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FAM222A encodes a protein which accumulates in plaques in Alzheimer’s disease

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  • Tingxiang Yan

    (Case Western Reserve University)

  • Jingjing Liang

    (Case Western Reserve University)

  • Ju Gao

    (Case Western Reserve University)

  • Luwen Wang

    (Case Western Reserve University)

  • Hisashi Fujioka

    (Case Western Reserve University)

  • Xiaofeng Zhu

    (Case Western Reserve University)

  • Xinglong Wang

    (Case Western Reserve University)

Abstract

Alzheimer’s disease (AD) is characterized by amyloid plaques and progressive cerebral atrophy. Here, we report FAM222A as a putative brain atrophy susceptibility gene. Our cross-phenotype association analysis of imaging genetics indicates a potential link between FAM222A and AD-related regional brain atrophy. The protein encoded by FAM222A is predominantly expressed in the CNS and is increased in brains of patients with AD and in an AD mouse model. It accumulates within amyloid deposits, physically interacts with amyloid-β (Aβ) via its N-terminal Aβ binding domain, and facilitates Aβ aggregation. Intracerebroventricular infusion or forced expression of this protein exacerbates neuroinflammation and cognitive dysfunction in an AD mouse model whereas ablation of this protein suppresses the formation of amyloid deposits, neuroinflammation and cognitive deficits in the AD mouse model. Our data support the pathological relevance of protein encoded by FAM222A in AD.

Suggested Citation

  • Tingxiang Yan & Jingjing Liang & Ju Gao & Luwen Wang & Hisashi Fujioka & Xiaofeng Zhu & Xinglong Wang, 2020. "FAM222A encodes a protein which accumulates in plaques in Alzheimer’s disease," Nature Communications, Nature, vol. 11(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-019-13962-0
    DOI: 10.1038/s41467-019-13962-0
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