Nicotinamide adenine dinucleotide (NAD+) plays an essential role as a redox cofactor in intermediary metabolism. NAD+ is also critical for the activity of several families of proteins, including sirtuins, cyclic ADP-ribose synthases and poly(ADP-ribose) polymerases, which together regulate fundamental biological processes, such as DNA repair, chromatin remodeling, metabolism or cellular senescence. Mounting evidence suggests that NAD+ content gradually declines in various tissues during aging, and that such decline is an essential contributor to most hallmarks of aging, including cellular senescence, mitochondrial dysfunction or DNA damage. These findings causally link NAD+ depletion to a number of age-associated diseases, such as neurodegeneration, muscle atrophy or insulin resistance. Conversely, evidence suggests that NAD+ repletion therapies may effectively counteract age-associated NAD+ decline, slowing down aspects of aging and alleviating the outcomes of several age-related disorders, though the therapeutic space around these therapies is still largely unexplored.
The aim of this Research Topic is to (1) highlight the state-of-the-art in the field of NAD+ and aging, (2) provide balanced perspectives on the therapeutic potential of this pathway for aging and age-related diseases; (3) explain opportunities for future developments in this field.
We welcome submissions ranging from fundamental to clinical research. Areas to be covered in this Research Topic may include, but are not limited to:
• Mechanisms driving age-associated NAD+ decline and associated diseases
• Contributions of NAD+ metabolism to hallmarks of aging
• Therapies targeting NAD+ metabolism in the context of age-associated disease
• Novel molecules and strategies to target NAD+ decline
Keywords:
Nicotinamide, NAD, age-related disease, metabolism, NAD repletion, NAD consumers
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Nicotinamide adenine dinucleotide (NAD+) plays an essential role as a redox cofactor in intermediary metabolism. NAD+ is also critical for the activity of several families of proteins, including sirtuins, cyclic ADP-ribose synthases and poly(ADP-ribose) polymerases, which together regulate fundamental biological processes, such as DNA repair, chromatin remodeling, metabolism or cellular senescence. Mounting evidence suggests that NAD+ content gradually declines in various tissues during aging, and that such decline is an essential contributor to most hallmarks of aging, including cellular senescence, mitochondrial dysfunction or DNA damage. These findings causally link NAD+ depletion to a number of age-associated diseases, such as neurodegeneration, muscle atrophy or insulin resistance. Conversely, evidence suggests that NAD+ repletion therapies may effectively counteract age-associated NAD+ decline, slowing down aspects of aging and alleviating the outcomes of several age-related disorders, though the therapeutic space around these therapies is still largely unexplored.
The aim of this Research Topic is to (1) highlight the state-of-the-art in the field of NAD+ and aging, (2) provide balanced perspectives on the therapeutic potential of this pathway for aging and age-related diseases; (3) explain opportunities for future developments in this field.
We welcome submissions ranging from fundamental to clinical research. Areas to be covered in this Research Topic may include, but are not limited to:
• Mechanisms driving age-associated NAD+ decline and associated diseases
• Contributions of NAD+ metabolism to hallmarks of aging
• Therapies targeting NAD+ metabolism in the context of age-associated disease
• Novel molecules and strategies to target NAD+ decline
Keywords:
Nicotinamide, NAD, age-related disease, metabolism, NAD repletion, NAD consumers
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.