Evidence map›Paper›PMID 34312771›Full record

ArticleMolecular neurobiology2021

Genetic Depletion of Amylin/Calcitonin Receptors Improves Memory and Learning in Transgenic Alzheimer's Disease Mouse Models.

Aarti Patel, Ryoichi Kimura, Wen Fu, Rania Soudy, David MacTavish, David Westaway, Jing Yang, Rachel A Davey, Jeffrey D Zajac, Jack H Jhamandas

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-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

7 citing papers in PubMed, 8 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

10 authors at 3 institutions in 4 countries.

Aarti Patel *Department of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, T6G 2S2, Canada.
Ryoichi Kimura *Department of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, T6G 2S2, Canada.
Wen Fu *Department of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, T6G 2S2, Canada.
Rania SoudyDepartment of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, T6G 2S2, Canada.
David MacTavishDepartment of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, T6G 2S2, Canada.
David WestawayDepartment of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, T6G 2S2, Canada.
Jing YangDepartment of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, T6G 2S2, Canada.
Rachel A DaveyDepartment of Medicine, University of Melbourne, Austin HealthHeidelberg, VIC, 3074, Australia.
Jeffrey D ZajacDepartment of Medicine, University of Melbourne, Austin HealthHeidelberg, VIC, 3074, Australia.
Jack H JhamandasDepartment of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, T6G 2S2, Canada. jack.jhamandas@ualberta.ca.ORCID http://orcid.org/0000-0002-4688-6500
University of Alberta · CAThe University of Melbourne · AUCairo University · EG

Funding

CIHR PS 159746Japan Society for the Promotion of Science KAKENHI Grant Number JP19K07014
6 · The paper itself

Abstract

Based upon its interactions with amyloid β peptide (Aβ), the amylin receptor, a class B G protein-coupled receptor (GPCR), is a potential modulator of Alzheimer's disease (AD) pathogenesis. However, past pharmacological approaches have failed to resolve whether activation or blockade of this receptor would have greater therapeutic benefit. To address this issue, we generated compound mice expressing a human amyloid precursor protein gene with familial AD mutations in combination with deficiency of amylin receptors produced by hemizygosity for the critical calcitonin receptor subunit of this heterodimeric GPCR. These compound transgenic AD mice demonstrated attenuated responses to human amylin- and Aβ-induced depression of hippocampal long-term potentiation (LTP) in keeping with the genetic depletion of amylin receptors. Both the LTP responses and spatial memory (as measured with Morris water maze) in these mice were improved compared to AD mouse controls and, importantly, a reduction in both the amyloid plaque burden and markers of neuroinflammation was observed. Our data support the notion of further development of antagonists of the amylin receptor as AD-modifying therapies.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsCells, CulturedEndothelium, VascularExcitatory Postsynaptic PotentialsFemaleHumansMaleMaze LearningMiceMice, Inbred C3HMice, Inbred C57BLMice, TransgenicOrgan Culture TechniquesReceptors, CalcitoninAmyloid beta-Protein PrecursorReceptors, CalcitoninReceptors, Islet Amyloid PolypeptideAlzheimer’s diseaseAmylinAmylin receptorAmyloid-β proteinCalcitonin receptorHippocampusLong-term potentiationSpatial memory

Identifiers

PMID34312771
PMCPMC8497456
OpenAlexW3164328066

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.