dc.contributor.author
Schreyer, Stefanie
dc.contributor.author
Klein, Charlotte
dc.contributor.author
Pfeffer, Anna
dc.contributor.author
Rasińska, Justyna
dc.contributor.author
Stahn, Laura
dc.contributor.author
Knuth, Karlotta
dc.contributor.author
Abuelnor, Basim
dc.contributor.author
Panzel, Alina Elisabeth Catharina
dc.contributor.author
Rex, André
dc.contributor.author
Koch, Stefan
dc.contributor.author
Hemmati-Sadeghi, Shabnam
dc.contributor.author
Steiner, Barbara
dc.date.accessioned
2022-05-24T09:31:12Z
dc.date.available
2022-05-24T09:31:12Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/35134
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-34851
dc.description.abstract
Glucose hypometabolism potentially contributes to Alzheimer’s disease (AD) and might even represent an underlying mechanism. Here, we investigate the relationship of diet-induced metabolic stress and AD as well as the therapeutic potential of chia seeds as a modulator of glucose metabolism in the APP23 mouse model. 4–6 (pre-plaque stage, PRE) and 28–32 (advanced-plaque stage, ADV) weeks old APP23 and wild type mice received pretreatment for 12 weeks with either sucrose-rich (SRD) or control diet, followed by 8 weeks of chia seed supplementation. Although ADV APP23 mice generally showed functioning glucose homeostasis, they were more prone to SRD-induced glucose intolerance. This was accompanied by elevated corticosterone levels and mild insulin insensitivity. Chia seeds improved spatial learning deficits but not impaired cognitive flexibility, potentially mediated by amelioration of glucose tolerance, attenuation of corticosterone levels and reversal of SRD-induced elevation of pro-inflammatory cytokine levels. Since cognitive symptoms and plaque load were not aggravated by SRD-induced metabolic stress, despite enhanced neuroinflammation in the PRE group, we conclude that impairments of glucose metabolism do not represent an underlying mechanism of AD in this mouse model. Nevertheless, chia seeds might provide therapeutic potential in AD as shown by the amelioration of cognitive symptoms.
en
dc.rights.uri
https://creativecommons.org/licenses/by/4.0/
dc.subject
Alzheimer Disease
en
dc.subject
Amyloid beta-Protein Precursor
en
dc.subject
Disease Models, Animal
en
dc.subject
Insulin Resistance
en
dc.subject
Mice, Inbred C57BL
en
dc.subject
Mice, Transgenic
en
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit
dc.title
Chia seeds as a potential cognitive booster in the APP23 Alzheimer’s disease model
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation.articlenumber
18215
dcterms.bibliographicCitation.doi
10.1038/s41598-020-75209-z
dcterms.bibliographicCitation.journaltitle
Scientific Reports
dcterms.bibliographicCitation.originalpublishername
Springer Nature
dcterms.bibliographicCitation.volume
10
refubium.affiliation
Charité - Universitätsmedizin Berlin
refubium.funding
Springer Nature DEAL
refubium.resourceType.isindependentpub
no
dcterms.accessRights.openaire
open access
dcterms.bibliographicCitation.pmid
33106576
dcterms.isPartOf.eissn
2045-2322