Anatomy and Neuroscience - Journal Articles
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Item Symposium: What does the microbiome tell us about prevention and treatment of AD/ADRD?(Society for Neuroscience, 2024-10-09) Capocchi, Joia K.; Figueroa-Romero, Claudia; Dunham, Sage J. B.; Faraci, Gina; Rothman, Jason A.; Whiteson, Katrine L.; Seo, Dong-oh; Holtzman, David M.; Grabrucker, Stefanie; Nolan, Yvonne M.; Kaddurah-Daouk, Rima; Jett, David A.; Good Ventures Foundation; Cure Alzheimer’s Fund; Science Foundation Ireland; National Institute on Aging; Foundation for the National Institutes of HealthAlzheimer's disease (AD) and Alzheimer's disease-related dementias (ADRDs) are broad-impact multifactorial neurodegenerative diseases. Their complexity presents unique challenges for developing effective therapies. This review highlights research presented at the 2024 Society for Neuroscience meeting which emphasized the gut microbiome's role in AD pathogenesis by influencing brain function and neurodegeneration through the microbiota–gut–brain axis. This emerging evidence underscores the potential for targeting the gut microbiota to treat AD/ADRD.Item Gut microbiota and eating behaviour in circadian syndrome(Elsevier Ltd., 2024-08-01) Soliz-Rueda, Jorge R.; Cuesta-Marti, Cristina; O’Mahony, Siobhain M.; Clarke, Gerard; Schellekens, Harriët; Muguerza, Begoña; Science Foundation Ireland; Ministerio de Ciencia e Innovación; Irish Research Council; Ministerio de Universidades; Biostime Institute for Nutrition and Care – Geneva; Food for Health IrelandEating behaviour and circadian rhythms are closely related. The type, timing, and quantity of food consumed, and host circadian rhythms, directly influence the intestinal microbiota, which in turn impacts host circadian rhythms and regulates food intake beyond homeostatic eating. This Opinion discusses the impact of food intake and circadian disruptions induced by an obesogenic environment on gut–brain axis signalling. We also explore potential mechanisms underlying the effects of altered gut microbiota on food intake behaviour and circadian rhythmicity. Understanding the crosstalk between gut microbiota, circadian rhythms, and unhealthy eating behaviour is crucial to addressing the obesity epidemic, which remains one of the biggest societal challenges of our time.Item A closer look at the subordinate population within the visible burrow system(Elsevier Inc., 2017-07-13) Melhorn, Susan J.; Elfers, Clinton T.; Scott, Karen A.; Sakai, Randall R.The visible burrow system (VBS) utilizes the natural social behavior of rodents to model chronic social stress. Classically, when male and female rats are housed together in the VBS a dominance hierarchy rapidly forms with one dominant (DOM) and three subordinate (SUB) males. SUB animals show signs of chronic social stress, including loss of body weight and elevated basal corticosterone. This study furthered examined differences among the SUB population. Quantitative observations across numerous VBS colonies within the Sakai Lab suggest that there is variability in the effects of stress on the SUB population, specifically that some animals may experience more severe effects of chronic social stress than others. To further examine this observation, SUB animals were classified as OMEGA if they received a disproportionate amount of their colonies' wounds. OMEGA animals received more wounds to their body compared to SUB (P < 0.0001) and lost significantly more weight throughout the stress period compared to all other VBS-housed animals (group × time interaction P < 0.0001). Following VBS housing it was determined the OMGEA also lost lean body mass (P < 0.01 vs. controls and DOM), are hyporesponsive to an acute restraint challenge (P < 0.01 vs all other groups) and show depressive-like behavior during a forced swim test. Furthermore, expression of neuropeptide Y within the amygdala, known for anxiolytic properties following chronic stress, was elevated among OMEGA (group × region interaction P < 0.001). Together these observations suggest that an additional phenotype exists among the SUB animals within a VBS colony and represents the variability of the effects of chronic social stress.Item Editorial: the role of stem cells, epigenetics and micrornas in parkinson’s disease(Frontiers Media S.A., 2020) Hegarty, Shane V.; Green, Holly F.; Niclis, Jonathan; O'Keeffe, Gerard W.; Sullivan, Aideen M.Item Association of distinct type 1 bone morphogenetic protein receptors with different molecular pathways and survival outcomes in neuroblastoma(Portland Press, 2020) Alshangiti, Amnah M.; Wyatt, Sean L.; McCarthy, Erin; Collins, Louise M.; Hegarty, Shane V.; Sullivan, Aideen M.; O'Keeffe, Gerard W.; Government of Saudi Arabia; Irish Research Council; Science Foundation IrelandNeuroblastoma (NB) is a paediatric cancer that arises in the sympathetic nervous system. Patients with stage 4 tumours have poor outcomes and 20% of high-risk cases have MYCN amplification. The bone morphogenetic proteins (BMPs) play roles in sympathetic neuritogenesis, by signalling through bone morphogenetic protein receptor (BMPR)2 and either BMPR1A or BMPR1B. Alterations in BMPR2 expression have been reported in NB; it is unknown if the expression of BMPR1A or BMPR1B is altered. We report lower BMPR2 and BMPR1B, and higher BMPR1A, expression in stage 4 and in MYCN-amplified NB. Kaplan–Meier plots showed that high BMPR2 or BMPR1B expression was linked to better survival, while high BMPR1A was linked to worse survival. Gene ontology enrichment and pathway analyses revealed that BMPR2 and BMPR1B co-expressed genes were enriched in those associated with NB differentiation. BMPR1A co-expressed genes were enriched in those associated with cell proliferation. Moreover, the correlation between BMPR2 and BMPR1A was strengthened, while the correlation between BMPR2 and BMPR1B was lost, in MYCN-amplified NB. This suggested that differentiation should decrease BMPR1A and increase BMPR1B expression. In agreement, nerve growth factor treatment of cultured sympathetic neurons decreased Bmpr1a expression and increased Bmpr1b expression. Overexpression of dominant negative BMPR1B, treatment with a BMPR1B inhibitor and treatment with GDF5, which signals via BMPR1B, showed that BMPR1B signalling is required for optimal neuritogenesis in NB cells, suggesting that loss of BMPR1B may alter neuritogenesis. The present study shows that expression of distinct BMPRs is associated with different survival outcomes in NB.