Evidence map›Paper›PMID 25883618›Full record

ReviewNeural regeneration research2015

Antagonizing amyloid-β/calcium-sensing receptor signaling in human astrocytes and neurons: a key to halt Alzheimer's disease progression?

Ilaria Dal Prà, Anna Chiarini, Ubaldo Armato

Open access · goldAbstract readReview
In one paragraph

Review in Neural regeneration research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

7 citing papers in PubMed, 17 citations in OpenAlex.

  1. Renal CaInternational journal of molecular sciences · 2019
    Review
  2. Review
  3. The Expression of Calcium Sensing Receptor in Normal and Diabetic Rat Eyes.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  4. Review
  5. Article
  6. Review
  7. 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

3 authors at 1 institution in 1 country.

Ilaria Dal PràHistology & Embryology Section, Department of Life & Reproduction Sciences, University of Verona Medical School, Verona, Venetia, I-37134, Italy.
Anna ChiariniHistology & Embryology Section, Department of Life & Reproduction Sciences, University of Verona Medical School, Verona, Venetia, I-37134, Italy.
Ubaldo ArmatoHistology & Embryology Section, Department of Life & Reproduction Sciences, University of Verona Medical School, Verona, Venetia, I-37134, Italy.
University of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astrocytes' roles in late-onset Alzheimer's disease (LOAD) promotion are important, since they survive soluble or fibrillar amyloid-β peptides (Aβs) neurotoxic effects, undergo alterations of intracellular and intercellular Ca(2+) signaling and gliotransmitters release via the Aβ/α7-nAChR (α7-nicotinic acetylcholine receptor) signaling, and overproduce/oversecrete newly synthesized Aβ42 oligomers, NO, and VEGF-A via the Aβ/CaSR (calcium-sensing receptor) signaling. Recently, it was suggested that the NMDAR (N-methyl-D-aspartate receptor) inhibitor nitromemantine would block the synapse-destroying effects of Aβ/α7-nAChR signaling. Yet, this and the progressive extracellular accrual and spreading of Aβ42 oligomers would be stopped well upstream by NPS 2143, an allosteric CaSR antagonist (calcilytic).

Indexed as

Alzheimer's diseaseamyloid-β; astrocytesCa2+calcilyticcalcium-sensing receptornitromemantineNPS 2143α7-nicotinic acetylcholine receptor

Identifiers

PMID25883618
PMCPMC4392667
OpenAlexW2073332176

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.