ArticleJournal of neuroinflammation2021
Administration of anti-ERMAP antibody ameliorates Alzheimer's disease in mice.
Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Beyond the Genotype: A Multi-Omic Analysis of APOEe4's Role in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2025Article
- ERMAP attenuates DSS-induced colitis in mice by regulating macrophage and T cell functions.BMC gastroenterology · 2025Article
- Expression analysis of inhibitory B7 family members in Alzheimer's disease.Metabolic brain disease · 2023Article
- Administration of recombinant FOXN1 protein attenuates Alzheimer's pathology in mice.Brain, behavior, and immunity · 2023Article
- N-acetylneuraminic acid links immune exhaustion and accelerated memory deficit in diet-induced obese Alzheimer's disease mouse model.Nature communications · 2023Article
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundAlzheimer's disease (AD) is a devastating age-related neurodegenerative disorder and characterized by progressive loss of memory and cognitive functions, which are associated with amyloid-beta (Aβ) plaques. Immune cells play an important role in the clearance of Aβ deposits. Immune responses are regulated by immune regulators in which the B7 family members play a crucial role. We have recently identified erythroid membrane-associated protein (ERMAP) as a novel B7 family-related immune regulator and shown that ERMAP protein affects T cell and macrophage functions.
methodsWe produced a monoclonal antibody (mAb) against ERMAP protein and then determined the ability of the mAb to affect cognitive performance and AD pathology in mice.
resultsWe have shown that the anti-ERMAP mAb neutralizes the T cell inhibitory activity of ERMAP and enhances macrophages to phagocytose Aβ in vitro. Administration of the mAb into AD mice improves cognitive performance and reduces Aβ plaque load in the brain. This is related to increased proportion of T cells, especially IFNγ-producing T cells, in the spleen and the choroid plexus (CP), enhanced expression of immune cell trafficking molecules in the CP, and increased migration of monocyte-derived macrophages into the brain. Furthermore, the production of anti-Aβ antibodies in the serum and the macrophage phagocytosis of Aβ are enhanced in the anti-ERMAP mAb-treated AD mice.
conclusionsOur results suggest that manipulating the ERMAP pathway has the potential to provide a novel approach to treat AD patients.
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Registered trials
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