Mitochondrial protein alterations in vascular dementia: evidence from Mendelian randomization, transcriptomics, and a chronic hypoperfusion model - Takeaways - MDSpire

Mitochondrial protein alterations in vascular dementia: evidence from Mendelian randomization, transcriptomics, and a chronic hypoperfusion model

  • By

  • Qian Liu

  • Huizhong Tan

  • Keke Tong

  • Ruhai Luo

  • Hanquan Li

  • Feng Qiu

  • Shiliang Wang

  • Le Xie

  • Xiuli Zhang

  • Dahua Wu

  • July 9, 2026

  • 0 min

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  • 1

    Mitochondrial dysfunction is a key pathological feature of vascular dementia (VaD), but specific proteins involved remain unclear.

  • 2

    Mendelian randomization analysis identified four proteins associated with VaD: AIFM1, COX5B, NDUFV2, and NUDT5.

  • 3

    COX5B was identified as the most robust target, showing consistent evidence across genetic, transcriptomic, and animal model analyses.

  • 4

    AIFM1 and NDUFV2 exhibited contradictions between genetic/transcriptomic data and in vivo protein expression.

  • 5

    The study emphasizes the need for a multi-layered approach to identify reliable biomarkers and therapeutic targets for VaD.

Original Source(s)

Mitochondrial protein alterations in vascular dementia: evidence from Mendelian randomization, transcriptomics, and a chronic hypoperfusion model

  • by Qian Liu, Huizhong Tan, Keke Tong, Ruhai Luo, Hanquan Li, Feng Qiu, Shiliang Wang, Le Xie, Xiuli Zhang, Dahua Wu

  • July 9, 2026

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