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Cited by 73Genetics and Neurodevelopmental DisordersAutism Spectrum Disorder ResearchPI3K/AKT/mTOR signaling in cancer

mTOR signalling pathway - A root cause for idiopathic autism?

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Ganesan, Harsha, Balasubramanian, Venkatesh, Iyer, Mahalaxmi, Venugopal, Anila, Subramaniam, Mohana Devi, Cho, Ssang-Goo, Vellingiri, Balachandar·2019·BMB Reports
DOI 10.5483/bmbrep.2019.52.7.137PMC PMC6675248
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Abstract

Autism spectrum disorder (ASD) is a complex neurodevelopmental monogenic disorder with a strong genetic influence. Idiopathic autism could be defined as a type of autism that does not have a specific causative agent. Among signalling cascades, mTOR signalling pathway plays a pivotal role not only in cell cycle, but also in protein synthesis and regulation of brain homeostasis in ASD patients. The present review highlights, underlying mechanism of mTOR and its role in altered signalling cascades as a triggering factor in the onset of idiopathic autism. Further, this review discusses how distorted mTOR signalling pathway stimulates truncated translation in neuronal cells and leads to downregulation of protein synthesis at dendritic spines of the brain. This review concludes by suggesting downstream regulators such as p70S6K, eIF4B, eIF4E of mTOR signalling pathway as promising therapeutic targets for idiopathic autistic individuals. [BMB Reports 2019; 52(7): 424-433].

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  • The mammalian target of rapamycin pathway is affected by cholesterol homeostatic changes and is dysregulated in individuals with phosphatase and tensin homolog mutations, tuberous sclerosis, neurofibromatosis, fragile X syndrome, and Rett syndrome.

    “Mammalian target of rapamycin pathway is affected by cholesterol homeostatic changes [37] and is dysregulated in individuals with phosphatase and tensin homolog mutations, tuberous sclerosis, neurofibromatosis, fragile X syndrome, and Rett syndrome [38].”

    From Sterol and lipid analyses identifies hypolipidemia and apolipoprotein disorders in autism associated with adaptive functioning deficits (2021) · cites this paper as [38]

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Authors
Ganesan, H., Balasubramanian, V., Iyer, M., Venugopal, A., Subramaniam, M. D., Cho, S.-G., & Vellingiri, B.
Affiliations
  • Bharathiar University (IN)
  • Avinashilingam University (IN)
  • Sankara Nethralaya (IN)
  • Konkuk University (KR)
Corresponding author
Vellingiri, Balachandar
ORCID
Venue
BMB Reports
Publisher
Korean Society for Biochemistry and Molecular Biology - BMB Reports
Published
2019-07-31
Volume
52
Issue
7
Pages
424-433
ISSN
  • 1976-6696 (ISSN-L)
  • 1976-670X
DOI
10.5483/bmbrep.2019.52.7.137
PMC
PMC6675248
OpenAlex
W2966313088
Cited by
73
References
92
Citations by year
2026: 9 · 2025: 8 · 2024: 12 · 2023: 5 · 2022: 9 · 2021: 19 · 2020: 11
FWCI
5.88
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • BMB Reports (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
  • Bharathiar University
  • Science and Engineering Research Board (ECR/2016/ 001688)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords
mTOR signaling, idiopathic autism, autism spectrum disorder, protein synthesis, dendritic spines, p70S6K, eIF4E, eIF4B, therapeutic target, neurodevelopmental disorders
MeSH terms
Autistic Disorder, Humans, Signal Transduction, TOR Serine-Threonine Kinases

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