The Silence of Biological Age Testing
Unparalleled in precision and reliability and built on decades of research
Over the past 10 years, science has gained a modern and reliable way to measure not only the various biomarkers associated with diseases, but the root cause of disease - aging. With the help of modern technologies in molecular biology and genetics, we are able to measure the rate of cell aging, which is reflected in the pattern of DNA methylation and is called epigenetic age.
Epigenetics is the study of how our environment and lifestyle affect the way our genes work. Thanks to epigenetic signatures, we can study the influence of various substances and lifestyle on the work of genes associated with human aging. And with the help of AI, we can get closer to the personalization of medicines and the individual selection of the optimal prolongation strategy.
Future of epigenetics?
Technology
Now there are more than 50 methods for determining biological age based on DNA methylation. We analyzed them all and identified the methylation sites that are common to all of them. Based on these shared sites, you created a model for determining biological age and validated it on a sample of people aged 9 to 100 years (R2 = 0.92). Our model proved to be as accurate as other models in predicting biological age (MAD 4.1). But it is 3 times cheaper in the execution of the text and faster in obtaining a result for the client. Due to some technical innovations in the method for determining the level of methylation, it is different from all competitors in the market and is patentable.
Technology
Now there are more than 50 methods for determining biological age based on DNA methylation. We analyzed them all and identified the methylation sites that are common to all of them. Based on these shared sites, you created a model for determining biological age and validated it on a sample of people aged 9 to 100 years (R2 = 0.92). Our model proved to be as accurate as other models in predicting biological age (MAD 4.1). But it is 3 times cheaper in the execution of the text and faster in obtaining a result for the client. Due to some technical innovations in the method for determining the level of methylation, it is different from all competitors in the market and is patentable.
01
Innovative technology, which speeds up sample processing and reduces costs
02
Own laboratory at Potsdam Science Park
Solutions For Every Business Need
Publication
Developmental programming of aging trajectory
Abstract: There is accumulating evidence that aging phenotype and longevity may be developmentally programmed. Main mechanisms linking developmental conditions to later-life health outcomes include persistent changes in epigenetic regulation, (re)programming of major endocrine axes such as growth hormone/insulin-like growth factor axis and hypothalamic-pituitary-adrenal axis and also early-life immune maturation. Recently, evidence has also been generated on the role of telomere biology in developmental programming of aging trajectory. In addition, persisting changes of intestinal microbiota appears to be crucially involved in these processes. In this review, experimental and epidemiological evidence on the role of early-life conditions in programming of aging phenotypes are presented and mechanisms potentially underlying these associations are discussed. Read more.
Vaiserman, Alexander, Alexander Koliada, and Oleh Lushchak. 2018. “Developmental Programming of Aging Trajectory.” Ageing Research Reviews 47 (November): 105–122.
Abstract: There is accumulating evidence that aging phenotype and longevity may be developmentally programmed. Main mechanisms linking developmental conditions to later-life health outcomes include persistent changes in epigenetic regulation, (re)programming of major endocrine axes such as growth hormone/insulin-like growth factor axis and hypothalamic-pituitary-adrenal axis and also early-life immune maturation. Recently, evidence has also been generated on the role of telomere biology in developmental programming of aging trajectory. In addition, persisting changes of intestinal microbiota appears to be crucially involved in these processes. In this review, experimental and epidemiological evidence on the role of early-life conditions in programming of aging phenotypes are presented and mechanisms potentially underlying these associations are discussed. Read more.
Vaiserman, Alexander, Alexander Koliada, and Oleh Lushchak. 2018. “Developmental Programming of Aging Trajectory.” Ageing Research Reviews 47 (November): 105–122.
Chapter 32 - Epigenetic Programming of Human Disease and Aging
Abstract: There is accumulating evidence that aging phenotype and longevity may be developmentally programmed. Main mechanisms linking developmental conditions to later-life health outcomes include persistent changes in epigenetic regulation, (re)programming of major endocrine axes such as growth hormone/insulin-like growth factor axis and hypothalamic-pituitary-adrenal axis and also early-life immune maturation. Recently, evidence has also been generated on the role of telomere biology in developmental programming of aging trajectory. In addition, persisting changes of intestinal microbiota appears to be crucially involved in these processes. In this review, experimental and epidemiological evidence on the role of early-life conditions in programming of aging phenotypes are presented and mechanisms potentially underlying these associations are discussed. Read more.
Vaiserman, Alexander, Alexander Koliada, and Oleh Lushchak. 2018. Chapter 32 - Epigenetic Programming of Human Disease and Aging. Epigenetics in Human Disease (Second Edition). January: 975–992.
Abstract: There is accumulating evidence that aging phenotype and longevity may be developmentally programmed. Main mechanisms linking developmental conditions to later-life health outcomes include persistent changes in epigenetic regulation, (re)programming of major endocrine axes such as growth hormone/insulin-like growth factor axis and hypothalamic-pituitary-adrenal axis and also early-life immune maturation. Recently, evidence has also been generated on the role of telomere biology in developmental programming of aging trajectory. In addition, persisting changes of intestinal microbiota appears to be crucially involved in these processes. In this review, experimental and epidemiological evidence on the role of early-life conditions in programming of aging phenotypes are presented and mechanisms potentially underlying these associations are discussed. Read more.
Vaiserman, Alexander, Alexander Koliada, and Oleh Lushchak. 2018. Chapter 32 - Epigenetic Programming of Human Disease and Aging. Epigenetics in Human Disease (Second Edition). January: 975–992.
Early-life adversity and long-term neurobehavioral outcomes: epigenome as a bridge?
Abstract: Accumulating evidence suggests that adversities at critical periods in early life, both pre- and postnatal, can lead to neuroendocrine perturbations, including hypothalamic-pituitary-adrenal axis dysregulation and inflammation persisting up to adulthood. This process, commonly referred to as biological embedding, may cause abnormal cognitive and behavioral functioning, including impaired learning, memory, and depressive- and anxiety-like behaviors, as well as neuropsychiatric outcomes in later life. Currently, the regulation of gene activity by epigenetic mechanisms is suggested to be a key player in mediating the link between adverse early-life events and adult neurobehavioral outcomes. Role of particular genes, including those encoding glucocorticoid receptor, brain-derived neurotrophic factor, as well as arginine vasopressin and corticotropin-releasing factor, has been demonstrated in triggering early adversity-associated pathological conditions. This review is focused on the results from human studies highlighting the causal role of epigenetic mechanisms in mediating the link between the adversity during early development, from prenatal stages through infancy, and adult neuropsychiatric outcomes. The modulation of epigenetic pathways involved in biological embedding may provide promising direction toward novel therapeutic strategies against neurological and cognitive dysfunctions in adult life. Read more.
Vaiserman, Alexander M, Alexander K. Koliada. 2017 “Early-life adversity and long-term neurobehavioral outcomes: epigenome as a bridge?” Hum Genomics 11: 34.
Abstract: Accumulating evidence suggests that adversities at critical periods in early life, both pre- and postnatal, can lead to neuroendocrine perturbations, including hypothalamic-pituitary-adrenal axis dysregulation and inflammation persisting up to adulthood. This process, commonly referred to as biological embedding, may cause abnormal cognitive and behavioral functioning, including impaired learning, memory, and depressive- and anxiety-like behaviors, as well as neuropsychiatric outcomes in later life. Currently, the regulation of gene activity by epigenetic mechanisms is suggested to be a key player in mediating the link between adverse early-life events and adult neurobehavioral outcomes. Role of particular genes, including those encoding glucocorticoid receptor, brain-derived neurotrophic factor, as well as arginine vasopressin and corticotropin-releasing factor, has been demonstrated in triggering early adversity-associated pathological conditions. This review is focused on the results from human studies highlighting the causal role of epigenetic mechanisms in mediating the link between the adversity during early development, from prenatal stages through infancy, and adult neuropsychiatric outcomes. The modulation of epigenetic pathways involved in biological embedding may provide promising direction toward novel therapeutic strategies against neurological and cognitive dysfunctions in adult life. Read more.
Vaiserman, Alexander M, Alexander K. Koliada. 2017 “Early-life adversity and long-term neurobehavioral outcomes: epigenome as a bridge?” Hum Genomics 11: 34.
