Evidence map›Paper›PMID 28866832›Full record

ArticleMolecular neurobiology2018

Increased Levels of Brain Adrenomedullin in the Neuropathology of Alzheimer's Disease.

Hilda Ferrero, Ignacio M Larrayoz, Eva Martisova, Maite Solas, David R Howlett, Paul T Francis, Francisco J Gil-Bea, Alfredo Martínez, María J Ramírez

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 33 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

9 authors at 4 institutions in 3 countries.

Hilda FerreroDepartment of Pharmacology and Toxicology, University of Navarra, Pamplona, Spain.
Ignacio M LarrayozOncology Area, Center for Biomedical Research of La Rioja (CIBIR), Logroño, Spain.
Eva MartisovaDepartment of Pharmacology and Toxicology, University of Navarra, Pamplona, Spain.
Maite SolasDepartment of Pharmacology and Toxicology, University of Navarra, Pamplona, Spain.
David R HowlettWolfson Centre for Age-Related Diseases, King's College, London, UK.
Paul T FrancisWolfson Centre for Age-Related Diseases, King's College, London, UK.
Francisco J Gil-BeaDepartment of Pharmacology and Toxicology, University of Navarra, Pamplona, Spain.
Alfredo MartínezOncology Area, Center for Biomedical Research of La Rioja (CIBIR), Logroño, Spain.
María J RamírezDepartment of Pharmacology and Toxicology, University of Navarra, Pamplona, Spain. mariaja@unav.es.ORCID http://orcid.org/0000-0002-3488-9579
Navarre Institute of Health Research · ESCenter for Biomedical Research of La Rioja · ESKing's College London · GBKarolinska Institutet · SE

Funding

Medical Research Council MR/L022656/1
6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by the loss of synaptic contacts caused in part by cytoskeleton disruption. Adrenomedullin (AM) is involved in physiological functions such as vasodilation, hormone secretion, antimicrobial activity, cellular growth, and angiogenesis. In neurons, AM and related peptides are associated with some structural and functional cytoskeletal proteins, causing microtubule destabilization. Here, we describe the relationships between AM and other signs of AD in clinical specimens. Frontal cortex from AD patients and controls were studied for AM, acetylated tubulin, NCAM, Ox-42, and neurotransmitters. AM was increased in AD compared with controls, while levels of acetylated tubulin, NCAM, and neurotransmitters were decreased. Interestingly, increases in AM statistically correlated with the decrease in these markers. Furthermore, Ox42 overexpression in AD correlated with levels of AM. It is proposed that AD patients may have neural cytoskeleton failure associated with increase of AM levels, resulting in axon transport collapse and synaptic loss. These observations suggest that reducing AM expression may constitute a new avenue to prevent/treat AD.

Indexed as

AdrenomedullinAlzheimer DiseaseBiomarkersBrainCD11b AntigenCell Adhesion Molecules, NeuronalFrontal LobeHumansMicrogliaTubulinAdrenomedullinBiomarkersCD11b AntigenCell Adhesion Molecules, NeuronalITGAM protein, humanTubulinAdrenomedullinAlzheimer’s diseaseCell-to-cell contactMicrogliaMicrotubulesNeurotransmitter contents

Identifiers

PMID28866832
OpenAlexW2753346007

What OpenQuestion holds

Textmetadata
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.