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Abstract Background Glucagon-like peptide-1 (GLP-1) plays a crucial role in metabolic disorders by enhancing insulin secretion, inhibiting glucagon release, and slowing gastric emptying, thereby improving glycemic control
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320 Similar protective roles are observed in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), where HSP70 and HSP90 suppress the aggregation of TDP-43, a protein that forms pathological cytoplasmic inclusions in affected neurons
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