Evidence map›Paper›PMID 35822151›Full record

ReviewCureus2022

Understanding Protein Protocadherin-19 (PCDH19) Syndrome: A Literature Review of the Pathophysiology.

Juan A Moncayo, Ivan N Ayala, Jennifer M Argudo, Alex S Aguirre, Jashank Parwani, Ana Pachano, Diego Ojeda, Steven Cordova, Maria Gracia Mora, Christiany M Tapia and 1 more

Open access · diamondAbstract readReview
In one paragraph

Review in Cureus, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Triplication of theGenes · 2024
    Article
  6. Article
  7. Article
  8. 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

11 authors at 7 institutions in 3 countries.

Juan A MoncayoNeurology, Pontificia Universidad Católica del Ecuador, Quito, ECU.
Ivan N AyalaEndocrinology, Mayo Clinic, Rochester, USA.
Jennifer M ArgudoChild Neurology, Universidad de Cuenca, Cuenca, ECU.
Alex S AguirreMedicine, Universidad San Francisco de Quito, Quito, ECU.
Jashank ParwaniNeurology, Lokmanya Tilak Municipal Medical College, Mumbai, IND.
Ana PachanoMedicine, Universidad de las Americas, Quito, ECU.
Diego OjedaNeurology, Universidad San Francisco de Quito, Quito, ECU.
Steven CordovaNeurology, Caduceus Healthcare, Miami, USA.
Maria Gracia MoraSurgery, Universidad de Cuenca, Cuenca, ECU.
Christiany M TapiaSurgery, Universidad de Cuenca, Cuenca, ECU.
Juan Fernando OrtizNeurology, Universidad San Francisco de Quito, Quito, ECU.
Universidad San Francisco de Quito · ECUniversity of Cuenca · ECLokmanya Tilak Municipal General Hospital and Lokmanya Tilak Municipal Medical College · INMiami VA Healthcare System · USPontificia Universidad Católica del Ecuador · ECUniversidad de Las Américas · ECWinnMed · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PCDH19 syndrome is a monogenic epilepsy related to the protein protocadherin-19 (PCDH19) gene, which encodes for a protein important for brain development. The protein also seems to regulate gamma-aminobutyric acid type A receptors (GABA(A)(R)). The disease presents with refractory epilepsy that is characterized by seizures occurring in clusters. Till now, the pathophysiology of the disease is mainly unknown, so we conducted a literature review to elucidate the pathophysiology of PCDH19-related epilepsy. We used two databases to investigate this literature review (Google Scholar and PubMed). We selected full-text papers that are published in the English language and published after the year 2000. We selected initially 64 papers and ended up with 29 to conduct this literature review. We found four main theories for the pathophysiology of PCDH19-related epilepsy: GABA(A)(R) dysregulation, blood-brain barrier (BBB) dysfunction, cellular interference, and the AKR1C1-3 gene product deficiency. GABA(A)(R) dysfunction and expression cause decreased effective inhibitory currents predisposing patients to epilepsy. BBB dysfunction allows the passage of methyl-D-aspartate (NMDA)-type glutamate receptor antibodies (abs-NR) through the BBB susceptible membrane. The cellular interference hypothesis establishes that the mutant and non-mutant cells interfere with each other's communication within the same tissue. Women are more susceptible to being affected by this hypothesis as men only have one copy of the x gene and interference is mediated by this gene, meaning that it cannot occur in them. Finally, downregulation and deficiency of the AKR1C3/AKR1C2 products lead to decreasing levels of allopregnanolone, which diminish the regulation of GABA(A)(R).

Indexed as

blood brain barriercellular interferenceclustersepilepsygaba r dysfuncitonpcdh19refractory epilepsy

Identifiers

PMID35822151
PMCPMC9271214
OpenAlexW4281710641

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.