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Abstract <p>Alzheimer’s disease (AD) is characterized by progressive neurodegeneration,synaptic dysfunction, and cognitive impairment. In this study, weexamined the effects of compound C20, a selective positive allostericmodulator of the TRPC6 channel, on the cognitive and motor functionof 5xFAD mice, a transgenic model of AD. Our results demonstratethat C20 effectively improves hippocampus-dependent (“Morris’s watermaze”, “Novel object recognition” tests) and hippocampus-independent(“Fear conditioning”) memory, which is consistent with its abilityto restore synaptic plasticity. However, C20 had no effect on motorimpairment in the “Beam walking” test. Thus, C20 exhibits an effectof protection of cognition but does not affect motor function in5xFAD mice. These findings support the potential of TRPC6 as a targetfor the treatment of cognitive impairment in a course of AD andhighlight the need for further investigation of the mechanisms underlyingmotor deficits.</p>

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Selective TRPC6 Modulator, C20, Improves Cognitive but Not Motor Function in a 5xFAD Mouse Model of Alzheimer’s Disease

  • 期刊论文

  • 发表日期：

    2025年5月1日

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  • N. Zernov,
  • D. M. Меlenteva,
  • Е. А. Popugaeva

摘要

Abstract

Alzheimer’s disease (AD) is characterized by progressive neurodegeneration,synaptic dysfunction, and cognitive impairment. In this study, weexamined the effects of compound C20, a selective positive allostericmodulator of the TRPC6 channel, on the cognitive and motor functionof 5xFAD mice, a transgenic model of AD. Our results demonstratethat C20 effectively improves hippocampus-dependent (“Morris’s watermaze”, “Novel object recognition” tests) and hippocampus-independent(“Fear conditioning”) memory, which is consistent with its abilityto restore synaptic plasticity. However, C20 had no effect on motorimpairment in the “Beam walking” test. Thus, C20 exhibits an effectof protection of cognition but does not affect motor function in5xFAD mice. These findings support the potential of TRPC6 as a targetfor the treatment of cognitive impairment in a course of AD andhighlight the need for further investigation of the mechanisms underlyingmotor deficits.