Evidence map›Paper›PMID 30051750›Full record

ReviewThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry2019

Amyloid Plaques of Alzheimer's Disease as Hotspots of Glutamatergic Activity.

Saak V Ovsepian, Valerie B O'Leary, Laszlo Zaborszky, Vasilis Ntziachristos, J Oliver Dolly

Abstract readReview
In one paragraph

Review in The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Molecular Biomarkers of Neuronal Injury in Epilepsy Shared with Neurodegenerative Diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. CYP46A1 Activation by Efavirenz Leads to Behavioral Improvement without Significant Changes in Amyloid Plaque Load in the Brain of 5XFAD Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Article
  18. Review
  19. Astroglia in Alzheimer's Disease.Advances in experimental medicine and biology · 2019
    Review
  20. Article
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.

Saak V OvsepianInstitute for Biological and Medical Imaging, Helmholtz Zentrum Munich, German Research Center for Environmental Health, Neuherberg, Germany.
Valerie B O'LearyInternational Centre for Neurotherapeutics, Dublin City University, Dublin, Ireland.
Laszlo ZaborszkyCenter for Molecular and Behavioral Neuroscience, Rutgers, the State University of New Jersey, Newark, NJ, USA.
Vasilis NtziachristosInstitute for Biological and Medical Imaging, Helmholtz Zentrum Munich, German Research Center for Environmental Health, Neuherberg, Germany.
J Oliver DollyInternational Centre for Neurotherapeutics, Dublin City University, Dublin, Ireland.

Funding

AFFERENT REGULATION OF CHOLINERGIC FOREBRAIN NEURONSR01NS023945 · NINDS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI ZABORSZKY, LASZLO · 1986 to 2019
$6.5M
NINDS NIH HHS R01 NS023945
6 · The paper itself

Abstract

Deposition of amyloid plaques in limbic and associative cortices is amongst the most recognized histopathologic hallmarks of Alzheimer's disease. Despite decades of research, there is a lack of consensus over the impact of plaques on neuronal function, with their role in cognitive decline and memory loss undecided. Evidence has emerged suggesting complex and localized axonal pathology around amyloid plaques, with a significant fraction of swellings and dystrophies becoming enriched with putative synaptic vesicles and presynaptic proteins normally colocalized at hotspots of transmitter release. In the absence of hallmark active zone proteins and postsynaptic receptive elements, the axonal swellings surrounding amyloid plaques have been suggested as sites for ectopic release of glutamate, which under reduced clearance can lead to elevated local excitatory drive. Throughout this review, we consider the emerging data suggestive of amyloid plaques as hotspots of compulsive glutamatergic activity. Evidence for local and long-range effects of nonsynaptic glutamate is discussed in the context of circuit dysfunctions and neurodegenerative changes of Alzheimer's disease.

Indexed as

Alzheimer DiseaseAnimalsAxonsBrainGlutamic AcidHumansPlaque, AmyloidPresynaptic TerminalsGlutamic AcidAlzheimer’s diseaseaxonal dystrophiesectopic releaseglutamatemetabotropic receptorsparacrine signaling

Identifiers

PMID30051750
PMCPMC6348130

What OpenQuestion holds

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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.