Evidence map›Paper›PMID 26519903›Full record

ReviewNeuropharmacology2016

Purinergic receptors as potential therapeutic targets in Alzheimer's disease.

Lucas T Woods, Deepa Ajit, Jean M Camden, Laurie Erb, Gary A Weisman

Open access · greenAbstract readReview
In one paragraph

Review in Neuropharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
8.1field-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

54 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Targeting the adenosine AChinese journal of traumatology = Zhonghua chuang shang za zhi · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. The ATP-dependent Pathways and Human Diseases.Current medicinal chemistry · 2023
    Article
  17. Review
  18. Review
  19. Review
  20. The Pharmacological Potential of Adenosine AMolecules (Basel, Switzerland) · 2022
    Review
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

5 authors at 1 institution in 1 country.

Lucas T WoodsDepartment of Biochemistry, University of Missouri, Columbia, MO, USA; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, MO, USA.
Deepa AjitDepartment of Biochemistry, University of Missouri, Columbia, MO, USA; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, MO, USA.
Jean M CamdenDepartment of Biochemistry, University of Missouri, Columbia, MO, USA; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, MO, USA.
Laurie ErbDepartment of Biochemistry, University of Missouri, Columbia, MO, USA; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, MO, USA.
Gary A WeismanDepartment of Biochemistry, University of Missouri, Columbia, MO, USA; Interdisciplinary Neuroscience Program, University of Missouri, Columbia, MO, USA; Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, MO, USA. Electronic address: weismang@missouri.edu.
University of Missouri · US

Funding

Restoring Salivary Gland Function by Reducing Nucleotide-induced InflammationR01DE023342 · NIDCR · UNIVERSITY OF MISSOURI-COLUMBIA · PI WEISMAN, GARY ANDREW · 2014 to 2018
$2.9M
NIDCR NIH HHS R01 DE023342
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a progressive loss of memory and cognitive ability and is a serious cause of mortality. Many of the pathological characteristics associated with AD are revealed post-mortem, including amyloid-β plaque deposition, neurofibrillary tangles containing hyperphosphorylated tau proteins and neuronal loss in the hippocampus and cortex. Although several genetic mutations and risk factors have been associated with the disease, the causes remain poorly understood. Study of disease-initiating mechanisms and AD progression in humans is inherently difficult as most available tissue specimens are from late-stages of disease. Therefore, AD researchers rely on in vitro studies and the use of AD animal models where neuroinflammation has been shown to be a major characteristic of AD. Purinergic receptors are a diverse family of proteins consisting of P1 adenosine receptors and P2 nucleotide receptors for ATP, UTP and their metabolites. This family of receptors has been shown to regulate a wide range of physiological and pathophysiological processes, including neuroinflammation, and may contribute to the pathogenesis of neurodegenerative diseases like Parkinson's disease, multiple sclerosis and AD. Experimental evidence from human AD tissue has suggested that purinergic receptors may play a role in AD progression and studies using selective purinergic receptor agonists and antagonists in vitro and in AD animal models have demonstrated that purinergic receptors represent novel therapeutic targets for the treatment of AD. This article is part of the Special Issue entitled 'Purines in Neurodegeneration and Neuroregeneration'.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAstrocytesBrainEncephalitisHumansMicrogliaPlaque, AmyloidReceptors, Purinergic P1Receptors, Purinergic P2Amyloid beta-PeptidesReceptors, Purinergic P1Receptors, Purinergic P2Alzheimer's diseaseNeuroinflammationP1 receptorP2X receptorP2Y receptor

Identifiers

PMID26519903
PMCPMC4848184
OpenAlexW2190308692

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.