Unraveling the Aging Secrets of the Unconventional Octodon degus

Published on June 30, 2022

Imagine a world where we could uncover the mysteries of aging and Alzheimer’s disease through the eyes of an unconventional rodent. Well, that world exists, my friends! Meet the degu, a diurnal long-lived creature that undergoes molecular and behavioral changes similar to those seen in humans as they age. Some degus even develop cognitive decline and brain pathology resembling Alzheimer’s disease. In a recent study, researchers sequenced the entire genome of these unique animals and found intriguing variations associated with aging and Alzheimer’s. They discovered specific gene variants linked to Alzheimer’s disease, including a new variation of the apolipoprotein E (Apoe) gene. This variant correlated with an increase in amyloid plaques in the brain, shedding light on their role in the disease. With this groundbreaking genome sequencing, scientists can unravel the molecular pathways involved in aging and propel us closer to effective treatments for Alzheimer’s. Don’t miss out on this fascinating research—dive into the full article to explore the hidden world of the octodon degus!

The degu (Octodon degus) is a diurnal long-lived rodent that can spontaneously develop molecular and behavioral changes that mirror those seen in human aging. With age some degu, but not all individuals, develop cognitive decline and brain pathology like that observed in Alzheimer’s disease including neuroinflammation, hyperphosphorylated tau and amyloid plaques, together with other co-morbidities associated with aging such as macular degeneration, cataracts, alterations in circadian rhythm, diabetes and atherosclerosis. Here we report the whole-genome sequencing and analysis of the degu genome, which revealed unique features and molecular adaptations consistent with aging and Alzheimer’s disease. We identified single nucleotide polymorphisms in genes associated with Alzheimer’s disease including a novel apolipoprotein E (Apoe) gene variant that correlated with an increase in amyloid plaques in brain and modified the in silico predicted degu APOE protein structure and functionality. The reported genome of an unconventional long-lived animal model of aging and Alzheimer’s disease offers the opportunity for understanding molecular pathways involved in aging and should help advance biomedical research into treatments for Alzheimer’s disease.

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