Early childhood is a vital period for brain development, characterized by rapid growth and high plasticity.
Adverse experiences during this time, such as abuse, neglect, violence, and poverty, can significantly affect
neurodevelopment and have lasting impacts on mental health and behavior. This review explores the
influence of early adversity on brain development, emphasizing key mecha-nisms and outcomes. Research
indicates that early adversity causes alterations in brain regions like the prefrontal cortex, amygdala, hippocampus,
and corpus callosum, impairing cognitive functions such as learning, memory, and executive
functioning. Chronic stress disrupts the hypothalamic-pituitary-adrenal (HPA) axis, resulting in elevated
cortisol levels that hinder emotional regulation and heighten the risk of mental health disorders such as
depression and anxiety. Epigenetic changes show how adversity can modify gene expression, affecting
brain development without altering the DNA sequence. The repercussions of early adversity include cognitive
deficits, emotional and beha-vioral problems, and social development challenges. However, resilience
factors, including indivi-dual traits and supportive environments, can mitigate these negative impacts.
Robust study designs, such as longitudinal and multidisciplinary approaches, are crucial for understanding
the long-term effects of early adversity. Ethical considerations and precise measurement are vital for
protecting vulnerable populations. Policy implications suggest that findings should inform child welfare,
edu-cation, and mental health policies, focusing on early identification and intervention. Practitioners
should adopt trauma-informed approaches, implement early intervention programs, and support parents
and caregivers. Addressing early childhood adversity is crucial for promoting healthy neu-rodevelopment
and well-being. Comprehensive interventions can reduce adverse effects, support healthy development,
and contribute to a resilient society.

This review explores the intricate relationship between hormonal fluctuations and emotional regulation,
emphasizing the critical role of hormones in mood, stress responses, and psychological well-being. By
examining key hormones involved in emotional regulation—such as those from the Hypothalamic-Pituitary-
Adrenal (HPA) axis, gonadal hormones (estrogen and testosterone), thyroid hormones, oxytocin,
and metabolic hormones like insulin, leptin, and ghrelin—we uncover how these biochemical messengers
impact emotional states and contribute to mood disorders. The paper discusses methodological challenges
and future research directions, highlighting the necessity for interdisciplinary approaches to deepen our
understanding of hormonal influences on emotional regulation.
The review underscores the importance of considering hormonal mechanisms in developing targeted treatments
for mood disorders, advocating for a holistic perspective that bridges endocrinology and psychology.
By integrating current research findings with clinical implications, our objective is to enhance the biological
foundation of emotional regulation, paving the way for innovative therapeutic strategies and improved
mental health care. This comprehensive overview aims not only to consolidate existing knowledge but also
to identify gaps in research, encouraging further exploration into the hormonal underpinnings of emotional
states. Through this endeavor, we aspire to contribute to a broader understanding of emotional regulation,
offering new perspectives on treating mood disorders and enhancing overall emotional well-being.

A hemispherectomy is a surgical procedure in which the basal ganglia are retained but the entire cerebral hemisphere is removed. This technique was used by Dandy in 1928 to remove a glioma. McKenzie, a Canadian doctor, performed the first hemispherectomy on an epileptic patient in 1938. A comprehensive review of the scientific literature was carried out using the recommended guidelines. Using PRISMA (Preferred Reporting Items for Systematic Reviews) guidelines, this study carefully evaluated the scholarly
literature on surgical outcomes and treatment regimens. We followed the EXCEL criteria, Rayyan
(Intelligent Systematic Review), and R software. Academic publications were found in databases such as
ScienceDirect and PubMed/MEDLINE Studies published in English up until January 2024. Our study
of epileptic patients with intractable epilepsy involved a total of 1157 patients, of whom 708 underwent
hemispherectomy. Table 1-2-3, and Figure 2,3,4, 5show the patients’ demographic breakdown: 195 patients,
or 27.54%, had cortical dysplasia, seizures, or Rasmussen encephalitis; 305 patients, or 43.08%, had
seizures; 87 patients, or 12.29%, had strokes or Weber syndrome; 449 patients, or 72.8% of the patients,
out of 325 patients, had the Engel type 1 classification; and 232 patients, or 51.67% of the patients, had
Engel type 2. The results of this pediatric systematic review led us to the conclusion that, once an infant’s
nonexistent seizure count is reached, either through conservative or immunoregulatory therapy or brain stimulation,
hemispherectomy is the most stable course of action. Intractable epilepsy is essentially treatable.

Muscle dysmorphia (MD) is a subtype of body dysmorphic disorder characterized by an obsessive
belief that one’s body is insufficiently muscular. This review provides a comprehensive examination of
the addiction cycle in MD, particularly in the context of anabolic steroid and performance‑enhancing
drug (PED) use. Utilizing a systematic search across databases such as PubMed, PsycINFO, Scopus,
and Web of Science, the review draws on peer‑reviewed literature published in the past two decades
to uncover the roles of hormonal and neural alterations in perpetuating this cycle. Inclusion and
exclusion criteria were meticulously applied to ensure a robust analysis of relevant studies. The
article details the interaction between exogenous hormonal supplementation from steroids and PEDs
and brain receptors, which significantly disrupt neurotransmitter systems and affect mood, cognition,
and stress responses. The synthesis of data reveals that hormonal imbalances due to substance abuse
lead to profound changes in brain plasticity and function, instigating psychiatric disorders and
complicating withdrawal and treatment. Therapeutic strategies are critically assessed, with emphasis
on the success of cognitive‑behavioral therapy, the role of pharmacological management, and the
promise of emerging treatments targeting neuroendocrine disruptions. The review suggests an
integrated, holistic treatment model that includes hormonal therapy and neurological considerations,
underscoring the importance of personalized and sustained interventions. In conclusion, the intricate
cycle of addiction in MD, fueled by the hormonal effects of steroids and PEDs on the brain, calls for
an integrated approach to treatment. Future research should focus on the neuroendocrine impact of
these substances to refine therapeutic strategies for MD.

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.

Aim: Emergentism as an ontology of consciousness leaves unanswered the question as to its
mechanism. I aim to solve the body–mind problem by explaining how conscious organisms
emerged on an evolutionary basis at various times in accordance with an accepted scientific
principle through a mechanism that cannot be understood, in principle. Proposal: The reason for
this cloak of secrecy is found in a seeming contradiction in the behavior of information with respect
to the first two laws of thermodynamics. Information, the microstate of particles within an isolated
system’s macrostate, can, like first‑law energy, be neither created nor destroyed, yet the information
in the system, like second‑law entropy, will inevitably increase. To explain information increasing
without being created, Laplace’s demon is invoked, able to predict where each particle is destined.
This doesn’t work for emerging events like consciousness, which are unpredictable. This can be
understood in terms of the derivation of entropy, and the emergence of classical physics, from the
Relativistic Transactional Interpretation of Quantum Mechanics. I propose that the increased entropy
in a time‑irreversible, unpredictable (emergent) isolated system requires the simultaneous deletion
of information concerning the steps, or calculations, involved. Conclusion: Thus, the steps leading
to consciousness are immediately destroyed and must remain a mystery. Implications include that
entropy, not panpsychism, is the universal principle generative of consciousness, that our being
conscious proves that we are not predetermined, and that consciousness requires assuming an
“entropy debt” that can only be repaid by living organisms, prohibiting the emergence of conscious
machines.

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.

Background: Epilepsy is a neurological illness that disturbs the central nervous system and is
characterized by regular convulsions. Over 70 million people worldwide are thought to have
epilepsy, with the prevalence rate estimated to be around 1%. Aims: The objective of this study
was to assess antiepileptic activities and histological changes after Mentat administration in the
hippocampus of pentylenetetrazole (PTZ)‑induced seizure mice. Materials and Methods: Twenty
Swiss albino mice (18–28 g) were divided into four groups (n = 5) and were given the following
intraperitoneally, 2 ml/kg distilled water and 50 mg/kg PTZ to Groups 1 and 2 animals, respectively.
Groups 3 and 4 animals were given 200 mg/kg and 400 mg/kg of Mentat, respectively, 1 h before
the administration of PTZ and were observed for 300 s. After the experiment, all surviving animals
in the various groups were humanely sacrificed and the brains were harvested and preserved in
10% buffered formalin. The brain tissues were processed using routine histological procedures
and stained with hematoxylin and eosin. Results: Results of this revealed that Mentat was able to
delay the onset time of seizure and offered quantal protection to the animals. Mentat also showed
a dose‑dependent ameliorative effect against histological changes following PTZ administration in
mice. Conclusion: Mentat attenuates PTZ‑induced seizure in mice.

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.