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Transcriptomic analysis of oligomeric amyloid-β treated primary cortical neurons reveals dysregulation of genes involved in the biosynthesis of steroids and cholesterol

Research output: Chapter in Book/Report/Conference proceedingChapter

Original languageEnglish
Title of host publicationMicroarrays: Principles, Applications and Technologies
PublisherNova Science Publishers Inc
Number of pages27
ISBN (Electronic)9781629487137
ISBN (Print)9781629486697
Published1 Jan 2014

King's Authors


Alzheimer's disease (AD) is a neurodegenerative disorder and is the most common cause of dementia. It is characterized by synaptic and neuronal loss, and the hallmark of AD is the presence of plaques in the brains of patients, which are primarily composed of the amyloid-β peptide (Aβ). However, the mechanisms by which Aβ gives rise to pathology have not been fully defined as yet. Evidence suggests that soluble oligomers of the peptide are the most potent and toxic form of Aβ. To uncover the potential mechanism by which Aβ may lead to toxicity in neurons, a transcriptomic profile of primary mouse cortical neurons in response to oligomeric Aβ (1-42) treatment was performed. The results show the differential regulation of genes involved in the biosynthesis of steroids and cholesterol, as well as other genes whose products are associated with lipid metabolism. Cholesterol may be a risk factor for development of the disease and several cholesterol-related genes linked to AD have been reported. The findings in this chapter highlight the importance of interactions between Aβ and cholesterol, and have potential implications for pathology in AD brain.

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