Amyloid beta (Aβ) peptides, known for their involvement in neurodegenerative diseases like Alzheimer's, have recently been recognized as significant contributors to metabolic disorders, including type 2 diabetes. This study examined the effects of Aβ40 and Aβ42 peptides on cell viability and glucose-stimulated insulin secretion in rat insulinoma (INS-1) cells. Aβ40 treatment demonstrated no significant toxicity at lower concentrations; however, it did reduce cell viability at higher concentrations and with prolonged exposure. Conversely, Aβ42 exhibited notable cytotoxicity even at lower concentrations within 24 hours. The combined treatment of Aβ40 and Aβ42 at a 10:1 ratio further accelerated the decline in cell viability, indicating a synergistic toxic effect. Importantly, Aβ40/42 treatment did not impair glucose-stimulated insulin secretion in INS-1 cells under the conditions tested. These findings suggest that Aβ peptides may contribute to β-cell loss in type 2 diabetes through their cytotoxic effects, although the direct impact on insulin secretion requires further study. Nutritional interventions aimed at reducing Aβ aggregation and associated oxidative stress could offer promising strategies to protect β-cell viability, warranting further research to clarify the underlying mechanisms of such dietary modulation.

disease is a characterized by cognitive impairment, progressive neurodegeneration and formation of amyloid-β (Aβ)-containing plaques and neurofibrillary tangles. In progress of disease, inflammation plays major role to lead the neuronal death. Previously Serum amyloid A (SAA1), one of the acute-phase proteins, was examined and found that this liver derived protein pass through the brain blood barrier (BBB). By making double transgenic mice through the crossing over APP c105 mice, produce amyloid beta1-42 in brain as a pathogen, and SAA1 overexpression mice confirm the SAA exacerbate inflammation that triggered by amyloid beta accumulation in brain. Followed behavior test also shows double transgenic mice have more damage in memory than the APP mouse that only designed to express the amyloid beta 1-42.