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1

The association between maternal immune activation and mitochondrial failure in adulthood: relevance to neurodevelopmental disorders

100%
Cieslik M., Adamczyk A.
Acta Neurobiologiae Experimentalis
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2019
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tom 79
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nr Suppl.1
Evidence suggests that maternal immune activation (MIA) during pregnancy is a risk factor for neurodevelopmental disturbances including autism spectrum disorders (ASDs). Animal models support this linkage and demonstrate that MIA in rodents leads to behavioral alterations in offspring that are characteristic of autism. However, the mechanism by which MIA causes long‑term behavioral deficits is unknown. Investigation of the links between maternal infection during pregnancy, mitochondrial dysfunction, and behavioral alterations in offspring. To induce MIA, pregnant Wistar rats were injected with lipopolysaccharide (LPS; 0.1mg/kg, intraperitoneally) on gestational day 9.5, a time point analogous to the first trimester of human gestation. Brains from adolescent offspring were evaluated for mitochondrial outcomes. Prenatal exposure to MIA led to anxiety and repetitive behavior. Adolescent offspring of MIA dams exhibited up-regulation of pro-inflammatory cytokines, oxidative stress, and disturbances in redox homoeostasis. Moreover, substantial mitochondrial abnormalities were observed. A significant decrease in mitochondrial membrane potential and changes in ATP production could be attributed to a downregulation of complex I and IV. Deregulated bioenergetics of mitochondria were accompanied by impaired mitochondrial dynamics, altered expression of fusion/fission machinery proteins including mitofusin 1 and 2 (Mfn1, Mfn2), Opa1, dynamin related protein‑1 (Drp1), and fission protein 1 (Fis1). We also demonstrated lower expression of the genes coding for PGC1α and TFAM (PPARGC1A and TFAM, respectively) that are responsible for mitochondrial biogenesis. MIA at early gestation leads to long-lasting effects on the mitochondrial bioenergetics, dynamics, and biogenesis in the offspring which can lead to synaptic dysfunction and behavioral abnormalities similar to ASD. FINANCIAL SUPPORT: Supported by the NSC grant 2016/23/D/NZ4/03572.
2

A prospective study of prenatal mercury exposure from maternal dental amalgams and autism severity

84%
Geier D. A., Kern J. K., Geier M. R.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 2
189-197
Dental amalgams containing 50% mercury (Hg) have been used in dentistry for the last 150 years, and Hg exposure during key developmental periods was associated with autism spectrum disorders (ASDs). This study examined increased Hg exposure from maternal dental amalgams during pregnancy among 100 qualifying participants born between 1990-1999 and diagnosed with DSM-IV autism (severe) or ASD (mild). Logistic regression analysis (age, gender, race, and region of residency adjusted) by quintile of maternal dental amalgams during pregnancy revealed the ratio of autism:ASD (severe:mild) were about 1 (no effect) for <5 amalgams and increased for >6 amalgams. Subjects with >6 amalgams were 3.2-fold significantly more likely to be diagnosed with autism (severe), in comparison to ASD (mild), than subjects with <5 amal­gams. Dental amalgam policies should consider Hg exposure in women before and during the child-bearing age and the possibility of subsequent fetal exposure and adverse outcomes.
3
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Intermingled modulatory and neurotoxic effects of thimerosal and mercuric ions on electrophysiological responses to GABA and NMDA in hippocampal neurons

84%
Wyrembek P., Szczuraszek K., Majewska M. D., Mozrzymas J. W.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 6
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