ArticleCNS neuroscience & therapeutics2023
Apicidin attenuates memory deficits by reducing the Aβ load in APP/PS1 mice.
Article in CNS neuroscience & therapeutics, 2023. 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, 8 citations in OpenAlex.
- Metformin Restores Innate Fear Deficits in Young Adult Female APP/PS1 Mice via Basolateral Amygdala Activation.Molecular neurobiology · 2026Article
- Investigating blood-brain barrier penetration and neurotoxicity of natural products for central nervous system drug development.Scientific reports · 2025Article
- SHMT2 Mediates Small-Molecule-Induced Alleviation of Alzheimer Pathology Via the 5'UTR-dependent ADAM10 Translation Initiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Immune-related gene characterization and biological mechanisms in major depressive disorder revealed based on transcriptomics and network pharmacology.Frontiers in psychiatry · 2024Article
- Apicidin attenuates memory deficits by reducing the Aβ load in APP/PS1 mice.CNS neuroscience & therapeutics · 2023Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
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Abstract
aimsAmyloid beta (Aβ) is an important pathological feature of Alzheimer's disease (AD). A disintegrin and metalloproteinase 10 (ADAM10) can reduce the production of toxic Aβ by activating the nonamyloidogenic pathway of amyloid precursor protein (APP). We previously found that apicidin, which is a histone deacetylase (HDAC) inhibitor, can promote the expression of ADAM10 and reduce the production of Aβ in vitro. This study was designed to determine the potential of apicidin treatment to reverse learning and memory impairments in an AD mouse model and the possible correlation of these effects with ADAM10.
methodsNine-month-old APP/PS1 mice and C57 mice received intraperitoneal injections of apicidin or vehicle for 2 months. At 11 months of age, we evaluated the memory performance of mice with Morris water maze (MWM) and context fear conditioning tests. The Aβ levels were assessed in mouse brain using the immunohistochemical method and ELISA. The expression of corresponding protein involved in proteolytic processing of APP and the phosphorylation of tau were assessed by Western blotting.
resultsApicidin reversed the deficits of spatial reference memory and contextual fear memory, attenuated the formation of Aβ-enriched plaques, and decreased the levels of soluble and insoluble Aβ40/42 in APP/PS1 mice. Moreover, apicidin significantly increased the expression of ADAM10, improved the level of sAPPα, and reduced the production of sAPPβ, but did not affect the levels of phosphorylated tau in APP/PS1 mice.
conclusionApicidin significantly improves the AD symptoms of APP/PS1 mice by regulating the expression of ADAM10, which may contribute to decreasing the levels of Aβ rather than decreasing the phosphorylation of tau.
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