image: Conceptual diagram summarizing the central experiment comparing cell death in amyloid-β treated neuronal cells with and without pancreatic β cell culture supernatant.
Credit: Yazawa et al.
Pancreas cells may produce a protein that can protect the brain from Alzheimer's disease. In individuals with Alzheimer's disease, a peptide known as amyloid-β accumulates and forms tangled plaques. People with diabetes have a higher probability of developing Alzheimer's disease, raising the possibility of a link between the cells that are disordered in diabetes—pancreatic β cells—and the onset of Alzheimer's disease. However, insulin supplementation may not halt the development of Alzheimer's disease. Toru Hosoi and colleagues hypothesized the existence of a neuroprotective agent secreted by pancreatic β cells, distinct from insulin, that could mitigate the onset of Alzheimer's disease. The authors cultured mouse pancreatic β cells, then exposed neuronal cells treated with amyloid-β to liquid from the pancreatic β cells. The liquid effectively stopped amyloid-β-induced neuronal cell death. The neuroprotective factor at work is thought to be Fibroblast Growth Factor 23 (FGF23), an endocrine protein. Treating neuronal cells subjected to amyloid-β with FGF23 alone significantly reduced cell death from amyloid-β toxicity. According to the authors, FGF23 may increase ribosomal proteins, helping to maintain the homeostasis of ribosomal components in neurons.
Journal
PNAS Nexus
Article Title
Pancreatic β cell-secreted factor FGF23 attenuates Alzheimer’s disease-related amyloid β-induced neuronal death
Article Publication Date
28-Jan-2025