Pancreatic islets contain beta cells that synthesize and release insulin, a key hormone in glucose metabolism. Islets are innervated by sympathetic innervation, which inhibits insulin release when activated. Research from our lab has shown an increase in sympathetic varicosity size in older animals, but the mechanism underlying this remains unclear. This research hypothesizes that the age-related increase in sympathetic varicosity size is associated with beta-amyloid aggregation. According to this hypothesis, beta-amyloid accumulation may compromise the release of the sympathetic neurotransmitter norepinephrine, thereby impacting hormone release. Using immunohistochemistry and confocal microscopy, we standardized labeling of the beta-amyloid and sympathetic varicosities within pancreatic islets from young (4-5months), middle (10-11 months), and old (18-22months) mouse groups. Our preliminary data shows a clear signal of beta-amyloid and sympathetic varicosities within pancreatic islets across different age groups. Our next step is to evaluate whether the two signals colocalize and if there are age-associated changes. This research will contribute to determining the specific mechanisms associated with the increase in sympathetic varicosities related to aging
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