type TP53 gene, the level of 8-oxo2dG was correlated with the level of protein p53 (R = +0.7388, p TP53 (p TP53 (C748A, C708T) may be associated with pathogenesis of AD.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_________::39c8f89bc4fde5b415400c55eb961fa3 https://doi.org/10.4236/aad.2014.31004 Zobrazit plný text záznamu