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.

Klüver–Bucy syndrome (KBS) is a neuropsychiatric disorder secondary to temporal lobe damage.
This can be associated with various causes. This syndrome is rarely caused by stroke. We describe the
case of a KBS, admitted to the neurology department of the military hospital of Agadir, in September
2022 secondary to ischemic stroke in middle cerebral artery territory. The patient presented most of the
clinical features of KBS. These neurobehavioral manifestations improved after the start of treatment.

Dear Editor,
Children living with autism spectrum disorder (ClwASD)
face challenges in social interactions and communication
across different settings (classroom, playground,
and home) due to socioemotional challenges.
The Diagnostic and Statistical Manual of Mental
Disorders – 5th Edition mentions deficits in conversations
involving expressive and receptive language for these
children due to abnormal social approaches such as sharing
of reduced interests, affect, pace of communication, social
skill deficits, and emotions.[1]
Lack of facial expressions and poor eye contact
make it nonverbally hard for ClwASD to participate
in communication in social situations. The ability to
integrate body language and gestures with communication
is essentially challenging for most of these children.
Misinterpretation of social cues and language hinders
comprehension of jokes, humors, and metaphors; ClwASD
face challenges in responding to peers and adults by
understanding their emotions and feelings. Many etiologies
are identified for causing ASD, and the spectrum also
encompasses a wide range of intellectual functioning
abilities beyond the neurophysiological changes in the brain.

Autism spectrum disorder (ASD) is an umbrella term
comprising a group of neurological conditions marked by
severe difficulties with social interaction and communication.
According to the World Health Organization,[1] in 100
children worldwide suffer from ASD, and 1 in 500 Indian
children receive an autistic diagnosis. With four men
diagnosed for every female, boys are more likely than
females to be impacted by autism. Compared to Down
syndrome, which affects one in 800 newborns, autism occurs
more often. Children may exhibit a spectrum of symptoms,
varying in intensity, from recurring patterns of limited
interests and unusual behaviors to challenges in transitioning
between activities or events, as well as unexpected reactions
to sensory cues in their surroundings. While a cure for
autism is not currently evident, interventions play a crucial
role in assisting children to effectively manage their
symptoms. By tailoring treatment plans to individual needs,
these interventions contribute to an improved quality of life.

Breastfeeding is the key element of infant feeding and has played a vital role in promoting infant
health throughout history. It provides all the necessary nutrients for infants to grow and develop.
The World Health Organization (WHO) recommends initiating breastfeeding right after birth and
continuing with exclusive breastfeeding for the first 6 months, followed by complementary feeding
up to 24 months of age. The WHO has also set targets to increase exclusive breastfeeding rates by
2025. As scientific research has advanced, the benefits of breastfeeding for infant health have become
increasingly apparent, not only for metabolic diseases but also for cognitive health. As a result,
researchers have started examining whether breastfeeding has any neurological or psychological
effects on lactating mothers. In this review, we examined current research on the neurological and
psychological effects of breastfeeding on women.

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.

The human mind receives, perceives, and processes visual and auditory input daily from the everyday
world of art and culture as an esthetic neural experience involving several regions of the cerebrum.
It is important to comprehend how this process of neuroesthetics works and how it affects each
individual’s emotions and behavior. This article will incorporate various clinical scanning techniques
and methods to examine the anatomical cerebral structures where the effects of external neuroesthetic
stimuli can be correlated with its resultant neural cognitive response. The effects of neuroesthetic
stimuli on the clinical improvement in patients experiencing depression, cognitive decline, and
other forms of behavioral manifestations will be reviewed. The results of these studies (including
international examples, along with various comparative analyses) demonstrate the beneficial effects
of art on the pleasure centers of the brain and its consequent positive effects on patients’ behavior and
emotions, thus exemplifying the short‑ and long‑term importance of incorporation of neuroesthetics
in not only the clinical setting but also in our global society.