Abstract
Aging is associated with cognitive declines that originate in impairments of function in the neurons that make up the nervous system. The marine mollusk Aplysia californica (Aplysia) is a premier model for the nervous system uniquely suited to investigation of neuronal aging due to uniquely identifiable neurons and molecular techniques available in this model. This study describes the molecular processes associated with aging in two populations of sensory neurons in Aplysia by applying RNA sequencing technology across the aging process (age 6–12 months). Differentially expressed genes clustered into four to five coherent expression patterns across the aging time series in the two neuron populations. Enrichment analysis of functional annotations in these neuron clusters revealed decreased expression of pathways involved in energy metabolism and neuronal signaling, suggesting that metabolic and signaling pathways are intertwined. Furthermore, increased expression of pathways involved in protein processing and translation suggests that proteostatic stress also occurs in aging. Temporal overlap of enrichment for energy metabolism, proteostasis, and neuronal function suggests that cognitive impairments observed in advanced age result from the ramifications of broad declines in energy metabolism.
Highlights
Aging can be summarized as a progressive decline in the physiological function and increased vulnerability to death of an organism over the course of the lifespan (Lopez-Otin et al, 2013; Dodig et al, 2019)
The calculated Gompertz actuarial aging rate G, which describes the change in mortality rate with change in time, was 0.047, similar to previously reported aging rates (Gerdes and Fieber, 2006)
Transcriptional profile clustering of transcripts differentially expressed in aging from Aplysia sensory neurons (SN) clusters identified four and five coherent transcriptional patterns from buccal S cluster (BSC) and pleural ventral caudal cluster (PVC), respectively
Summary
Aging can be summarized as a progressive decline in the physiological function and increased vulnerability to death of an organism over the course of the lifespan (Lopez-Otin et al, 2013; Dodig et al, 2019). Several of the most prevalent neurological diseases, such as Alzheimer’s disease and Parkinson’s disease, have age-associated onset (Hou et al, 2019). The nervous system is profoundly affected with age, resulting in cognitive impairments and susceptibility to neurodegenerative disorders (Reuter-Lorenz, 2002; Yankner et al, 2008; Anderson and Craik, 2017; Bettio et al, 2017). The long-lived, post-mitotic, and energetically expensive nature of neurons results in a suite of age-associated changes that underpin cognitive changes observed at the whole organism level (Grimm and Eckert, 2017)
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