Aim: Autism spectrum disorder (ASD) is a common neurodevelopmental disorder affecting
multiple levels of social and cognitive skills and causing a significant health‑care burden.
Currently, there is no approved treatment for ASD. Methods: In this study, 10 children with
ASD between the ages 6 and 19 years (M = 12.3, standard deviation = 3.94) were recruited.
Repetitive transcranial magnetic stimulation (rTMS) was applied and symptom severity was
measured before and after treatment using the Childhood Autism Rating Scale (CARS) and
Autistic Behavior Checklist (ABC). All children received sessions of low‑frequency rTMS to the
bilateral prefrontal cortices. Results: The results showed that the children improved according
to both symptom ratings. Specifically, both the relating (z = −2.02, P < 0.05), body and object
use (z = −2.03, P < 0.05) and language (z = −2.21, P < 0.05) subscale scores and the total
score of ABC (z = −2.37, P < 0.05) decreased. Regarding CARS, visual response (z = −2.06,
P < 0.05), verbal communication (z = −2.12, P < 0.05) subscale scores, and the total score (z
= −2.52, P = 0.01) decreased significantly after TMS therapy. Conclusion: Our study was open
label and in terms of sample size should be considered a pilot study. Although the results should
be evaluated cautiously, the findings suggest that rTMS might be a safe and useful tool for
improving deficits related to ASD in children.

Aim: COVID‑19 pandemic response measures adversely affected the psychological effects of health‑care professionals due to disruption of daily life, sense of uncertainty, fear of getting sick, and the perception of working in a dangerous environment. In this study, we assessed the level of depression and anxiety symptoms in health‑care professionals who had interaction with COVID‑19 patients both before and after vaccination. Materials and Methods: The participants in this prospective cohort study, which took place between July 24, 2020 and April 30, 2021, were 233 health‑care workers who were employed in the hospital’s COVID area. Participants were divided into two groups as pre‑COVID‑19 vaccine group (Group 1; n = 98) and postvaccine group (Group 2; n = 135), both groups received the Hospital Anxiety and Depression Scale. Results: The mean score of the Group 1 anxiety subscale was 15.64 ± 2.112, and the mean score of the depression subscale was 15.19 ± 1.762. The same scores were 9.65 ± 5.535 and 9.13 ± 4.984, respectively, in Group 2. There was a statistically significant difference between the groups (P = 0.001). Conclusion: In our research, we have seen that the application of the vaccine has positive effects on the psychological state of health workers who are directly exposed to COVID‑19 patients. We think that the therapies or preventive measures that are developed during the pandemic phase will lessen the possibility of sadness and anxiety in health‑care personnel and boost the effectiveness of the effort to combat the disease.

Background: Heavy metals such as lead are ubiquitous elements at exposure causing deleterious
effects on the brain and leading to neurodegenerative diseases. Aim: In this investigation, the
neurotherapeutic effects of ethanol extract of Curcuma longa (EECl) against lead‑induced hippocampal
neurotoxicity in rats were examined. Biochemical examination for antioxidant enzyme activity and
lipid peroxide level (malondialdehyde [MDA], superoxide dismutase [SOD], and glutathione [GSH])
was evaluated, the Barnes maze for learning and memory, and histological analysis (H and E stain)
for general histoarchitectural features to investigate the neurotherapeutic characteristics of EECl.
Materials and Methods: Six groups totalling 36 rats were created (n = 6). In the first group, rats
received distilled water (2 mg/kg), in the second, lead acetate (LA) (120 mg/kg), in the third, ascorbic
acid (100 mg/kg), and the 4th, 5th, and 6th groups, rats received LA (120 mg/kg) and EECl (375 mg/kg,
750 mg/kg, and 1500 mg/kg, respectively) for 14 days. Results: A significant learning and memory
deficit was seen in the LA‑treated group’s results, but a significant improvement was seen in the
EECl‑treated group. Increased oxidative stress was seen in the LA‑treated group, as evidenced by
an increase in MDA levels and a decrease in antioxidant enzymes (SOD and GSH). A decline in
MDA levels and an increase in SOD and GSH activity was the evidence of the ameliorative effects of
EECl treatment. Cytoarchitectural distortions relative to the control were observed with the LA‑treated
group. Mild distortion was however detected with EECl treatment. Conclusion: EECl has possible
neurotherapeutic properties against LA‑induced pathological changes in the hippocampus of Wistar
rats. EECl may have neuroprotective effects against degenerative alterations brought on by LA.

Aim: The purpose of this study is to predict the possible impact of missense single‑nucleotide polymorphisms (SNPs) in CHRNA7 and GRIN1 genes associated with AD on protein structure, function, and stabilization and to analyze gene–gene interactions via in silico methods. Materials and Methods: SIFT, PolyPhen‑2, SNPsandGO, PROVEAN, SNAP2, PhD‑SNP, and Meta‑SNP were used to estimate high‑risk SNPs. The impact of SNPs on protein stabilization was evaluated with I‑Mutant 3.0 and MUpro software. Three‑dimensional models of amino acid changes were determined with the Project HOPE software. Furthermore, the gene–gene interactions were analyzed via GeneMANIA. Results: According to the results of 603 missense SNPs in the CHRNA7 gene, rs142728508 (Y233C), rs12899798 (W77G), rs138222088 (R227H), rs140316734 (R227C), rs199633275 (P322R), rs199819119 (L29F), rs200147286 (Q49P), rs200908085 (Y115C), rs201094833 (Q61R), rs201473594 (N69D), rs201210785 (E195K), and rs368352998 (S48W) polymorphisms were predicted as deleterious. Similarly, rs193920837 (P117 L), rs3181457 (I540M), and rs201764643 (R217P) polymorphisms in the GRIN1 were estimated as deleterious. Conclusion: It is thought that the results of this study will provide useful information to guide future diagnostic and experimental strategies for AD.

Background: Cadmium (Cd) and bisphenol A (BPA) are known industrial additives and
environmental toxicants that have been extensively reported for their various deleterious effects
on biological systems, particularly endocrine disruption and neurotoxicity. In high‑fat diet‑induced
insulin‑resistant model rats, we studied the neurotoxicity and oxidative stress effects of co‑exposure to
Cd and BPA. Aims: This study aims to look at prefrontal microarchitecture and antioxidant profiles in
insulin‑resistant rats. Materials and Methods: Twenty‑five adult Wistar rats were randomly assigned
into five groups (A– E; n = 5). With A receiving normal saline; B: 40 mg/kg. bw CdCl2 + high‑fat
diet (HFD) + Suc; C: 40 mg/kg. bw BPA + HFD + Suc; D: 40 mg/kg. bw BPA + 40 mg/kg. bw
CdCl2 + HFD + Suc; and E: HFD + Suc orally for 56 days. Finally, brains were excised from each
group and the medial prefrontal cortex was dissected from both hemispheres with right hemisphere
samples processed for hematoxylin and eosin histology and left hemisphere samples homogenized
for biochemical evaluation of oxidative stress markers. One‑way analysis of variance and Tukey’s
post hoc test were used for data analysis with P < 0.05 considered statistically significant.
Results: From our findings, prefrontal glutathione levels were significantly lower (P < 0.05) in the
insulin‑resistant rats (Cd + BPA + HFD + Suc: 120.9 ± 21.89, HFD + Suc: 93.27 ± 17.29) compared
with control rats (244.0 ± 11.57), while prefrontal glutathione reductase activity was significantly
elevated (Cd + BPA + HFD + Suc: 41.02 ± 5.5, HFD + Suc: 41.09 ± 1.68, P < 0.05) compared
to the control rats (20.17 ± 3.27). Prefrontal neurons showed nuclear condensation, cytoplasmic
vacuolations, and clumping of cells. Conclusion: Morphological and biochemical evidence from
the present study suggests that environmental and metabolic factors do combine to induce profound
adverse effects on prefrontal microanatomy and antioxidant system.

Background: Tramadol has a high potential for misuse resulting in cognitive impairment.
Zingiber officinale, however, possesses neuroprotective qualities. Objective: Microscopically
assessed hippocampal CA1 and CA3 following Z. officinale and tramadol treatment.
Materials and Methods: Two milliliters/kilogram of distilled water was given to Group 1,
Groups 2–5 were administered 50 mg/kg of tramadol while Group 3 was also administered 12.5 mg/
kg of naltrexone, and Groups 4 and 5 were also administered 500, and 1000 mg/kg ethanol extract of
Z. officinale (EEZO), respectively, orally for 21 days. The rats were euthanized and their brains were
collected, fixed in 10% formal saline, and processed routinely using crystal fast violet (CFV) stain for
the demonstration of Nissl substance, glial fibrillary acidic protein (GFAP) for the demonstration of
astrocytes, and Hematoxylin and Eosin for general histoarchitecture and estimation of cell number and
volume using physical dissector and Cavalieri estimator, respectively. Results: CFV stain revealed
alterations in regions of CA1 and CA3 of the hippocampus presenting as indistinct staining intensity
and peripheral Nissl substance accumulation in the tramadol‑treated group. GFAP revealed numerous
reactive astrocyte processes. The area of reactive astrocytes remarkably increased (P < 0.05) and
the intensity of the Nissl substance remarkably reduced in the tramadol-exposed group. When
compared to the control, the tramadol-exposed group’s hippocampal volume considerably (P < 0.05)
decreased (coefficient of error [CE] =0.050). The tramadol treatment group (CE = 0.090) relative to
the control group (CE = 0.060) showed a striking decrease (P < 0.05) in the number of pyramidal
cells in the CA3 region. The tramadol treatment group (CE = 0.090) compared to the control
group (CE = 0.060) showed a striking decrease (P < 0.05) in the number of pyramidal cells in the
CA3 region. Tramadol toxicity was attenuated in the groups treated with EEZO in a dose-dependent
manner. Conclusion: Z. officinale possesses a potential neuroprotective effect against tramadol‑induced
neurotoxicity.