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논문 기본 정보

자료유형
학술저널
저자정보
박수미 (Korea University) Anu Shahapal (Korea University) Sangjin Yoo (Neuracle Science Co., Ltd.) Hoyun Kwak (Neuracle Science Co., Ltd) Minhyeok Lee (Neuracle Science Co., Ltd) Sang-Myeong Lee (Neuracle Science Co., Ltd) Jong-Ik Hwang (Korea University) Jae Young Seong (Korea University)
저널정보
한국뇌신경과학회 Experimental Neurobiology Experimental Neurobiology Vol.33 No.4
발행연도
2024.8
수록면
193 - 201 (9page)

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초록· 키워드

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FAM19A5, a novel secretory protein highly expressed in the brain, is potentially associated with the progression of Alzheimer's disease (AD). However, its role in the AD pathogenesis remains unclear. Here, we investigated the potential function of FAM19A5 in the context of AD. We generated APP/PS1 mice with partial FAM19A5 deficiency, termed APP/PS1/FAM19A5+/LacZ mice. Compared with control APP/PS1 mice, APP/PS1/FAM19A5+/LacZ mice exhibited significantly lower Aβ plaque density and prolonged the lifespan of the APP/PS1 mice. To further explore the therapeutic potential of targeting FAM19A5, we developed a FAM19A5 antibody. Administration of this antibody to APP/PS1 mice significantly improved their performance in the Y-maze and passive avoidance tests, indicating enhanced cognitive function. This effect was replicated in 5XFAD mice, a model of early-onset AD characterized by rapid Aβ accumulation. Additionally, FAM19A5 antibody treatment in 5XFAD mice led to enhanced exploration of novel objects and increased spontaneous alternation behavior in the novel object recognition and Y-maze tests, respectively, indicating improved cognitive function. These findings suggest that FAM19A5 plays a significant role in AD pathology and that targeting with FAM19A5 antibodies may be a promising therapeutic strategy for AD.

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