Evidence map›Paper›PMID 29067318›Full record

ArticleAlzheimer's & dementia (New York, N. Y.)2017

Cyclic AC253, a novel amylin receptor antagonist, improves cognitive deficits in a mouse model of Alzheimer's disease.

Rania Soudy, Aarti Patel, Wen Fu, Kamaljit Kaur, David MacTavish, David Westaway, Rachel Davey, Jeffrey Zajac, Jack Jhamandas

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's & dementia (New York, N. Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Mechanism of Metal Complexes in Alzheimer's Disease.International journal of molecular sciences · 2024
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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

9 authors at 4 institutions in 4 countries.

Rania SoudyDepartment of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Alberta, Canada.
Aarti PatelDepartment of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Alberta, Canada.
Wen FuDepartment of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Alberta, Canada.
Kamaljit KaurFaculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada.
David MacTavishDepartment of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Alberta, Canada.
David WestawayDepartment of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Alberta, Canada.
Rachel DaveyDepartment of Medicine, Austin Health, University of Melbourne, Heidelberg, Victoria, Australia.
Jeffrey ZajacDepartment of Medicine, Austin Health, University of Melbourne, Heidelberg, Victoria, Australia.
Jack JhamandasDepartment of Medicine (Neurology), Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Alberta, Canada.
University of Alberta · CAAustin Health · AUWomen and Children’s Health Research Institute · CACairo University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAmylin receptor serves as a portal for the expression of deleterious effects of amyloid β-protein (Aβ), a key pathologic hallmark of Alzheimer's disease. Previously, we showed that AC253, an amylin receptor antagonist, is neuroprotective against Aβ toxicity in vitro and abrogates Aβ-induced impairment of hippocampal long-term potentiation.

methodsAmyloid precursor protein-overexpressing TgCRND8 mice received intracerebroventricularly AC253 for 5 months. New cyclized peptide cAC253 was synthesized and administered intraperitoneally three times a week for 10 weeks in the same mouse model. Cognitive functions were monitored, and pathologic changes were quantified biochemically and immunohistochemically.

resultsAC253, when administered intracerebroventricularly, improves spatial memory and learning, increases synaptic integrity, reduces microglial activation without discernible adverse effects in TgCRND8 mice. cAC253 demonstrates superior brain permeability, better proteolytic stability, and enhanced binding affinity to brain amylin receptors after a single intraperitoneal injection. Furthermore, cAC253 administered intraperitoneally also demonstrates improvement in spatial memory in TgCRND8 mice. DISCUSSION: Amylin receptor is a therapeutic target for Alzheimer's disease and represents a disease-modifying therapy for this condition.

Indexed as

AC253 peptideAlzheimer's diseaseAmylin receptorAmyloid βBrain penetrationIn vivo imaging

Identifiers

PMID29067318
PMCPMC5651374
OpenAlexW2560348603

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.