Abstract
Background
A major pathological hallmark of Alzheimer's disease (AD), the most common cause of dementia, is the accumulation of amyloid-β (Aβ) plaques. However, currently approved therapeutic agents fail to fundamentally halt disease progression and have limitations in terms of efficacy, sustainability, and safety. CD300c is an immunoregulatory molecule that modulates monocyte differentiation and activates macrophages. We recently developed a fully human anti-CD300c antibody, CB201, demonstrating its therapeutic potential in early and late 5xFAD mice.
Objective
This study investigated the efficacy of CB201 in late-stage AD using the APP/PS1 transgenic mouse model. We analyzed the effects of administering CB201 on changes in memory and cognitive function and Aβ and tau protein accumulation in the brain.
Methods
To assess long- and short-term memory improvements, behavioral tests were conducted using the Morris water maze and fear conditioning. Immunostaining was performed to quantify changes in Aβ and tau accumulation.
Results
CB201-treated late-stage AD mice demonstrated improved cognitive performance and memory, comparable to wild-type controls. Histopathological analysis further revealed that CB201 treatment reduced Aβ and tau accumulation.
Conclusions
CB201 exerts significant therapeutic effects on functional impairments and pathological alterations in late-stage AD. These results confirm CB201 as a potential immunotherapeutic for the treatment of AD.
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