Abstract
Aging of the nervous system is typified by depressed metabolism, compromised proteostasis, and increased inflammation that results in cognitive impairment. Differential expression analysis is a popular technique for exploring the molecular underpinnings of neural aging, but technical drawbacks of the methodology often obscure larger expression patterns. Co-expression analysis offers a robust alternative that allows for identification of networks of genes and their putative central regulators. In an effort to expand upon previous work exploring neural aging in the marine model Aplysia californica, we used weighted gene correlation network analysis to identify co-expression networks in a targeted set of aging sensory neurons in these animals. We identified twelve modules, six of which were strongly positively or negatively associated with aging. Kyoto Encyclopedia of Genes analysis and investigation of central module transcripts identified signatures of metabolic impairment, increased reactive oxygen species, compromised proteostasis, disrupted signaling, and increased inflammation. Although modules with immune character were identified, there was no correlation between genes in Aplysia that increased in expression with aging and the orthologous genes in oyster displaying long-term increases in expression after a virus-like challenge. This suggests anti-viral response is not a driver of Aplysia sensory neuron aging.
Highlights
As an organ composed of long-lived cells, the brain is uniquely susceptible to the deleterious effects of aging, the outcome of which is often cognitive impairment [1,2]
Removal of transcripts with zero total count and variance filtering with the geneFilter package yielded 11,703 analysis ready transcripts, out of approximately 12,000 transcripts expressed in these sensory neuron types described previously [24]
While enrichment analysis and eigengene expression profiles suggested strong overlap with our previous study, several modules and enrichment results identified many facets to the transcriptional dynamics in aging of these sensory neurons not detected in our previous differential expression analysis (DEA) study [24]
Summary
As an organ composed of long-lived cells, the brain is uniquely susceptible to the deleterious effects of aging, the outcome of which is often cognitive impairment [1,2]. Common hallmarks of brain aging include impaired metabolism, compromised proteostasis, mitochondrial dysfunction, and neuro-inflammation [3,4,5]. What causes these hallmark phenotypes is not well understood and still debated [6,7,8]. The marine model Aplysia californica is well suited for study of aging neurons. These mollusks live approximately one year in the wild and mariculture setting and have relatively simple nervous systems of only approximately 10,000 neurons grouped into well mapped circuits [9,10,11]
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