Aim: The study's long-term goals, such as determining supratherapeutic ranges according to age distributions
specific to the country, adjusting dosages for additional drugs used by patients in different disease
groups, and providing the opportunity for etiological studies in the light of diagnosis and drug metabolism
perspective, are of great importance in defining the study. Method: Population pharmacokinetics is a
method expressed to evaluate processes such as absorption, distribution, metabolism, and elimination of a
drug from an individual's blood-plasma concentration. In drug pharmacokinetic experiments, generating
data without considering any pharmacokinetic differences among patients prevents the measurement or
observation of variability among individuals in the population as a simple approach. The dose-concentration
relationship is crucial for individualized dose adjustment. Additionally, the impact of other drugs used
by the individual on metabolite levels and the metabolic interactions between drugs play a critical role in
the development of personalized treatments. Population approaches provide a foundation that benefits the
observation of these effects. The variability in drug metabolism among individuals forms one of the fundamental
building blocks of personalized treatment approaches, specifically through Therapeutic Drug Monitoring
(TDM), which plays an important role in determining the therapeutic range of drugs. Materials:
In this study, drug metabolism findings of patients served at NP Istanbul Brain Hospital between 2010 and
2022 were examined within the repository created along with other patient-specific parameters. Results
and Conclusion: The analysis results have been followed up longitudinally, partially demographically,
and retrospectively. Thanks to the repository of NP Istanbul Brain Hospital, population pharmacokinetic
analyses aimed in this study are being conducted for the first time globally and nationally in terms of
scope. The repository has been studied with TDM for individualized treatment methods, and within this
project, it is anticipated to perform phenotyping with the population pharmacokinetic approach.

Background: Lead acetate (Pb) exposure during frontal cortex development is associated with developmental
toxicity later in life, causing both morphological and functional alterations. Curcuma longa,
however, has been suggested to possess neuroprotective qualities that could lessen these adverse effects.
Objective: Assessed the frontal cortex following treatment with Curcuma longa. Materials and Methods:
Twenty adult female Wistar rats and ten adult male Wistar rats were matched during the proestrous phase
of the estrous cycle in order to mate and create five groups of six (n=6) in a 4:2 (4 females to 2 males)
ratio. Gestational day 0 was marked as the confirmation of pregnancy based on if sperm is present and a
vaginal plug in the vaginal smear. Four (n=4) pregnant Wistar rats were put together. Group 1 (control) rats
were given 2 milliliters per kilogram of distilled water. Pb was given at a dose of 120 mg/kg to Group 2.
Group 3 rats were given 120 mg/kg of lead and 100 mg/kg of vitamin C. The animals in Group 4 received
750 mg/kg of Curcuma longa and 120 mg/kg of Pb. The animals in Group 5 rats were given 1500 mg/kg
of Curcuma longa and 120 mg/kg of Pb. From gestational day 7 to day 21 (14 days), the medication was
administered orally. The animals were allowed to litter naturally. At postnatal day (PND) 1, some pups
were euthanized using chloroform inhalation and their brains were harvested for Oxidative stress markers,
histology, histochemical assessments. While some pups were kept for Cliff avoidance test at PND 4-7.
Results: The study found that lead acetate (Pb) exposure during gestation significantly decreased the mean
turning latency in the cliff avoidance test and increased lipid peroxidation (MDA) levels, while decreasing
antioxidant enzyme levels (SOD, CAT, GSH) compared to the control group. These neurological and oxidative
changes were mitigated by co-administration of Curcuma longa, with a notable improvement in the
cliff avoidance test performance and restoration of the altered histological and histochemical markers. The
results suggest that Curcuma longa, a natural antioxidant, has neuroprotective properties that can counteract
the adverse effects of lead toxicity during gestational development. Conclusion: N-Butanol Fraction
of Curcuma Longa ameliorated lead-induced neurotoxicity in rat pups.

Background: Benzodiazepines (BZDs) are a class of depressant drugs that have enjoyed widespread use
in conventional clinical management of anxiety-related conditions such as panic disorders that require
therapeutic central relaxation and sedation. Meanwhile, prolonged administration of benzodiazepines even
at low doses has however been linked to variety of undesirable effects such as discontinuation relapse with
the associated risk of abuse and dependency. Aim: This study investigated the behavioral, histological
and biochemical outcomes of long-term low dose diazepam use and explored the potential role of nigella
sativa oil (NSO) in the amelioration of the associated side effects. Methods: Adult Wistar rats (n=32)
were randomized into four groups that received normal saline; diazepam; diazepam + NSO; or NSO only,
respectively for 14 days. At the end of the period of the various exposures, the rats were taken through
behavioral paradigms after which they were sacrificed for chemical and histological profiling. Results:
diazepam-exposed rats exhibited stress-related manifestations with relatively poor performance in memory-
related tasks. Repeated diazepam ingestion reduced brain antioxidant biomarkers while causing elevation
of brain oxidative stress markers. On histological observation, mild degenerative changes were evident
in the various brain regions of the diazepam-exposed rats. Conclusion: Interventional nigella sativa oil
administration showed therapeutic potentials by mitigating and reversing the observed effects of diazepam,
largely due to its antioxidant and anti-inflammatory effects as observed in the present study.

Background: Pyrethroids pose health risks to humans. Therefore, it is imperative to assess the preventive
benefits of thymoquinone against neurotoxicity induced by cypermethrin- in the hippocampal dentate
gyrus. Methods: Forty male adult Wistar rats with an average weight of 180-200g were randomly allocated
to five (5) groups, and each comprising eight rats (n=8 per group). The groups were designated
as follows, through oral administrations for 14 days: 0.5ml phosphate- buffered saline (PBS) was given
to group one; Group two received 20mg/kg of cypermethrin (CYM); Group three received 10 mg/kg of
thymoquinone (THQ); Group four received 20 mg/kg of cypermethrin followed by 10mg/kg of thymoquinone
(CYM-10mgTHQ); and Group five received 20 mg/kg and 5mg/kg cypermethrin and thymoquinone
respectively (CYM-5 mgTHQ). Behavioral, histological, immunohistochemical, and biochemical analyses
were conducted post-treatment. Results: Cypermethrin administration caused the rise in pro-inflammatory
cytokine TNF-α, Nuclear Factor-kappa B (NF-κB) and increased expression of astrocytes, microglia, and
pro-apoptotic protein Bax. Additionally, cypermethrin reduced levels of anti-inflammatory cytokine IL-10
and acetylcholinesterase (AChE) activity. Cytoarchitectural disruption of dentate gyrus were observed.
Cognitive deficits were evident. Thymoquinone treatment attenuated TNF-α and NF-κB elevation, reduced
astrocyte, microglial, and Bax expression, and increased IL-10 and AChE. Conclusion: Thymoquinone
demonstrated anti-inflammatory and anti-apoptotic effects against cypermethrin-induced neurotoxicity,
improving cognitive function in rats.

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.