Abstract
Alzheimer's disease (AD) is the most common neurodegenerative disease among the elderly and has become a growing global health problem causing great concern. However, the pathogenesis of AD is unclear and no specific therapeutics are available to provide the sustained remission of the disease. In this study, we used comprehensive bioinformatics to determine 158 potential genes, whose expression levels changed between the entorhinal and temporal lobe cortex samples from cognitively normal individuals and patients with AD. Then, we clustered these genes in the protein-protein interaction analysis and identified six significant genes that had more biological functions. Besides, we conducted a drug-gene interaction analysis of module genes in the drug-gene interaction database and obtained 26 existing drugs that might be applied for the prevention and treatment of AD. In addition, a predictive model was built based on the selected genes using different machine learning algorithms to identify individuals with AD. These findings may provide new insights into AD therapy.
Highlights
Alzheimer’s disease (AD) is the most common neurodegenerative disease among the elderly and has become a growing global health problem of great concern [1]
A previous study identified that the expression of genes highly correlates with AD tau pathology and is most significantly increased in the entorhinal cortex, followed by the temporal cortex [6]; tau pathology usually begins in the medial temporal lobe in the allogeneic cortex
The differential expression analysis showed 691 upregulated and 636 downregulated genes in the entorhinal cortex that were detected based on the following cut-off criteria: ∣log2 fold change ðFCÞ ∣ >0:5 and P value < 0.05, as well as 116 upregulated and 243 downregulated genes that were identified in the temporal lobe cortex
Summary
Alzheimer’s disease (AD) is the most common neurodegenerative disease among the elderly and has become a growing global health problem of great concern [1]. The most typical clinical manifestations of AD are progressive memory loss and cognitive function decline. There are approximately 47 million individuals who suffer from dementia across the globe, and the number is expected to increase to 100 million by 2050 [2]. The most characteristic symptoms of AD are mild memory loss and fatigue, anxiety, or negative emotions. The cognitive impairment becomes more serious and widespread, making the person incapable of simple daily life tasks such as dressing and eating; at this time, the individual may be diagnosed with AD dementia. AD pathology is confirmed in the entorhinal and temporal cortexes. The brains of AD patients show greater volume loss in the entorhinal cortex [9]. No specific therapeutics are currently available to provide the sustained remission of AD
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