Evidence map›Paper›PMID 33106576›Full record

ArticleScientific reports2020

Chia seeds as a potential cognitive booster in the APP23 Alzheimer's disease model.

Stefanie Schreyer, Charlotte Klein, Anna Pfeffer, Justyna Rasińska, Laura Stahn, Karlotta Knuth, Basim Abuelnor, Alina Elisabeth Catharina Panzel, André Rex, Stefan Koch and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 13 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Stefanie SchreyerDepartment of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany. stefanie.schreyer@charite.de.
Charlotte KleinDepartment of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Anna PfefferDepartment of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Justyna RasińskaDepartment of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Laura StahnDepartment of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Karlotta KnuthDepartment of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Basim AbuelnorDepartment of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Alina Elisabeth Catharina PanzelDepartment of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
André RexDepartment of Experimental Neurology and Center for Stroke Research Berlin, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Stefan KochDepartment of Experimental Neurology and Center for Stroke Research Berlin, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Shabnam Hemmati-SadeghiDepartment of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Barbara SteinerDepartment of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DEFreie Universität Berlin · DEBerlin Institute of Health at Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Disease Models, AnimalInsulin ResistanceAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimal FeedAnimalsCognitionDietFemaleGlucoseMaleMiceMice, Inbred C57BLMice, TransgenicMutationSalviaAmyloid beta-Protein PrecursorAPP protein, humanGlucose

Identifiers

PMID33106576
PMCPMC7589531
OpenAlexW3093881843

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.