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<p>Alzheimer’s disease (AD) is the leading neurodegenerative disease manifesting cognitive impairment. Its procession is regulated by activated glial cell–mediated neuroinflammation. Although estrogen deprivation is a known risk factor for AD in females, the impact of androgen deprivation on AD pathology in males, particularly regarding neuroinflammation, remains unclear. This study investigates the effects of long-term systemic androgen deprivation on AD pathology, including glial cell–specific gene expression, amyloid β (Aβ) pathology, and cognitive function in male castrated <i>App</i><sup><i>NL−G−F/NL−G−F</i></sup> (App) mice. We found significantly reduced androgen receptor (<i>AR/Ar</i>) expression levels in the precunei of male patients with early AD pathology and isolated brain microglia of male App mice compared with their nonpathological controls. In castrated App mice, microglial <i>Tnf</i> and <i>Il6</i> and astrocytic <i>Socs3</i> were downregulated, indicating that androgens may promote inflammation in the brain. However, Aβ accumulation and cognitive function were unaffected. These results suggest that although systemic androgen deprivation modulates neuroinflammation, the changes are insufficient to alter the AD phenotype or pathology in male App mice.</p>

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Long-term systemic androgen deprivation partially modulates neuroinflammation in male AppNL−G−F/NL−G−F mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月27日

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  • Kasumi Maekawa,
  • Akira Sobue,
  • Okiru Komine,
  • Yuko Saito,
  • Shigeo Murayama,
  • Takaomi C. Saido,
  • Takashi Saito,
  • Koji Yamanaka

摘要

Alzheimer’s disease (AD) is the leading neurodegenerative disease manifesting cognitive impairment. Its procession is regulated by activated glial cell–mediated neuroinflammation. Although estrogen deprivation is a known risk factor for AD in females, the impact of androgen deprivation on AD pathology in males, particularly regarding neuroinflammation, remains unclear. This study investigates the effects of long-term systemic androgen deprivation on AD pathology, including glial cell–specific gene expression, amyloid β (Aβ) pathology, and cognitive function in male castrated AppNL−G−F/NL−G−F (App) mice. We found significantly reduced androgen receptor (AR/Ar) expression levels in the precunei of male patients with early AD pathology and isolated brain microglia of male App mice compared with their nonpathological controls. In castrated App mice, microglial Tnf and Il6 and astrocytic Socs3 were downregulated, indicating that androgens may promote inflammation in the brain. However, Aβ accumulation and cognitive function were unaffected. These results suggest that although systemic androgen deprivation modulates neuroinflammation, the changes are insufficient to alter the AD phenotype or pathology in male App mice.