Evidence map›Paper›PMID 22925831›Full record

ReviewMolecular psychiatry2013

What's hAPPening at synapses? The role of amyloid β-protein precursor and β-amyloid in neurological disorders.

C J Westmark

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
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  15. Review
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  18. Article
  19. Amyloid-Beta Mediates Homeostatic Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  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

1 author at 1 institution in 1 country.

C J WestmarkWaisman Center for Developmental Disabilities, University of Wisconsin, Madison, Madison, WI 53705, USA. westmark@wisc.edu
Wisconsin Disability Association · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence suggests that dysregulated levels of amyloid β-protein precursor (APP) and its catabolites contribute to the impaired synaptic plasticity and seizure incidence observed in several neurological disorders, including Alzheimer's disease, fragile X syndrome, Down's syndrome, autism, epilepsy and Parkinson's disease as well as in brain injury. This review article summarizes what is known regarding the synaptic synthesis, processing and function of APP and amyloid-beta (Aβ), as well as discusses how these proteins could contribute to the altered synaptic plasticity and pathology of the aforementioned disorders. In addition, APP and its proteolytic fragments are emerging as biomarkers for neurological health, and pharmacological interventions that modulate their levels, such as secretase inhibitors, passive immunotherapy against Aβ and mGluR5 antagonists, are reviewed.

Indexed as

Amyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesBiomarkersEnzyme InhibitorsExcitatory Amino Acid AntagonistsHumansImmunization, PassiveModels, NeurologicalNervous System DiseasesNeuronal PlasticitySynapsesAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesBiomarkersEnzyme InhibitorsExcitatory Amino Acid Antagonists

Identifiers

PMID22925831
OpenAlexW1601830790

What OpenQuestion holds

Textmetadata
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.