中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (8): 3525-3526.doi: 10.4103/NRR.NRR-D-25-00456

• 观点:退行性病与再生 • 上一篇    下一篇

阿尔茨海默病中性别偏倚的内含子保留

  

  • 出版日期:2026-08-18 发布日期:2026-04-25

Sex-biased intron retention in Alzheimer’s disease

Ching-Thong Choo, Chin-Tong Ong*   

  1. Temasek Life Sciences Laboratory, Singapore (Choo CT, Ong CT)
    Department of Biological Sciences, National University of Singapore, Singapore (Choo CT, Ong CT)
  • Online:2026-08-18 Published:2026-04-25
  • Contact: Chin-Tong Ong, PhD, chintong@tll.org.sg.
  • Supported by:
    This work was supported by Temasek Life Sciences Laboratory core funding (3160) (to CTO).

摘要: https://orcid.org/0000-0002-5450-4760 (Chin-Tong Ong)
https://orcid.org/0000-0003-4058-8235 (Ching-Thong Choo)

Abstract: Higher prevalence of sporadic Alzheimer’s disease in women: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder caused by the accumulation of amyloid-β (Aβ) plaques and Tau neurofibrillary tangles in the affected brain regions. The clearance of these pathological protein aggregates by microglia can trigger excessive neuroinflammation, which contributes to brain atrophy. AD exhibits clinical heterogeneity and is characterized by highly complex, multifactorial etiology (Lopez-Lee et al., 2024). In the rare autosomal dominant forms of familial AD, patients inherit mutations in genes encoding amyloid precursor protein or presenilins. In contrast, the majority of the cases are classified as late-onset sporadic AD, in which aging is the primary risk factor. Disease susceptibility is sexbiased, with approximately 1 in 5 women at risk of developing AD during their lifetime, compared to 1 in 10 men. Beyond socio-cultural factors, a previous study suggests that inherent biological differences between the sexes contribute to the higher prevalence of AD in women (Lopez-Lee et al., 2024). For example, hormonal fluctuations during menopause can disrupt metabolic and inflammatory processes, increasing vulnerability to AD. Sex-specific differences in gene regulation and autophagy may also significantly impair protein homeostasis in females, thereby exacerbating AD pathology. Identifying other sex-biased mechanisms will deepen our understanding of AD etiology and lead to more effective treatment.