Aging is a natural consequence of cells as they undergo replication. Occasionally, coding errors may occur within the human genome and cause the processes responsible for maintaining the body’s normal function to become dysfunctional.
Our investigations include research on molecules and mechanisms associated with metabolism and aging, such as regulators of the mammalian target of rapamycin (mTOR) and nicotinamide adenine dinucleotide (NAD+) pathways. By understanding the ways in which mTOR and other genes are involved in the regulation of metabolic pathways, we aim to develop novel techniques toward slowing the human biological clock.
We are working toward achieving this outcome through methods encompassing Metabolism, Genomics, and Gene Therapy. Our techniques include genomic analysis in determining biomarkers correlating with age and developing gene therapy vectors to restore their functions.
Through an extensive database collected from our research on human genomes, we have developed machine learning algorithms that can assess an individual's genome and identify markers of gene expression correlated with metabolic disorders and abnormal aging. This acts as an early predictive tool for health diagnostic purposes. We believe that the use of artificial intelligence within the field of genomics may yield novel and accurate solutions to age-associated health conditions on a hereditary level.
Our research on aging directly involves addressing the ways in which cellular metabolism changes over time. Body systems decline as individuals age, leading to age-associated health conditions such as Alzheimer's Disease and Type II Diabetes. These conditions pose a difficult burden on the world’s health systems and thus we strive to find a solution by reversing the decline caused by the aging process.
As we identify cellular targets that can be modulated to restore metabolic function, we hope to indirectly reduce the burden presented by these health conditions. We are investigating controllers of mitochondrial function and cellular repair machineries. Our findings suggest that a number of mTOR modulators may serve to improve age-associated health conditions and more research is underway.
We are also actively investigating a class of proteins called sirtuins, which can be modulated by the presence of compounds such as NAD+. Deficiencies in sirtuin function can lead to large-scale repercussions such as the development of insulin resistance, a key symptom in the diagnosis of Type II diabetes. Our investigations aim to find efficient ways to replenish available NAD+ supply within cellular mitochondria, so that cells of older individuals may function at a renewed level.
Using the data acquired from our genomics database, we can assess genes that can be targeted for modification.
Using our AI-driven genomic platforms to compare an individual’s genome with a target population, we can identify early symptoms of altered homeostasis resulting from aging or metabolic conditions. Our goal is to develop a method to correct detrimental downregulation and upregulation changes and restore corresponding biological functions, using our advanced gene delivery techniques.