Результаты исследований: Научные публикации в периодических изданиях › статья › Рецензирование
Candidate SNP markers of familial and sporadic Alzheimer's diseases are predicted by a significant change in the affinity of TATA-binding protein for human gene promoters. / Ponomarenko, Petr; Chadaeva, Irina; Rasskazov, Dmitry A. и др.
в: Frontiers in Aging Neuroscience, Том 9, № JUL, 231, 20.07.2017, стр. 231.Результаты исследований: Научные публикации в периодических изданиях › статья › Рецензирование
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TY - JOUR
T1 - Candidate SNP markers of familial and sporadic Alzheimer's diseases are predicted by a significant change in the affinity of TATA-binding protein for human gene promoters
AU - Ponomarenko, Petr
AU - Chadaeva, Irina
AU - Rasskazov, Dmitry A.
AU - Sharypova, Ekaterina
AU - Kashina, Elena V.
AU - Drachkova, Irina
AU - Zhechev, Dmitry
AU - Ponomarenko, Mikhail P.
AU - Savinkova, Ludmila K.
AU - Kolchanov, Nikolay
PY - 2017/7/20
Y1 - 2017/7/20
N2 - While year after year, conditions, quality, and duration of human lives have been improving due to the progress in science, technology, education, and medicine, only eight diseases have been increasing in prevalence and shortening human lives because of premature deaths according to the retrospective official review on the state of US health, 1990-2010. These diseases are kidney cancer, chronic kidney diseases, liver cancer, diabetes, drug addiction, poisoning cases, consequences of falls, and Alzheimer's disease (AD) as one of the leading pathologies. There are familial AD of hereditary nature (~4% of cases) and sporadic AD of unclear etiology (remaining ~96% of cases; i.e., non-familial AD). Therefore, sporadic AD is no longer a purely medical problem, but rather a social challenge when someone asks oneself: "What can I do in my own adulthood to reduce the risk of sporadic AD at my old age to save the years of my lifespan from the destruction caused by it?" Here, we combine two computational approaches for regulatory SNPs: Web service SNP_TATA_Comparator for sequence analysis and a PubMed-based keyword search for articles on the biochemical markers of diseases. Our purpose was to try to find answers to the question: "What can be done in adulthood to reduce the risk of sporadic AD in old age to prevent the lifespan reduction caused by it?" As a result, we found 89 candidate SNP markers of familial and sporadic AD (e.g., rs562962093 is associated with sporadic AD in the elderly as a complication of stroke in adulthood, where natural marine diets can reduce risks of both diseases in case of the minor allele of this SNP). In addition, rs768454929, and rs761695685 correlate with sporadic AD as a comorbidity of short stature, where maximizing stature in childhood and adolescence as an integral indicator of health can minimize (or even eliminate) the risk of sporadic AD in the elderly. After validation by clinical protocols, these candidate SNP markers may become interesting to the general population [may help to choose a lifestyle (in childhood, adolescence, and adulthood) that can reduce the risks of sporadic AD, its comorbidities, and complications in the elderly].
AB - While year after year, conditions, quality, and duration of human lives have been improving due to the progress in science, technology, education, and medicine, only eight diseases have been increasing in prevalence and shortening human lives because of premature deaths according to the retrospective official review on the state of US health, 1990-2010. These diseases are kidney cancer, chronic kidney diseases, liver cancer, diabetes, drug addiction, poisoning cases, consequences of falls, and Alzheimer's disease (AD) as one of the leading pathologies. There are familial AD of hereditary nature (~4% of cases) and sporadic AD of unclear etiology (remaining ~96% of cases; i.e., non-familial AD). Therefore, sporadic AD is no longer a purely medical problem, but rather a social challenge when someone asks oneself: "What can I do in my own adulthood to reduce the risk of sporadic AD at my old age to save the years of my lifespan from the destruction caused by it?" Here, we combine two computational approaches for regulatory SNPs: Web service SNP_TATA_Comparator for sequence analysis and a PubMed-based keyword search for articles on the biochemical markers of diseases. Our purpose was to try to find answers to the question: "What can be done in adulthood to reduce the risk of sporadic AD in old age to prevent the lifespan reduction caused by it?" As a result, we found 89 candidate SNP markers of familial and sporadic AD (e.g., rs562962093 is associated with sporadic AD in the elderly as a complication of stroke in adulthood, where natural marine diets can reduce risks of both diseases in case of the minor allele of this SNP). In addition, rs768454929, and rs761695685 correlate with sporadic AD as a comorbidity of short stature, where maximizing stature in childhood and adolescence as an integral indicator of health can minimize (or even eliminate) the risk of sporadic AD in the elderly. After validation by clinical protocols, these candidate SNP markers may become interesting to the general population [may help to choose a lifestyle (in childhood, adolescence, and adulthood) that can reduce the risks of sporadic AD, its comorbidities, and complications in the elderly].
KW - Alzheimer's disease
KW - Expression change
KW - Gene
KW - Promoter
KW - Single nucleotide polymorphism
KW - SNP marker
KW - TATA-binding protein
KW - TBP-binding site
KW - TRANSCRIPTION FACTOR-BINDING
KW - MYOCARDIAL-INFARCTION
KW - gene
KW - single nucleotide polymorphism
KW - AMYOTROPHIC-LATERAL-SCLEROSIS
KW - POLYMERASE-II TRANSCRIPTION
KW - SENILE PLAQUES
KW - DIABETES-MELLITUS
KW - HUMAN HEREDITARY-DISEASES
KW - expression change
KW - AMYLOID-BETA
KW - MOUSE MODEL
KW - promoter
KW - PARKINSONS-DISEASE
UR - http://www.scopus.com/inward/record.url?scp=85027168071&partnerID=8YFLogxK
U2 - 10.3389/fnagi.2017.00231
DO - 10.3389/fnagi.2017.00231
M3 - Article
C2 - 28775688
AN - SCOPUS:85027168071
VL - 9
SP - 231
JO - Frontiers in Aging Neuroscience
JF - Frontiers in Aging Neuroscience
SN - 1663-4365
IS - JUL
M1 - 231
ER -
ID: 9965653