picture:
Moreover, detailed aggregation dynamics experiments were performed to elucidate the effect of Cu(II) on the fibrillation of Aβ, as well as a global fit analysis, which revealed a specific inhibitory effect of Cu(II) on the fiber end elongation process.
These results were then rationalized in a model describing the molecular mechanism by which Cu(II) inhibits Aβ self-regulation by forming a complex with monomeric Aβ, which prevents fibril formation.
“Our model is transferrable to other related metal ions,” says the associate professor. Axel Abilene, who co-authored with Dr Henrik Biverstål in the study. “This contributes to a general understanding of the impact of metal ions on Aβ accumulation, which may be useful for designing specific medical strategies against Alzheimer’s disease.”
In the future, this approach could also be applied to other amyloidogenic systems and thus aid in understanding behavior in vivo of Aβ aggregation, in which metal ions are important environmental factors.
Thanks to the KI researchers Swedish Society for Medical ResearchAnd the formedAnd the Åke Wiberg FoundationAnd the Hedlund FoundationAnd the Magnus Bergvall FoundationAnd the Ahlin FoundationAnd the KI Research Foundation grantsAnd the Geriatrics FoundationAnd the Sigurd & Elsa Golje Memory FoundationAnd the JPco FundAnd the Osterman Foundation And the I’m next.
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