Evidence map›Paper›PMID 35805109›Full record

ReviewCells2022

GLP-1 Receptor Agonists in Neurodegeneration: Neurovascular Unit in the Spotlight.

Giulia Monti, Diana Gomes Moreira, Mette Richner, Henricus Antonius Maria Mutsaers, Nelson Ferreira, Asad Jan

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
6.6field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 55 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

6 authors at 2 institutions in 2 countries.

Giulia MontiDepartment of Biomedicine, Aarhus University, Høegh-Guldbergs Gade 10, DK-8000 Aarhus, Denmark.ORCID 0000-0001-9404-1273
Diana Gomes MoreiraVIB-KU Leuven Center for Brain & Disease Research, Herestraat 49, 3000 Leuven, Belgium.ORCID 0000-0003-2937-1772
Mette RichnerDepartment of Biomedicine, Aarhus University, Høegh-Guldbergs Gade 10, DK-8000 Aarhus, Denmark.
Henricus Antonius Maria MutsaersDepartment of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 82, DK-8200 Aarhus, Denmark.
Nelson FerreiraDepartment of Biomedicine, Aarhus University, Høegh-Guldbergs Gade 10, DK-8000 Aarhus, Denmark.ORCID 0000-0002-0305-9097
Asad JanDepartment of Biomedicine, Aarhus University, Høegh-Guldbergs Gade 10, DK-8000 Aarhus, Denmark.ORCID 0000-0002-3636-0070
Aarhus University · DKVIB-KU Leuven Center for Brain & Disease Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defects in brain energy metabolism and proteopathic stress are implicated in age-related degenerative neuronopathies, exemplified by Alzheimer's disease (AD) and Parkinson's disease (PD). As the currently available drug regimens largely aim to mitigate cognitive decline and/or motor symptoms, there is a dire need for mechanism-based therapies that can be used to improve neuronal function and potentially slow down the underlying disease processes. In this context, a new class of pharmacological agents that achieve improved glycaemic control via the glucagon-like peptide 1 (GLP-1) receptor has attracted significant attention as putative neuroprotective agents. The experimental evidence supporting their potential therapeutic value, mainly derived from cellular and animal models of AD and PD, has been discussed in several research reports and review opinions recently. In this review article, we discuss the pathological relevance of derangements in the neurovascular unit and the significance of neuron-glia metabolic coupling in AD and PD. With this context, we also discuss some unresolved questions with regard to the potential benefits of GLP-1 agonists on the neurovascular unit (NVU), and provide examples of novel experimental paradigms that could be useful in improving our understanding regarding the neuroprotective mode of action associated with these agents.

Indexed as

Alzheimer DiseaseNeuroprotective AgentsParkinson DiseaseAnimalsGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorNeuroprotective AgentsAlzheimer’s diseaseglucagon-like peptide-1 (GLP-1)neurodegenerationneurovascular unitParkinson’s disease

Identifiers

PMID35805109
PMCPMC9265397
OpenAlexW4283460245

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.