Neural Regeneration Research ›› 2026, Vol. 21 ›› Issue (8): 3545-3546.doi: 10.4103/NRR.NRR-D-25-00793

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Deconvolution in Alzheimer´s disease

Sho Oasa, Marianne Schultzberg, Lars Terenius*   

  1. Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden (Oasa S, Terenius L)
    Department of Neurobiology, Care Sciences & Society, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden (Schultzberg M)
  • Online:2026-08-18 Published:2026-04-25
  • Contact: Lars Terenius, PhD, lars.terenius@ki.se.

Abstract: Alzheimer’s disease (AD) is the most common origin of sporadic dementia. Rare familial forms have identified a central role for toxicity based on aggregation of peptide fragments generated from amyloid precursor protein (APP), named amyloid-beta (Aβ), which exists in two common forms, Aβ1–40 (Aβ40) and Aβ1–42 (Aβ42). The latter is more neurotoxic. A common clinical biomarker measured in blood is the ratio Aβ42/Aβ40.

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