A peptide that links diabetes and Alzheimer’s

MELIS-UPF leads a study showing how the accumulation of β-amyloid peptide, which causes Alzheimer’s, leads to insulin resistance.

Peptide aggregation and subsequent oligomer formation is a common cause of neurodegenerative diseases such as Alzheimer's, Parkinson's or Amyotrophic Lateral Sclerosis. Credit: Robina Weermeijer for Unsplash.

Monomeric β-amyloid peptide is secreted by all cells in the body, with the brain being where it is produced most. Although its precise function is still unknown, a recent collaboration between several labs from the Department of Medicine and Life Sciences at Pompeu Fabra University (MELIS-UPF) shows how its function changes over the years, going from activating the sugar uptake by neurons, to inhibit it.

The research team has worked with human cell cultures and prepared a computational analysis that mimics the physiological and pathological functioning of the peptide. This has allowed them to see that, over time, the β-amyloid peptide aggregates from a monomeric to an oligomeric configuration. This new beta-sheet conformation, typical of Alzheimer’s, is capable of blocking the insulin receptor of neurons, preventing them from obtaining the glucose needed to function.

During the early stages of Alzheimer’s, a reduction in the metabolic activity of neurons and in glucose uptake is seen
Francisco Muñoz, MELIS-UPF

Thus, the study points out that the accumulation of β-amyloid, which causes Alzheimer’s disease, in turn produces insulin resistance, damaging neuronal metabolism. “Studying drugs that are already used successfully for the treatment of type 2 diabetes could be useful for the treatment of Alzheimer’s disease”, adds Francisco Muñoz, researcher at MELIS-UPF and senior author of the article.

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