Evidence map›Paper›PMID 33467075›Full record

ArticleInternational journal of molecular sciences2021

RETRACTED: Liraglutide Has Anti-Inflammatory and Anti-Amyloid Properties in Streptozotocin-Induced and 5xFAD Mouse Models of Alzheimer's Disease.

Leela Paladugu, Abeer Gharaibeh, Nivya Kolli, Cameron Learman, Tia C Hall, Lixin Li, Julien Rossignol, Panchanan Maiti, Gary L Dunbar

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 42 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 3 pooled it
5.9field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 3 syntheses or guidelines pooled it, 77 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Leela PaladuguField Neurosciences Institute Laboratory for Restorative Neurology, Central Michigan University, Mount Pleasant, MI 48859, USA.
Abeer GharaibehField Neurosciences Institute Laboratory for Restorative Neurology, Central Michigan University, Mount Pleasant, MI 48859, USA.ORCID 0000-0003-3549-1826
Nivya KolliField Neurosciences Institute Laboratory for Restorative Neurology, Central Michigan University, Mount Pleasant, MI 48859, USA.ORCID 0000-0001-9010-9998
Cameron LearmanField Neurosciences Institute Laboratory for Restorative Neurology, Central Michigan University, Mount Pleasant, MI 48859, USA.
Tia C HallField Neurosciences Institute Laboratory for Restorative Neurology, Central Michigan University, Mount Pleasant, MI 48859, USA.
Lixin LiPhysician Assistant Program, Central Michigan University, Mount Pleasant, MI 48859, USA.
Julien RossignolField Neurosciences Institute Laboratory for Restorative Neurology, Central Michigan University, Mount Pleasant, MI 48859, USA.ORCID 0000-0002-8662-0547
Panchanan MaitiField Neurosciences Institute Laboratory for Restorative Neurology, Central Michigan University, Mount Pleasant, MI 48859, USA.ORCID 0000-0003-3213-8015
Gary L DunbarField Neurosciences Institute Laboratory for Restorative Neurology, Central Michigan University, Mount Pleasant, MI 48859, USA.
Central Michigan University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent clinical and epidemiological studies support the contention that diabetes mellitus (DM) is a strong risk factor for the development of Alzheimer's disease (AD). The use of insulin cell toxin, streptozotocin (STZ), when injected into the lateral ventricles, develops an insulin resistant brain state (IRBS) and represents a non-transgenic, or sporadic AD model (SAD), with several AD-like neuropathological features. The present study explored the effects of an anti-diabetic drug, liraglutide (LIR), in reversing major pathological hallmarks in the prodromal disease stage of both the 5xFAD transgenic and SAD mouse models of AD. Three-month-old 5xFAD and age-matched wild type mice were given a single intracerebroventricular (i.c.v) injection of STZ or vehicle (saline) and were subsequently treated with LIR, intraperitoneally (IP), once a day for 30 days. The extent of neurodegeneration, Aβ plaque load, and key proteins associated with the insulin signaling pathways were measured using Western blot and neuroinflammation (via immunohistological assays) in the cortical and hippocampal regions of the brain were assessed following a series of behavioral tests used to measure cognitive function after LIR or vehicle treatments. Our results indicated that STZ significantly increased neuroinflammation, Aβ plaque deposition and disrupted insulin signaling pathway, while 25 nmol/kg LIR, when injected IP, significantly decreased neuroinflammatory responses in both SAD and 5xFAD mice before significant cognitive changes were observed, suggesting LIR can reduce early neuropathology markers prior to the emergence of overt memory deficits. Our results indicate that LIR has neuroprotective effects and has the potential to serve as an anti-inflammatory and anti-amyloid prophylactic therapy in the prodromal stages of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAnti-Inflammatory AgentsLiraglutideMiceNeuroprotective AgentsPresenilinsStreptozocinAmyloid beta-PeptidesAnti-Inflammatory AgentsLiraglutideNeuroprotective AgentsPresenilinsStreptozocinAlzheimer’s diseaseamyloid beta proteindiabetes mellitusliraglutideneuroinflammationsporadic Alzheimer’s diseasestreptozotocin

Identifiers

PMID33467075
PMCPMC7829894
OpenAlexW3121912114

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.