Oxidative Stress Indicated by Nuclear Transcription Factor Nrf2 and Glutathione Status in the Blood of Young Children with Autism Spectrum Disorder: Pilot Study

Antioxidants, Год журнала: 2025, Номер 14(3), С. 320 - 320

Опубликована: Март 6, 2025

This pilot study investigated the relationship between nuclear transcription factor Nrf2 and glutathione homeostasis in children with autism spectrum disorder (ASD), addressing role of oxidative stress ASD pathophysiology. Oxidative stress, characterized by an imbalance reactive oxygen species antioxidant defenses, has been implicated may contribute to neuroinflammation mitochondrial dysfunction. Nrf2, a key regulator response, influences synthesis recycling, making it critical for cellular redox balance. included 23 21 neurotypical healthy controls, measured levels Keap1 (Kelch-like ECH-associated protein 1), reduced (GSH), oxidized (GSSG), reductase (GR), peroxidase (GPx3) blood samples. Our reveals altered defense disorder, as evidenced Keap1, GSH, GR, along elevated GSSG lower GSH/GSSG ratio. These findings indicate increased burden this population. Additionally, observed positive correlation GR suggests important maintaining homeostasis. results underscore potential involvement emphasize need further research into targeted therapeutic approaches address imbalance.

Язык: Английский

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Delving into the Complexity of Valproate-Induced Autism Spectrum Disorder: The Use of Zebrafish Models

Cells, Год журнала: 2024, Номер 13(16), С. 1349 - 1349

Опубликована: Авг. 14, 2024

Autism spectrum disorder (ASD) is a multifactorial neurodevelopmental condition with several identified risk factors, both genetic and non-genetic. Among these, prenatal exposure to valproic acid (VPA) has been extensively associated the development of disorder. The zebrafish, cost- time-effective model, useful for studying ASD features. Using validated VPA-induced zebrafish models, we aimed provide new insights into VPA effects during embryonic identify potential biomarkers ASD-like Dose-response analyses were performed in vivo study larval phenotypes mechanisms underlying neuroinflammation, mitochondrial dysfunction, oxidative stress, microglial cell status, motor behaviour. Wild-type transgenic

Язык: Английский

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Advances in Understanding Biomarkers and Treating Neurological Diseases -Role of the Cerebellar Dysfunction and Emerging Therapies

Ageing Research Reviews, Год журнала: 2024, Номер unknown, С. 102519 - 102519

Опубликована: Сен. 1, 2024

Язык: Английский

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The effectiveness of hyperbaric oxygen therapy in children and adolescents and with autism spectrum disorders: A systematic review and meta-analysis

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Год журнала: 2025, Номер unknown, С. 111257 - 111257

Опубликована: Янв. 1, 2025

Язык: Английский

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Neurodegeneration in Autism: A Study of Clusterin, Very Long-Chain Fatty Acids, and Carnitine

Journal of Molecular Neuroscience, Год журнала: 2025, Номер 75(1)

Опубликована: Фев. 11, 2025

Язык: Английский

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A Mitochondrial Supplement Improves Function and Mitochondrial Activity in Autism: A Double-Blind Placebo-Controlled Cross-Over Trial

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(6), С. 2479 - 2479

Опубликована: Март 10, 2025

Autism spectrum disorder (ASD) is associated with mitochondrial dysfunction, but studies demonstrating the efficacy of treatments are scarce. We sought to determine whether a mitochondrial-targeted dietary supplement designed for children ASD improved function and symptomatology using double-blind placebo-controlled cross-over design. Sixteen [mean age 9 years 4 months; 88% male] non-syndromic enzyme abnormalities, as measured by MitoSwab (Religen, Plymouth Meeting, PA, USA), received weight-adjusted SpectrumNeeds® (NeuroNeeds, Old Lyme, CT, USA) QNeeds® placebos matched on taste, texture appearance during two separate 12-week blocks. Which product was first randomized. The treatment significantly normalized citrate synthase complex IV activity MitoSwab. Mitochondrial respiration peripheral blood mononuclear cell respiration, Seahorse XFe96 (Agilent, Santa Clara, CA, oxidative stress test, became more resilient after treatment, particularly in poor neurodevelopment. demonstrated significant improvement standardized parent-rated scales neurodevelopment, social withdrawal, hyperactivity large effect sizes (Cohen’s d’ = 0.77–1.25), while changes clinical psychometric instruments were not different. Adverse effects minimal. This small study abnormalities demonstrates that simple, well-tolerated can improve physiology symptoms. Further larger controlled need verify extend these findings. These findings have few other effective treatments.

Язык: Английский

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Gamma-aminobutyric acid and glutamate system dysregulation in a small population of Egyptian children with autism spectrum disorder

Metabolic Brain Disease, Год журнала: 2025, Номер 40(3)

Опубликована: Март 13, 2025

Язык: Английский

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Examining mitochondrial genetic variation in obsessive-compulsive disorder

Research Square (Research Square), Год журнала: 2025, Номер unknown

Опубликована: Март 27, 2025

Obsessive-compulsive disorder (OCD) is a severe neuropsychiatric with clear evidence of genetic vulnerability, although specific risk factors are not fully understood. Mitochondrial dysfunction has been implicated in other disorders, particularly through its role oxidative stress, and thus merits exploration OCD. Here we first examined the association set 59 mitochondrial single nucleotide polymorphisms (SNPs) OCD symptom severity. These SNPs located inside 28 nuclear-encoded genes involved phosphorylation, biogenesis, inflammation, apoptosis. We used linear regression to test for this SNP severity using Yale-Brown Obsessive Compulsive Scale (YBOCS). found nominally significant rs3820189 5’ MFN2 gene YBOCS total score (N = 346; P_uncorrected= 0.002). also conducted gene-based gene-set (pathway) analyses on pathways MAGMA. ADCK1 be associated (p 0.00005, q 0.05). No were risk. To further examine variation risk, then (mt) DNA (mtDNA), circular genome each mitochondrion. utilized Toronto sample 215) 1000 Genome Project 485) as healthy controls discovery. For replication, compared individual-level data from Psychiatric Genomics Consortium (PGC) Working Group release 2017 1691) Wellcome Trust 2616) controls. After cleaning, 58 common mtDNA (minor allele frequency greater than 1%) available analysis. Meta-analysis across variants shared between both samples revealed five significantly which survived Nyholt correction: NC_012920.1:m.1719G > A (P 1.489E-05), NC_012920.1:m.3010G 2.423E-05), NC_012920.1:m.10398A G 3.172E-04), NC_012920.1:m.11914G 6.085E-04) NC_012920.1:m.6260G 7.792E-04). best our knowledge, largest study report involvement Further investigations validation findings warranted.

Язык: Английский

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Oxidative Stress Response and NRF2 Signaling Pathway in Autism Spectrum Disorder

Redox Biology, Год журнала: 2025, Номер 83, С. 103661 - 103661

Опубликована: Май 2, 2025

Язык: Английский

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Deletion of Mex3c gene leads to autistic-like behavior in mice by inhibiting AMPK signal pathway

Frontiers in Behavioral Neuroscience, Год журнала: 2025, Номер 19

Опубликована: Май 20, 2025

Autism Spectrum Disorder (ASD) is a hereditary neurodevelopmental condition influenced by genetic alterations, particularly in genes regulating neural development and synaptic plasticity. Emerging evidence suggests that the Mex3c gene plays role energy metabolism neuronal development, indicating its potential relevance to ASD pathogenesis. To investigate of ASD, we generated knockout (KO) mice conducted series behavioral tests, histological analyses, molecular assays. Behavioral phenotyping included elevated plus maze, open-field test, three-chamber social interaction test. Histological assessments Nissl staining, Golgi-Cox transmission electron microscopy. Molecular evaluations Western blotting analysis AMPK/SIRT1/PGC1α signaling pathway. KO exhibited autistic-like behaviors, including deficits anxiety-like traits. These abnormalities were accompanied reduced number, decreased dendritic spine density, impaired protein expression hippocampus. Mitochondrial structural damage dysfunction observed, alongside suppression Our findings suggest deletion induces ASD-like phenotypes mice, potentially through disruption mitochondrial function integrity via AMPK/SIRT1/PGC1? results support candidacy as susceptibility for highlight pathways therapeutic targets.

Язык: Английский

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