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CD36-mediated ROS/PI3K/AKT signaling pathway exacerbates cognitive impairment in APP/PS1 mice after noise exposure
Zan Zhou1, Wen-Jun Jiang2, Yan-Ping Wang3
1Department of Physiology, Medical College of Jiaxing University, Jiaxing, Zhejiang 314000, China; Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang 832000, China; The Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Medical College of Shihezi University, Shihezi 832000, Xinjiang, China.
Noise exposure worsens cognitive impairment in Alzheimer's disease (AD) models by increasing CD36 expression, leading to neuroinflammation and neuronal damage. This highlights CD36 as a potential therapeutic target for noise-induced cognitive decline.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Noise exposure is linked to cognitive impairment, with potentially greater effects in Alzheimer's disease (AD) and mild cognitive impairment.
- The underlying mechanisms connecting noise exposure to cognitive decline, particularly in AD, require further elucidation.
Purpose of the Study:
- To investigate the impact of noise exposure on cognitive function in an AD mouse model (APP/PS1) compared to a normal control group (C57BL/6J).
- To identify molecular changes, specifically Cluster of Differentiation (CD) molecules, associated with noise exposure in the AD model.
- To explore the role of the identified CD molecule, CD36, in mediating noise-induced cognitive impairment and neuroinflammation.
Main Methods:
- Utilized APP/PS1 mice as an AD model and C57BL/6J mice as controls.
- Assessed cognitive abilities following controlled noise exposure.
- Employed transcriptomics to analyze differential CD molecule expression.
- Quantified CD36 protein levels using Western Blot in the hippocampus and entorhinal cortex.
- Investigated the mechanistic pathway involving CD36, oxidative stress, PI3K/AKT signaling, and microglial/astrocyte polarization.
- Intervened using a CD36 pharmacological inhibitor.
Main Results:
- Noise exposure significantly exacerbated cognitive impairment in APP/PS1 mice compared to controls.
- Transcriptomic analysis revealed significant differences in CD molecule expression trends between the two mouse types.
- CD36 expression was notably upregulated in the hippocampus and entorhinal cortex of APP/PS1 mice post-noise exposure.
- Elevated CD36 levels correlated with increased oxidative stress, reduced PI3K/AKT phosphorylation, and a shift towards pro-inflammatory M1/A1 microglia/astrocytes.
- Pharmacological inhibition of CD36 ameliorated noise-induced neuroinflammation and cognitive deficits.
Conclusions:
- Noise exposure disproportionately affects cognitive function in AD models, mediated by CD36 upregulation.
- CD36 plays a critical role in noise-induced neuroinflammation, oxidative stress, and synaptic damage in the context of Alzheimer's disease.
- Targeting CD36 may offer a novel therapeutic strategy to mitigate cognitive impairment associated with noise exposure in AD patients.
