Evidence map›Paper›PMID 27084356›Full record

ReviewProgress in neurobiology2017

Monoaminergic neuropathology in Alzheimer's disease.

Goran Šimić, Mirjana Babić Leko, Selina Wray, Charles R Harrington, Ivana Delalle, Nataša Jovanov-Milošević, Danira Bažadona, Luc Buée, Rohan de Silva, Giuseppe Di Giovanni and 2 more

Open access · greenAbstract readReview
In one paragraph

Review in Progress in neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed, 1 pooled it
15.0field-weighted citation impact, top 1% 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

159 citing papers in PubMed, 1 synthesis or guideline pooled it, 288 citations in OpenAlex.

  1. Pooled it
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  6. Vulnerability of locus coeruleus connections to aging and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  17. The impact of polygenic risk for alzheimer's disease on neurotransmitter-related grey matter atrophy in the alzheimer continuum.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  18. Review
  19. Article
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99 more citing papers are in PubMed but not listed here.

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

12 authors at 8 institutions in 5 countries.

Goran ŠimićDepartment of Neuroscience, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Zagreb, Croatia. Electronic address: gsimic@hiim.hr.
Mirjana Babić LekoDepartment of Neuroscience, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Zagreb, Croatia.
Selina WrayReta Lila Weston Institute and Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Charles R HarringtonSchool of Medicine and Dentistry, University of Aberdeen, Aberdeen, UK.
Ivana DelalleDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
Nataša Jovanov-MiloševićDepartment of Neuroscience, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Zagreb, Croatia.
Danira BažadonaDepartment of Neurology, University Hospital Center Zagreb, Zagreb, Croatia.
Luc BuéeUniversity of Lille, Inserm, CHU-Lille, UMR-S 1172, Alzheimer & Tauopathies, Lille, France.
Rohan de SilvaReta Lila Weston Institute and Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Giuseppe Di GiovanniDepartment of Physiology and Biochemistry, Faculty of Medicine and Surgery, University of Malta, Msida, Malta.
Claude M WischikSchool of Medicine and Dentistry, University of Aberdeen, Aberdeen, UK.
Patrick R HofFishberg Department of Neuroscience, Ronald M. Loeb Center for Alzheimer's Disease, and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
University of Zagreb · HRUniversity College London · GBUniversity of Aberdeen · GBBoston University · USIcahn School of Medicine at Mount Sinai · USUniversité de Lille · FRUniversity Hospital Centre Zagreb · HRUniversity of Malta · MT

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
Medical Research Council G0501560NIA NIH HHS P50 AG005138Parkinson's UK K-1212
6 · The paper itself

Abstract

None of the proposed mechanisms of Alzheimer's disease (AD) fully explains the distribution patterns of the neuropathological changes at the cellular and regional levels, and their clinical correlates. One aspect of this problem lies in the complex genetic, epigenetic, and environmental landscape of AD: early-onset AD is often familial with autosomal dominant inheritance, while the vast majority of AD cases are late-onset, with the ε4 variant of the gene encoding apolipoprotein E (APOE) known to confer a 5-20 fold increased risk with partial penetrance. Mechanisms by which genetic variants and environmental factors influence the development of AD pathological changes, especially neurofibrillary degeneration, are not yet known. Here we review current knowledge of the involvement of the monoaminergic systems in AD. The changes in the serotonergic, noradrenergic, dopaminergic, histaminergic, and melatonergic systems in AD are briefly described. We also summarize the possibilities for monoamine-based treatment in AD. Besides neuropathologic AD criteria that include the noradrenergic locus coeruleus (LC), special emphasis is given to the serotonergic dorsal raphe nucleus (DRN). Both of these brainstem nuclei are among the first to be affected by tau protein abnormalities in the course of sporadic AD, causing behavioral and cognitive symptoms of variable severity. The possibility that most of the tangle-bearing neurons of the LC and DRN may release amyloid β as well as soluble monomeric or oligomeric tau protein trans-synaptically by their diffuse projections to the cerebral cortex emphasizes their selective vulnerability and warrants further investigations of the monoaminergic systems in AD.

Indexed as

NeuropathologyAlzheimer DiseaseAnimalsBiogenic MonoaminesHumansPhosphorylationtau ProteinsBiogenic Monoaminestau Proteins5-hydroxytryptamine (serotonin)Alzheimer’s diseaseAmyloid beta (Aβ) peptideBlood-brain barrierCerebrospinal fluidEpigeneticsLocus coeruleusMetalsMonoaminesNeurofibrillary degenerationNon-cognitive symptomsNucleus raphe dorsalisPhosphorylationSleep-wake cycleTau protein

Identifiers

PMID27084356
PMCPMC5061605
OpenAlexW2336131134

What OpenQuestion holds

Textmetadata
LicenceTDM
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.