Evidence map›Paper›PMID 24587388›Full record

ArticlePloS one2014

Blood platelets in the progression of Alzheimer's disease.

Nina S Gowert, Lili Donner, Madhumita Chatterjee, Yvonne S Eisele, Seyda T Towhid, Patrick Münzer, Britta Walker, Isabella Ogorek, Oliver Borst, Maria Grandoch and 7 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
7.5field-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

75 citing papers in PubMed, 141 citations in OpenAlex.

  1. Trial
  2. Unveiling the procoagulant state in Alzheimer's disease: A novel PET imaging strategy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  19. Advances in Alzheimer's Disease Biomarkers.Current Alzheimer research · 2024
    Review
  20. Article

15 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

17 authors at 4 institutions in 1 country.

Nina S GowertDepartment of Clinical and Experimental Hemostasis, Hemotherapy and Transfusion Medicine, Heinrich-Heine-University, Düsseldorf, Germany.
Lili DonnerDepartment of Clinical and Experimental Hemostasis, Hemotherapy and Transfusion Medicine, Heinrich-Heine-University, Düsseldorf, Germany.
Madhumita ChatterjeeMedizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard-Karls-Universität, Tübingen, Germany.
Yvonne S EiseleDepartment of Cellular Neurology, Hertie-Institut for Clinical Brain Research, Eberhard-Karls University, Tübingen, Germany ; DZNE, German Center for Neurodegenerative Diseases, Tübingen, Germany.
Seyda T TowhidDepartment of Physiology, Eberhard-Karls University, Tübingen, Germany.
Patrick MünzerDepartment of Physiology, Eberhard-Karls University, Tübingen, Germany.
Britta WalkerDepartment of Physiology, Eberhard-Karls University, Tübingen, Germany.
Isabella OgorekDepartment of Neuropathology, Heinrich-Heine-University, Düsseldorf, Germany.
Oliver BorstMedizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard-Karls-Universität, Tübingen, Germany ; Department of Physiology, Eberhard-Karls University, Tübingen, Germany.
Maria GrandochInstitut für Pharmakologie u. Klinische Pharmakologie, Universitätsklinikum der Heinrich-Heine-Universität, Düsseldorf, Germany.
Martin SchallerDepartment of Dermatology, Eberhard-Karls University, Tübingen, Germany.
Jens W FischerInstitut für Pharmakologie u. Klinische Pharmakologie, Universitätsklinikum der Heinrich-Heine-Universität, Düsseldorf, Germany.
Meinrad GawazMedizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard-Karls-Universität, Tübingen, Germany.
Sascha WeggenDepartment of Neuropathology, Heinrich-Heine-University, Düsseldorf, Germany.
Florian LangDepartment of Physiology, Eberhard-Karls University, Tübingen, Germany.
Mathias JuckerDepartment of Cellular Neurology, Hertie-Institut for Clinical Brain Research, Eberhard-Karls University, Tübingen, Germany.
Margitta ElversDepartment of Clinical and Experimental Hemostasis, Hemotherapy and Transfusion Medicine, Heinrich-Heine-University, Düsseldorf, Germany ; Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard-Karls-Universität, Tübingen, Germany.
University of Tübingen · DEHeinrich Heine University Düsseldorf · DEHertie Institute for Clinical Brain Research · DEDüsseldorf University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by neurotoxic amyloid-ß plaque formation in brain parenchyma and cerebral blood vessels known as cerebral amyloid angiopathy (CAA). Besides CAA, AD is strongly related to vascular diseases such as stroke and atherosclerosis. Cerebrovascular dysfunction occurs in AD patients leading to alterations in blood flow that might play an important role in AD pathology with neuronal loss and memory deficits. Platelets are the major players in hemostasis and thrombosis, but are also involved in neuroinflammatory diseases like AD. For many years, platelets were accepted as peripheral model to study the pathophysiology of AD because platelets display the enzymatic activities to generate amyloid-ß (Aß) peptides. In addition, platelets are considered to be a biomarker for early diagnosis of AD. Effects of Aß peptides on platelets and the impact of platelets in the progression of AD remained, however, ill-defined. The present study explored the cellular mechanisms triggered by Aß in platelets. Treatment of platelets with Aß led to platelet activation and enhanced generation of reactive oxygen species (ROS) and membrane scrambling, suggesting enhanced platelet apoptosis. More important, platelets modulate soluble Aß into fibrillar structures that were absorbed by apoptotic but not vital platelets. This together with enhanced platelet adhesion under flow ex vivo and in vivo and platelet accumulation at amyloid deposits of cerebral vessels of AD transgenic mice suggested that platelets are major contributors of CAA inducing platelet thrombus formation at vascular amyloid plaques leading to vessel occlusion critical for cerebrovascular events like stroke.

Indexed as

AdultAlzheimer DiseaseAmyloidAmyloid beta-PeptidesAnimalsApoptosisBlood PlateletsCells, CulturedCerebral Amyloid AngiopathyDisease Models, AnimalDisease ProgressionHumansMice, Inbred C57BLMice, TransgenicMicroscopy, ElectronMicroscopy, FluorescenceAmyloidAmyloid beta-PeptidesReactive Oxygen Species

Identifiers

PMID24587388
PMCPMC3938776
OpenAlexW2133885791

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.