Role of SHANK3 in concentrated ambient PM2. 5 exposure induced autism-like phenotype

Li, Kang; Liang, Xiao‐Tian; Xie, Xiaoqian; Tian, Lei; Yan, Jun; Lin, Bencheng; Liu, Huanliang; Lai, Wenqin; Liu, Xiaohua; Xi, Zhuge

doi:10.1016/j.heliyon.2023.e14328

Cited by 2 publications

(2 citation statements)

References 65 publications

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“…60 A recent study also confirmed the role of SHANK3 in concentrated ambient PM2.5 exposure-induced autism-like phenotype, providing new ideas for the etiology and prevention of autism. 68…”

Section: Pm25 and Neurodevelopmental Disorders (Ndds)mentioning

confidence: 99%

“…60 A recent study also confirmed the role of SHANK3 in concentrated ambient PM2.5 exposure-induced autism-like phenotype, providing new ideas for the etiology and prevention of autism. 68 Moreover, studies have identified a significant reduction in Reelin expression in the brains of ASD individuals and a methylation pattern of its promoter. [69][70][71] Reelin is a signaling glycoprotein secreted in the limbic region of the developing cerebral cortex.…”

Section: Mechanisms Associated With Pm25-induced Asdmentioning

confidence: 99%

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Neurodevelopmental toxicity induced by PM2.5 Exposure and its possible role in Neurodegenerative and mental disorders

et al. 2023

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Recent extensive evidence suggests that ambient fine particulate matter (PM2.5, with an aerodynamic diameter ≤2.5 μm) may be neurotoxic to the brain and cause central nervous system damage, contributing to neurodevelopmental disorders, such as autism spectrum disorders, neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, and mental disorders, such as schizophrenia, depression, and bipolar disorder. PM2.5 can enter the brain via various pathways, including the blood–brain barrier, olfactory system, and gut-brain axis, leading to adverse effects on the CNS. Studies in humans and animals have revealed that PM2.5-mediated mechanisms, including neuroinflammation, oxidative stress, systemic inflammation, and gut flora dysbiosis, play a crucial role in CNS damage. Additionally, PM2.5 exposure can induce epigenetic alterations, such as hypomethylation of DNA, which may contribute to the pathogenesis of some CNS damage. Through literature analysis, we suggest that promising therapeutic targets for alleviating PM2.5-induced neurological damage include inhibiting microglia overactivation, regulating gut microbiota with antibiotics, and targeting signaling pathways, such as PKA/CREB/BDNF and WNT/β-catenin. Additionally, several studies have observed an association between PM2.5 exposure and epigenetic changes in neuropsychiatric disorders. This review summarizes and discusses the association between PM2.5 exposure and CNS damage, including the possible mechanisms by which PM2.5 causes neurotoxicity.

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“…60 A recent study also confirmed the role of SHANK3 in concentrated ambient PM2.5 exposure-induced autism-like phenotype, providing new ideas for the etiology and prevention of autism. 68…”

Section: Pm25 and Neurodevelopmental Disorders (Ndds)mentioning

confidence: 99%

Section: Mechanisms Associated With Pm25-induced Asdmentioning

confidence: 99%

Neurodevelopmental toxicity induced by PM2.5 Exposure and its possible role in Neurodegenerative and mental disorders

et al. 2023

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Spotted around the web: GABA interneurons; CDEP4; Black researchers

Adams¹,

Dattaro²,

Askham³

2023

Spectrum

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Autistic people tend to have fewer GABA-ergic interneurons than non-autistic people, and autistic people with intellectual disability have the fewest. Autism Young children who attend more to the toys than to an ongoing social interaction in a video, as measured by eye tracking, are less likely to engage with their parents while playing with their own toys. Autism Research Glutamate AMPA receptors accumulate in the dendritic spines of motor cortex neurons of wildtype mice after the animals learn a motor skill, an upregulation that is absent in a mouse model of fragile X syndrome. eNeuro Rats exposed to particulate-matter air pollution show autism-like behaviors that seem to be accompanied by changes in SHANK3 expression and methylation. Heliyon Repetitive behaviors in children with behavioral, emotional or cognitive difficulties -not only in those with autism -are associated with heightened anxiety levels. Frontiers in Behavioral Neuroscience Autistic toddlers are less likely than those with other neurodevelopmental conditions to have gastrointestinal or sleep problems, though they still have high rates of both issues. Clinical Pediatrics Human neurodevelopment: Connections between the thalamus and the cortex are evident by 9 to 10 weeks after conception.

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Role of SHANK3 in concentrated ambient PM2. 5 exposure induced autism-like phenotype

Cited by 2 publications

References 65 publications

Neurodevelopmental toxicity induced by PM2.5 Exposure and its possible role in Neurodegenerative and mental disorders

Neurodevelopmental toxicity induced by PM2.5 Exposure and its possible role in Neurodegenerative and mental disorders

Spotted around the web: GABA interneurons; CDEP4; Black researchers

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