Evidence map›Paper›PMID 27376697›Full record

ReviewJournal of neuroscience research2017

Defective phosphoinositide metabolism in autism.

Christina Gross

Open access · greenAbstract readReview
In one paragraph

Review in Journal of neuroscience research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Role of Lysosomal Cholesterol in Regulating PI(4,5)PAdvances in experimental medicine and biology · 2023
    Article
  9. Article
  10. Article
  11. Striking a balance: PIPExploration of neuroprotective therapy · 2021
    Article
  12. Article
  13. Review
  14. Review
  15. Biofluid lipidome: a source for potential diagnostic biomarkers.Clinical and translational medicine · 2017
    Review
  16. Dysregulation of mRNA Localization and Translation in Genetic Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    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

1 author at 1 institution in 1 country.

Christina GrossDivision of Neurology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.ORCID 0000-0001-6057-2527
Cincinnati Children's Hospital Medical Center · US

Funding

Selective targeting of P13K to restore higher cognitive function in FXSR21MH103748 · NIMH · CINCINNATI CHILDRENS HOSP MED CTR · PI GROSS, CHRISTINA · 2014 to 2015
$461k
Targeting the PI3K Enhancer PIKE to Reverse FXS-associated PhenotypesR21MH105353 · NIMH · EMORY UNIVERSITY · PI BASSELL, GARY J, GROSS, CHRISTINA · 2014 to 2015
$366k
NIMH NIH HHS R21 MH103748NIMH NIH HHS R21 MH105353
6 · The paper itself

Abstract

Phosphoinositides are essential components of lipid membranes and crucial regulators of many cellular functions, including signal transduction, vesicle trafficking, membrane receptor localization and activity, and determination of membrane identity. These functions depend on the dynamic and highly regulated metabolism of phosphoinositides and require finely balanced activity of specific phosphoinositide kinases and phosphatases. There is increasing evidence from genetic and functional studies that these enzymes are often dysregulated or mutated in autism spectrum disorders; in particular, phosphoinositide 3-kinases and their regulatory subunits appear to be affected frequently. Examples of autism spectrum disorders with defective phosphoinositide metabolism are fragile X syndrome and autism disorders associated with mutations in the phosphoinositide 3-phosphatase tensin homolog deleted on chromosome 10 (PTEN), but recent genetic analyses also suggest that select nonsyndromic, idiopathic forms of autism may have altered activity of phosphoinositide kinases and phosphatases. Isoform-specific inhibitors for some of the phosphoinositide kinases have already been developed for cancer research and treatment, and a few are being evaluated for use in humans. Altogether, this offers exciting opportunities to explore altered phosphoinositide metabolism as a therapeutic target in individuals with certain forms of autism. This review summarizes genetic and functional studies identifying defects in phosphoinositide metabolism in autism and related disorders, describes published preclinical work targeting phosphoinositide 3-kinases in neurological diseases, and discusses the opportunities and challenges ahead to translate these findings from animal models and human cells into clinical application in humans. © 2016 Wiley Periodicals, Inc.

Indexed as

AnimalsAutistic DisorderDisease Models, AnimalHumansMetabolic DiseasesPhosphatidylinositolsPhosphatidylinositolsautismbiomarkerfragile X syndromephosphoinositide 3-kinasePTENschizophreniasignal transductiontherapeutic strategy

Identifiers

PMID27376697
PMCPMC5214992
OpenAlexW2468666265

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.