Decoding microRNAs in autism spectrum disorder

Li, Jinyu; Xu, Xiaohui; Liu, Jiane; Zhang, Sudan; Tan, Xiaohua; Li, Zhiqiang; Zhang, Jian; Wang, Zheng

doi:10.1016/j.omtn.2022.11.005

Cited by 12 publications

(10 citation statements)

References 151 publications

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“…To explain the selected miRNAs, the most downregulated miR-219 in ASD patients was found to be involved in the control of the circadian rhythm in the SCN. miR-219 can directly target polo-like kinase 2 (PLK2), and PLK2 overexpression can reduce synaptic strength and neuroexcitability, leading to synaptic dysfunction in patients with ASD (Sarachana et al 2010 ; Li et al 2022 ). miR-219 is a target of the master circadian regulators CLOCK and BMAL1 (brain and muscle ANT-like 1) complexes, shows strong circadian rhythmic expression, and finely adjusts the length of the circadian rhythm in mice (Cheng et al 2007 ; Kojima et al 2011 ).…”

Section: Micrornas Influencing Both Circadian Rhythm and Asdmentioning

confidence: 99%

The role of microRNAs in the molecular link between circadian rhythm and autism spectrum disorder

Kim

Lee

2023

Animal Cells and Systems

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Circadian rhythm regulates physiological cycles of awareness and sleepiness. Melatonin production is primarily regulated by circadian regulation of gene expression and is involved in sleep homeostasis. If the circadian rhythm is abnormal, sleep disorders, such as insomnia and several other diseases, can occur. The term ‘autism spectrum disorder (ASD)’ is used to characterize people who exhibit a certain set of repetitive behaviors, severely constrained interests, social deficits, and/or sensory behaviors that start very early in life. Because many patients with ASD suffer from sleep disorders, sleep disorders and melatonin dysregulation are attracting attention for their potential roles in ASD. ASD is caused by abnormalities during the neurodevelopmental processes owing to various genetic or environmental factors. Recently, the role of microRNAs (miRNAs) in circadian rhythm and ASD have gained attraction. We hypothesized that the relationship between circadian rhythm and ASD could be explained by miRNAs that can regulate or be regulated by either or both. In this study, we introduced a possible molecular link between circadian rhythm and ASD. We performed a thorough literature review to understand their complexity.

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Section: Micrornas Influencing Both Circadian Rhythm and Asdmentioning

confidence: 99%

The role of microRNAs in the molecular link between circadian rhythm and autism spectrum disorder

Kim

Lee

2023

Animal Cells and Systems

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“…Resultant ADAM 10 increase, therefore, favors increased sAPPα. Likewise, miR 145-5p, is downregulated in ASD blood ( Vaccaro et al, 2018 ), miR 338-3p is downregulated in ASD brain ( Li J. et al, 2022 ), and (normally) both decrease α-secretase ADAM17 ( Doberstein et al, 2013 ; Chen et al, 2015 ). Therefore, increase in ADAM17 favors increased sAPPα.…”

Section: Microrna and α-Secretase In Asdmentioning

confidence: 99%

“…Therefore, increase in ADAM17 favors increased sAPPα. Finally, miR 146a, upregulation occurs in ASD brain ( Mor et al, 2015 ; Nguyen et al, 2018 ) and olfactory mucosa ( Nguyen et al, 2016 ), and is the “most common miRNA deregulation in neurodevelopmental disorders such as ASD”( Li J. et al, 2022 ). miR146a also is dysregulated in AD ( Wang et al, 2019 ) and in brain of AD mouse models, as reported by Lahiri et al (2018) .…”

Section: Microrna and α-Secretase In Asdmentioning

confidence: 99%

APPlications of amyloid-β precursor protein metabolites in macrocephaly and autism spectrum disorder

Sokol,

Lahiri

2023

Front. Mol. Neurosci.

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Metabolites of the Amyloid-β precursor protein (APP) proteolysis may underlie brain overgrowth in Autism Spectrum Disorder (ASD). We have found elevated APP metabolites (total APP, secreted (s) APPα, and α-secretase adamalysins in the plasma and brain tissue of children with ASD). In this review, we highlight several lines of evidence supporting APP metabolites’ potential contribution to macrocephaly in ASD. First, APP appears early in corticogenesis, placing APP in a prime position to accelerate growth in neurons and glia. APP metabolites are upregulated in neuroinflammation, another potential contributor to excessive brain growth in ASD. APP metabolites appear to directly affect translational signaling pathways, which have been linked to single gene forms of syndromic ASD (Fragile X Syndrome, PTEN, Tuberous Sclerosis Complex). Finally, APP metabolites, and microRNA, which regulates APP expression, may contribute to ASD brain overgrowth, particularly increased white matter, through ERK receptor activation on the PI3K/Akt/mTOR/Rho GTPase pathway, favoring myelination.

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“…The complexity of miRNA-mediated gene regulation is highlighted by a single miRNA’s ability to regulate hundreds of proteins, and multiple miRNAs dynamically regulating many mRNAs [ 6 ]. Consequently, dysregulation of miRNAs is a common feature in neurodevelopmental, neurodegenerative, and psychiatric disorders [ 7 , 8 , 9 , 10 , 11 ], making them potential biomarkers for diagnosis and prognosis in conditions like autism spectrum disorder (ASD) or schizophrenia (SCZ) [ 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Exploratory Analysis of MicroRNA Alterations in a Neurodevelopmental Mouse Model for Autism Spectrum Disorder and Schizophrenia

García-Cerro,

Gómez-Garrido,

Garcia

et al. 2024

IJMS

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MicroRNAs (miRNAs) play a crucial role in the regulation of gene expression levels and have been implicated in the pathogenesis of autism spectrum disorder (ASD) and schizophrenia (SCZ). In this study, we examined the adult expression profiles of specific miRNAs in the prefrontal cortex (PFC) of a neurodevelopmental mouse model for ASD and SCZ that mimics perinatal pathology, such as NMDA receptor hypofunction, and exhibits behavioral and neurophysiological phenotypes related to these disorders during adulthood. To model the early neuropathogenesis of the disorders, mouse pups were administered subcutaneously with ketamine (30 mg/Kg) at postnatal days 7, 9, and 11. We focused on a set of miRNAs most frequently altered in ASD (miR-451a and miR-486-3p) and in SCZ (miR-132-3p and miR-137-3p) according to human studies. Additionally, we explored miRNAs whose alterations have been identified in both disorders (miR-21-5p, miR-92a-2-5p, miR-144-3p, and miR-146a-5p). We placed particular emphasis on studying the sexual dimorphism in the dynamics of these miRNAs. Our findings revealed significant alterations in the PFC of this ASD- and SCZ-like mouse model. Specifically, we observed upregulated miR-451a and downregulated miR-137-3p. Furthermore, we identified sexual dimorphism in the expression of miR-132-3p, miR-137-3p, and miR-92a-2-5p. From a translational perspective, our results emphasize the potential involvement of miR-92a-2-5p, miR-132-3p, miR-137-3p, and miR-451a in the pathophysiology of ASD and SCZ and strengthen their potential as biomarkers and therapeutic targets of such disorders.

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Decoding microRNAs in autism spectrum disorder

Cited by 12 publications

References 151 publications

The role of microRNAs in the molecular link between circadian rhythm and autism spectrum disorder

The role of microRNAs in the molecular link between circadian rhythm and autism spectrum disorder

APPlications of amyloid-β precursor protein metabolites in macrocephaly and autism spectrum disorder

Exploratory Analysis of MicroRNA Alterations in a Neurodevelopmental Mouse Model for Autism Spectrum Disorder and Schizophrenia

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