Autism is neurodevelopmental disorder that is characterized by developmental, behavioral, social and sensory abnormalities. Researchers have focused in last years in immunological alteration and inflammation as a hot subject in autism field. This work aims to study the alteration in phospholipids (PE, PS, and PC) together with the change in cPLA2 concentration as the main phospholipid hydrolytic enzyme in autistic patients compared to control. It was also extended to find a correlation between these biomarkers and severity of autism measured as childhood autism rating scale (CARS), Social responsiveness scale (SRS), and Short sensory profile (SSP). Phospholipids (PE, PS, PC) and cPLA2 as biochemical parameters were determined in the plasma of 48 Saudi autistic male patients, categorized as mild-moderate and severe as indicated by their Childhood Autism Rating Scale (CARS), social responsiveness scale (SRS) and short sensory profile (SSP) and compared to 40 age- and gender-matched control samples. The reported data demonstrate significantly lower levels of PE, PS, and PC together with a significant increase in cPLA2. While association between severity of autism and impaired phospholipid concentration was completely lacked, an association between cPLA2 and impaired sensory processing was observed. The impaired phospholipid level and remarkable increased in cPLA2 concentration asserted their roles in the etiology of autism. Receiver operating characteristic analysis together with predictiveness diagrams proved that the measured parameters could be used as predictive biomarkers of clinical symptoms and provide significant guidance for future therapeutic strategy to re-establish physiological homeostasis.

This study was conducted to examine if modulating transporters like transient receptor potential cation channels, subfamily M, member 7 (TRPM7) underlies the hippocampal neuroprotection afforded by melatonin (Mel) in rats exposed to cerebral hypoperfusion (CHP). Experimental groups included control, Mel-treated (1.87 g/kg), CHP, and CHP + Mel (1.87 g/kg)-treated rats. CHP was induced by the permanent bilateral occlusion of the common carotid arteries (2VO) method and treatments were conducted for 7 days, orally. Mel prevented the damage of the dental gyrus and memory loss in CHP rats and inhibited the hippocampal reactive oxygen species (ROS), lipid peroxidation levels of tumor necrosis factor-α (TNF-α), interleukine-6 (IL-6), interleukine-1 beta (IL-1β), and prostaglandin E2 (PGE2). It also reduced the hippocampal transcription of the TRPM7 channels and lowered levels of calcium (Ca²⁺) and zinc (Zn²⁺). Mel Also enhanced the levels of total glutathione (GSH) and superoxide dismutase (SOD) in the hippocampus of the control and CHP-treated rats. In conclusion, downregulation of TRPM7 seems to be one mechanism underlying the neuroprotective effect of Mel against global ischemia and is triggered by its antioxidant potential.

Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by defective social communication and interaction with a repetitive pattern of monotonous or stereotyped behavior. Although the exact etiology of ASD is unknown, many factors may be implicated in the development of ASD. We aimed to determine the correlation between specific parental factors and Autism Treatment Evaluation Checklist (ATEC) scores. This cross-sectional study was conducted at the Prince Nasser Bin Abdulaziz Center for Autism, Autism Center for Excellence, and Academy of Special Education for Autism in Riyadh, Saudi Arabia. We enrolled children diagnosed with ASD and their parents from these centers. Data were collected through self-administered questionnaires to the patients’ parents. All included children were <18 years old. In total, 71 (92.2%) children were male and six (7.8%) were female. Further, 77 (100%) patients were diagnosed with autistic disorder. Children of consanguineous parents, underweight mothers and obese fathers, mothers with a history of depression during pregnancy, and mothers aged ≥31 years during pregnancy tend to have a higher mean ATEC score. The health domain was the most significantly correlated with ATEC scores, with a Pearson correlation of 0.880. In linear regression analysis, only maternal depression during pregnancy was significantly correlated with ATEC scores. Our patients had a mean ATEC score of 86.2. The health domain was the most significantly correlated with ATEC scores, with a Pearson correlation of 0.880. Linear regression analysis revealed that consanguinity, parental chronic disease, parental allergy, smoking, drug use during pregnancy, paternal and maternal body mass index (BMI), and sibling number were not significantly correlated with ATEC scores (P=0.701, 0.693, 0.133, 0.874, 0.982, 0.255, 0.778, and 0.502, respectively). However, maternal depression during pregnancy was significantly correlated with ATEC scores (P=0.055).

Introduction: Carvacrol, a phenolic monoterpene and putative TRPM7 inhibitor, has demonstrated neuroprotective activity in cerebral ischemia models. This systematic review synthesizes preclinical evidence on carvacrol across focal and global ischemia, separating outcomes by disease model and summarizing mechanisms of action and translational barriers. Methods: Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, PubMed, ScienceDirect, and Google Scholar were searched from inception to 06-20-2025. Inclusion criteria (PICOS) targeted rodent models of focal (MCAO or hypoxia–ischemia) or global ischemia (BCCAO), with carvacrol administered systemically or centrally and reporting infarct size, behavior, oxidative stress, apoptosis, or pathway markers. Dual, independent screening, extraction, and SYRCLE risk-of-bias appraisal were performed. A prospectively registered protocol (KAIMRC NRR25/050/9) guided this review. Results: Seven studies met criteria. In focal ischemia (3 studies), individual experiments reported reduced infarct volume (up to 44%) and improved neurological scores when carvacrol was given before or shortly after injury. In global ischemia (4 studies), carvacrol improved memory/behavioral outcomes and neuronal survival in hippocampal CA1, with mixed effects on infarct surrogates. Across models, studies showed reduced oxidative damage (MDA, 4-HNE), increased antioxidant enzymes (SOD, CAT, GPx), lower apoptosis (cleaved caspase-3), and variable changes in TRPM7 expression. No study directly linked carvacrol’s outcome benefits to contemporaneous measurement of TRPM7 channel activity in vivo . Conclusion: Carvacrol demonstrates promising neuroprotective signals in both focal and global ischemia models, with convergent antioxidant and anti-apoptotic effects and suggestive TRPM7 involvement. However, evidence certainty is limited by small study numbers, heterogeneity, and methodological risks. Translation will require optimization of delivery, improved study design aligned with STAIR, and mechanistic validation using selective TRPM7 modulators. Systematic Review Registration: identifier NRR25/050/9.

It is now scientifically accepted that neurons have the ability to release multiple transmitter substances simultaneously, yet, cotransmission's functionality is still limited to the scientific community. Acetylcholine is released by the noradrenergic neurons, and then the acetylcholine works prejunctionally in the promotion of the noradrenaline release. This hypothesis significantly challenged the previous idea of autonomic transmission as being a simple process that had a single transmitter. Norepinephrine was thought to be the single transmitter at the sympathetic neurovascular junction according to “Dale’s principle". However, more evidence of the involvement of other neurotransmitters has been shown by many researchers in conjunction with Dale's principle and established terms such as adrenergic, purinergic, and peptidergic nerves. With the discovery of cotransmission, we now understand the existence of more than one neurotransmitter at a sympathetic neurovascular junction.