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Characterization of Uranyl (UO22+) Ion Binding to Amyloid Beta (Aβ) Peptides : Effects on Aβ Structure and Aggregation

Berntsson, Elina (author)
Stockholms universitet,Institutionen för biokemi och biofysik
Vosough, Faraz, 1986- (author)
Stockholms universitet,Institutionen för biokemi och biofysik
Noormagi, Andra (author)
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Padari, Kärt (author)
Asplund, Fanny (author)
Stockholms universitet,Institutionen för biokemi och biofysik
Gielnik, Maciej (author)
Paul, Suman, 1984- (author)
Stockholms universitet,Institutionen för biokemi och biofysik
Jarvet, Jüri (author)
Stockholms universitet,Institutionen för biokemi och biofysik
Tõugu, Vello (author)
Roos, Per M. (author)
Karolinska Institutet
Kozak, Maciej (author)
Gräslund, Astrid, 1945- (author)
Stockholms universitet,Institutionen för biokemi och biofysik,CellPept Sweden AB, Sweden
Barth, Andreas, 1960- (author)
Stockholms universitet,Institutionen för biokemi och biofysik
Pooga, Margus (author)
Palumaa, Peep (author)
Wärmländer, Sebastian, 1970- (author)
Stockholms universitet,Institutionen för biokemi och biofysik,CellPept Sweden AB, Sweden
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 (creator_code:org_t)
2023
2023
English.
In: ACS Chemical Neuroscience. - 1948-7193. ; 14:15, s. 2618-2633
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Uranium (U) is naturally present in ambient air, water, and soil, and depleted uranium (DU) is released into the environment via industrial and military activities. While the radiological damage from U is rather well understood, less is known about the chemical damage mechanisms, which dominate in DU. Heavy metal exposure is associated with numerous health conditions, including Alzheimer’s disease (AD), the most prevalent age-related cause of dementia. The pathological hallmark of AD is the deposition of amyloid plaques, consisting mainly of amyloid-β (Aβ) peptides aggregated into amyloid fibrils in the brain. However, the toxic species in AD are likely oligomeric Aβ aggregates. Exposure to heavy metals such as Cd, Hg, Mn, and Pb is known to increase Aβ production, and these metals bind to Aβ peptides and modulate their aggregation. The possible effects of U in AD pathology have been sparsely studied. Here, we use biophysical techniques to study in vitro interactions between Aβ peptides and uranyl ions, UO22+, of DU. We show for the first time that uranyl ions bind to Aβ peptides with affinities in the micromolar range, induce structural changes in Aβ monomers and oligomers, and inhibit Aβ fibrillization. This suggests a possible link between AD and U exposure, which could be further explored by cell, animal, and epidemiological studies. General toxic mechanisms of uranyl ions could be modulation of protein folding, misfolding, and aggregation. 

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Neurosciences (hsv//eng)
NATURVETENSKAP  -- Biologi -- Biokemi och molekylärbiologi (hsv//swe)
NATURAL SCIENCES  -- Biological Sciences -- Biochemistry and Molecular Biology (hsv//eng)

Keyword

Alzheimer's disease
amyloid aggregation
metal-protein binding
neurodegeneration
heavy metal toxicity

Publication and Content Type

ref (subject category)
art (subject category)

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