Transcriptomic Profiling Reveals Neuroinflammation in the Corpus Callosum of a Transgenic Mouse Model of Alzheimer’s Disease

Jan 26, 2024Journal of Alzheimer's disease : JAD

Gene Activity Shows Brain Inflammation in the Connecting Pathway of a Mouse Model of Alzheimer's Disease

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Abstract

Cognitive decline and demyelination were observed in the corpus callosum of 5xFAD transgenic mice.

Gene expression analysis showed a predominance of upregulated genes in AD mice, particularly those linked to immune cells like microglia.
Downregulation of genes associated with chaperone function and circadian rhythms, including Per1, Per2, and Cry1, was noted.
The findings indicate that neuroinflammation, disruption of chaperone function, and circadian dysfunction may be involved in the development of white matter lesions in Alzheimer's disease.

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BACKGROUND: Alzheimer's disease (AD) is a widespread neurodegenerative disorder characterized by progressive cognitive decline, affecting a significant portion of the aging population. While the cerebral cortex and hippocampus have been the primary focus of AD research, accumulating evidence suggests that white matter lesions in the brain, particularly in the corpus callosum, play an important role in the pathogenesis of the disease.

OBJECTIVE: This study aims to investigate the gene expression changes in the corpus callosum of 5xFAD transgenic mice, a widely used AD mouse model.

METHODS: We conducted behavioral tests for spatial learning and memory in 5xFAD transgenic mice and performed RNA sequencing analyses on the corpus callosum to examine transcriptomic changes.

RESULTS: Our results show cognitive decline and demyelination in the corpus callosum of 5xFAD transgenic mice. Transcriptomic analysis reveals a predominance of upregulated genes in AD mice, particularly those associated with immune cells, including microglia. Conversely, downregulation of genes related to chaperone function and clock genes such as Per1, Per2, and Cry1 is also observed.

CONCLUSIONS: This study suggests that activation of neuroinflammation, disruption of chaperone function, and circadian dysfunction are involved in the pathogenesis of white matter lesions in AD. The findings provide insights into potential therapeutic targets and highlight the importance of addressing white matter pathology and circadian dysfunction in AD treatment strategies.

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Transcriptomic Profiling Reveals Neuroinflammation in the Corpus Callosum of a Transgenic Mouse Model of Alzheimer’s Disease

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