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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Menopause, a natural biological process marking the end of a woman's fertility, typically occurs between the fifth and sixth decade of life. This phase is characterized by the exhaustion of the ovarian follicle pool, leading to less responsive ovaries despite the high levels of Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH). The consequential decrease in estrogen production results in symptoms like hot flashes, heavy sweating, headaches, hair loss, muscle pains, vaginal...
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A decrease in NAD+ contributes to the loss of osteoprogenitors and bone mass with aging.

Ha-Neui Kim1, Filipa Ponte1, Aaron Warren1

  • 1Division of Endocrinology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.

NPJ Aging and Mechanisms of Disease
|April 2, 2021
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Summary
This summary is machine-generated.

Aging reduces bone formation due to decreased NAD+ levels, which impairs osteoblast function via the Sirt1/FoxO/β-catenin pathway. Supplementing NAD+ precursor nicotinamide riboside (NR) can restore bone mass in aging mice.

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Area of Science:

  • Gerontology
  • Cell Biology
  • Bone Biology

Background:

  • Age-related osteoporosis is linked to reduced osteoblast numbers and increased cellular senescence.
  • Forkhead box O (FoxO) transcription factors inhibit osteoprogenitor proliferation and bone formation.
  • Sirtuin1 (Sirt1) deacetylates FoxOs and β-catenin, promoting bone mass.

Purpose of the Study:

  • To investigate the role of the Sirt1/FoxO/β-catenin pathway in age-related bone loss.
  • To determine if NAD+ levels decline in aging osteoblast progenitors.
  • To assess the therapeutic potential of NAD+ precursors in counteracting age-related bone loss.

Main Methods:

  • Cultured osteoblast progenitors from young and old mice.
  • Measured NAD+ levels, FoxO1 and β-catenin acetylation, and senescence markers.
  • Administered nicotinamide riboside (NR) to cell cultures and aged mice.
  • Assessed osteoblastogenesis and bone mass.

Main Results:

  • Old mice exhibited decreased NAD+ levels, increased FoxO1/β-catenin acetylation, and cellular senescence.
  • NR treatment reduced acetylation and senescence, enhancing osteoblastogenesis in aged cells.
  • NR administration to aged mice prevented bone loss.
  • Reduced NAD+ levels in young cells inhibited osteoblastogenesis in a FoxO-dependent manner.

Conclusions:

  • Decreased NAD+ and dysregulated Sirt1/FoxO/β-catenin signaling contribute to age-related bone loss.
  • NAD+ repletion via NR is a promising therapeutic strategy for skeletal involution.