ArticleExperimental neurobiology2024
FAM19A5 Deficiency Mitigates the Aβ Plaque Burden and Improves Cognition in Mouse Models of Alzheimer's Disease.
Article in Experimental neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Therapeutic Efficacy of Autologous Blood-Derived Stem Cells with Growth Factors in Moderate to Severe Alzheimer's Disease: A Clinical Trial.Molecular neurobiology · 2025Trial
- Inhibition of FAM19A5 reverses synaptic loss and cognitive decline in mouse models of Alzheimer's disease.Alzheimer's research & therapy · 2025Trial
- Partial FAM19A5 deficiency in mice leads to disrupted spine maturation, hyperactivity, and an altered fear response.PloS one · 2025Article
- Is FAM19A5 an adipokine? Peripheral FAM19A5 in wild-type, FAM19A5 knockout, and LacZ knockin mice.Molecules and cells · 2024Article
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Authors and funding
8 authors.
Funding
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Abstract
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
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