Evidence map›Paper›PMID 37101819›Full record

ReviewIBRO neuroscience reports2023

Correlation of mutated gene and signalling pathways in ASD.

Madhavi Apte, Aayush Kumar

Open access · goldAbstract readReview
In one paragraph

Review in IBRO neuroscience reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
    Review
  2. Article
  3. Review
  4. Novel mouse line with D277N mutation in theFrontiers in cell and developmental biology · 2026
    Article
  5. Review
  6. Review
  7. Article
  8. Review of autism spectrum disorder databases for the identification of candidate genes.Database : the journal of biological databases and curation · 2025
    Review
  9. Article
  10. Autism-RelatedBiomolecules · 2024
    Article
  11. Decoding the genetic landscape of autism: A comprehensive review.World journal of clinical pediatrics · 2024
    Article
  12. Article
  13. 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

2 authors at 1 institution in 1 country.

Madhavi ApteQuality Assurance and Pharmacognosy and Phytochemistry, SVKM's Dr. Bhanuben Nanavati College of Pharmacy, Vile Parle, 400056 Mumbai, India.
Aayush KumarQuality Assurance, SVKM's Dr. Bhanuben Nanavati College of Pharmacy, Vile Parle, 400056 Mumbai, India.
Shri Vile Parle Kelavani Mandal · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism is a complicated spectrum of neurodevelopmental illnesses characterized by repetitive and constrained behaviors and interests, as well as social interaction and communication difficulties that are first shown in infancy. More than 18 million Indians, according to the National Health Portal of India, and 1 in 160 children worldwide, according to the WHO, are diagnosed with autism spectrum disorders. This review aims to discuss the complex genetic architecture that underlies autism and summarizes the role of proteins likely to play in the development of autism. We also consider how genetic mutations can affect convergent signaling pathways and hinder the development of brain circuitry and the role of cognition development and theory of mind with Cognition-behavior therapy benefits in autism.

Indexed as

AutismCognition developmentCognitive behavioral therapyEpigenetic RegulationGene mutationGenetic architectureGeneticsSignaling pathwayTheory of mind

Identifiers

PMID37101819
PMCPMC10123338
OpenAlexW4360998512

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.