自己紹介・研究目的
令和4年度修了／ ■SPRING事業 採択学生紹介
東西統合医学専攻
令和4年度 大学院入学
Mariam Karim
マリアム カリム
Maintenance of NAD+ levels during young age prevents sarcopenia （幼少期におけるNAD+レベルの維持はサルコペニアを予防する）
Hi everyone, it is honor for me to introduce myself. My name is Mariam Karim and I am from Pakistan. I am 4rth year doctoral student in Professor Takashi Nakagawa Lab, Department of Molecular and Medical Pharmacology.
NAD+ depletion associated with hallmark of aging in many medical conditions such as metabolic disorder, neurodegenerative disorders, Parkinson’s disease, Alzheimer’s disease, skeletal muscle aging, obesity, ocular aging. NAD+ metabolism in skeletal muscle aging is the focus of my study.
Nicotinamide adenine dinucleotide is an essential pyridine nucleotide that serves as an essential cofactor and substrate for a number of important cellular processes involved in oxidative phosphorylation and ATP production, DNA repair, epigenetically altered gene expression, cellular stress response .Therefore; NAD+ regulates many important metabolic pathways, such as glycolysis, fatty acid β-oxidation, the tricarboxylic acid cycle, and mitochondrial oxidative phosphorylation. NAD+ also serves as a substrate for poly (ADP-ribose) polymerase (PARP) and sirtuins.
According to the findings, age-related NAD+ depletion is caused by a combination of 1) increased activity of NAD+ consumption enzymes and 2) impaired NAD+ production as the age advances.
Increasing evidence show that poor NAD+ biosynthesis and degradation triggers the vicious cycle, which is the root cause of age-related diseases.
NAD+ supplementation is one of the strategies to prevent age related pathologies by break this cycle and maintain NAD+ levels in tissues which are crucial for delay in senescence.
Sarcopenia is age related progressive and generalized muscular weakness which is characterized by loss of function and mass of skeletal muscle. This pathological state is a high cost global burden as it causes increased risk of fall, frailty, immobility leading to death. Prevention, therapeutics and etiology are still unknown. My study is unique in that it can reverse skeletal muscle aging by increasing NAD+ levels in skeletal muscle.
I employ metabolomics technology and various NAD synthesis/degrading enzyme KO mice in my study. I elucidate the role of NAD metabolism in skeletal muscle and hope that this research work would be extremely beneficial in sarcopenia study by filling the gap of unknown etiology and helps in developing therapeutics against sarcopenia.
NAD+ depletion associated with hallmark of aging in many medical conditions such as metabolic disorder, neurodegenerative disorders, Parkinson’s disease, Alzheimer’s disease, skeletal muscle aging, obesity, ocular aging. NAD+ metabolism in skeletal muscle aging is the focus of my study.
Nicotinamide adenine dinucleotide is an essential pyridine nucleotide that serves as an essential cofactor and substrate for a number of important cellular processes involved in oxidative phosphorylation and ATP production, DNA repair, epigenetically altered gene expression, cellular stress response .Therefore; NAD+ regulates many important metabolic pathways, such as glycolysis, fatty acid β-oxidation, the tricarboxylic acid cycle, and mitochondrial oxidative phosphorylation. NAD+ also serves as a substrate for poly (ADP-ribose) polymerase (PARP) and sirtuins.
According to the findings, age-related NAD+ depletion is caused by a combination of 1) increased activity of NAD+ consumption enzymes and 2) impaired NAD+ production as the age advances.
Increasing evidence show that poor NAD+ biosynthesis and degradation triggers the vicious cycle, which is the root cause of age-related diseases.
NAD+ supplementation is one of the strategies to prevent age related pathologies by break this cycle and maintain NAD+ levels in tissues which are crucial for delay in senescence.
Sarcopenia is age related progressive and generalized muscular weakness which is characterized by loss of function and mass of skeletal muscle. This pathological state is a high cost global burden as it causes increased risk of fall, frailty, immobility leading to death. Prevention, therapeutics and etiology are still unknown. My study is unique in that it can reverse skeletal muscle aging by increasing NAD+ levels in skeletal muscle.
I employ metabolomics technology and various NAD synthesis/degrading enzyme KO mice in my study. I elucidate the role of NAD metabolism in skeletal muscle and hope that this research work would be extremely beneficial in sarcopenia study by filling the gap of unknown etiology and helps in developing therapeutics against sarcopenia.
