Evidence map›Paper›PMID 31771069›Full record

ArticleJournal of Alzheimer's disease : JAD2020

Relationships of Cerebrospinal Fluid Alzheimer's Disease Biomarkers and COMT, DBH, and MAOB Single Nucleotide Polymorphisms.

Mirjana Babić Leko, Matea Nikolac Perković, Nataša Klepac, Dubravka Švob Štrac, Fran Borovečki, Nela Pivac, Patrick R Hof, Goran Šimić

Abstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Review
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  6. Article
  7. Parkinson's disease · 2022
    Article
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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

8 authors.

Mirjana Babić LekoDepartment of Neuroscience, Croatian Institute for Brain Research, University of Zagreb Medical School, Zagreb, Croatia.
Matea Nikolac PerkovićDepartment of Molecular Medicine, Institute Ruđer Bošković, Zagreb, Croatia.
Nataša KlepacDepartment of Neurology, University Hospital Centre Zagreb, Zagreb, Croatia.
Dubravka Švob ŠtracDepartment of Molecular Medicine, Institute Ruđer Bošković, Zagreb, Croatia.
Fran BorovečkiDepartment of Neurology, University Hospital Centre Zagreb, Zagreb, Croatia.
Nela PivacDepartment of Molecular Medicine, Institute Ruđer Bošković, Zagreb, Croatia.
Patrick R HofNash Family Department of Neuroscience, Friedman Brain Institute, and Ronald M. Loeb Center for Alzheimer's Disease, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Goran ŠimićDepartment of Neuroscience, Croatian Institute for Brain Research, University of Zagreb Medical School, Zagreb, Croatia.

Funding

VESICULAR LOCALIZATION AND FUNCTION OF PRESENILIN 1 FRAGMENTP50AG005138 · NIA · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GROSSMAN, HILLEL · 1985 to 2019
$37.9M
NIA NIH HHS P50 AG005138
6 · The paper itself

Abstract

The noradrenergic and dopaminergic systems are affected in Alzheimer's disease (AD). Polymorphisms in genes encoding enzymes and proteins that are components of these systems can affect products of transcription and translation and lead to altered enzymatic activity and alterations in overall dopamine and noradrenaline levels. Catechol-O-methyltransferase (COMT) and monoamine oxidase B (MAOB) are the enzymes that regulate degradation of dopamine, while dopamine β-hydroxylase (DBH) is involved in synthesis of noradrenaline. COMT Val158Met (rs4680), DBH rs1611115 (also called -1021C/T or -970C/T), and MAOB rs1799836 (also called A644G) polymorphisms have been previously associated with AD. We assessed whether these polymorphisms are associated with cerebrospinal fluid (CSF) AD biomarkers including total tau (t-tau), phosphorylated tau proteins (p-tau181, p-tau199, and p-tau231), amyloid-β42 (Aβ42), and visinin-like protein 1 (VILIP-1) to test possible relationships of specific genotypes and pathological levels of CSF AD biomarkers. The study included 233 subjects: 115 AD, 53 mild cognitive impairment, 54 subjects with other primary causes of dementia, and 11 healthy controls. Significant decrease in Aβ42 levels was found in patients with GG compared to AG COMT Val158Met genotype, while t-tau and p-tau181 levels were increased in patients with AA compared to AG COMT Val158Met genotype. Aβ42 levels were also decreased in carriers of A allele in MAO-B rs1799836 polymorphism, while p-tau181 levels were increased in carriers of T allele in DBH rs1611115 polymorphism. These results indicate that COMT Val158Met, DBH rs1611115, and MAOB rs1799836 polymorphisms deserve further investigation as genetic markers of AD.

Indexed as

AgedAlzheimer DiseaseCatechol O-MethyltransferaseCognitive DysfunctionCroatiaDNADopamine beta-HydroxylaseFemaleGene FrequencyGenotypeHeterozygoteHumansMaleMiddle AgedMonoamine OxidasePolymorphism, Single NucleotideCatechol O-MethyltransferaseCOMT protein, humanDNADopamine beta-HydroxylaseMAPT protein, humanMonoamine Oxidasetau ProteinsAlzheimer’s diseasebiomarkersCOMTDBHdopamineMAOBnoradrenalinepolymorphisms

Identifiers

PMID31771069
PMCPMC7029364

What OpenQuestion holds

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Registered trials

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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.