Mechanosensory Neuron Aging: Differential Trajectories with Lifespan-Extending Alaskan Berry and Fungal Treatments in Caenorhabditis elegans

Abstract

Many nutritional interventions that increase lifespan are also proposed to postpone age-related declines in motor and cognitive function. Potential sources of anti-aging compounds are the plants and fungi that have adapted to extreme environments. We studied the effects of four commonly consumed and culturally relevant Interior Alaska berry and fungus species (bog blueberry, lowbush cranberry, crowberry, and chaga) on the decline in overall health and neuron function and changes in touch receptor neuron morphology associated with aging. We observed increased wild-type Caenorhabditis elegans lifespan and improved markers of healthspan upon treatment with Alaskan blueberry, lowbush cranberry, and chaga extracts. Interestingly, although all three treatments increased lifespan, they differentially affected the development of aberrant morphologies in touch receptor neurons. Blueberry treatments decreased anterior mechanosensory neuron (ALM) aberrations (i.e., extended outgrowths and abnormal cell bodies) while lowbush cranberry treatment increased posterior mechanosensory neuron (PLM) aberrations, namely process branching. Chaga treatment both decreased ALM aberrations (i.e., extended outgrowths) and increased PLM aberrations (i.e., process branching and loops). These results support the large body of knowledge positing that there are multiple cellular strategies and mechanisms for promoting health with age. Importantly, these results also demonstrate that although an accumulation of abnormal neuron morphologies is associated with aging and decreased health, not all of these morphologies are detrimental to neuronal and organismal health.

A robust and miniaturized screening platform to study natural products affecting metabolism and survival in Caenorhabditis elegans

“…Our findings are in line and complement recent preclinical studies on the beneficial effects of I. obliquus extracts in different mammal models of obesity and diabetes [73][74][75][76] . Longevity effects of I. obliquus in C. elegans were already reported by Scerbak et al 77,78 , and in Drosophila melanogaster by Zhang et al 79 .…”

Genetic Silencing of Fatty Acid Desaturases Modulates α-Synuclein Toxicity and Neuronal Loss in Parkinson-Like Models of C. elegans

“…The survival was determined daily by visual observation under dissecting microscope or by gentle prodding with a platinum wire. “Bagged” animals and animals crawling off the plates were censored (Scerbak et al, 2016). Each experiment was repeated at least three times.…”

Potential ofCaenorhabditis elegansas an antiaging evaluation model for dietary phytochemicals: A review

“…Caenorhabditis elegans has neuronal, gut, and muscle cells homologous to those of humans that are vital for nervous system and metabolic functions, rendering this species powerful and suitable model for the study of processes related to aging including neurodegeneration (Daskalaki, Markaki, & Tavernarakis, 2019; Pallauf, Duckstein, & Rimbach, 2017; Scerbak, Vayndorf, Hernandez, McGill, & Taylor, 2016). Notably, numerous genes and signaling pathways regulating the lifespan and related molecules in C. elegans are highly conserved between worms and mammals (Alexander et al., 2014; Lin, Xiao et al., 2019; Martorell et al., 2011; Nakagawa et al., 2016).…”