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Parkinson’s disease is the second most common neurodegenerative disease after Alzheimer’s disease characterized by early degeneration of dopaminergic neurons in the substantia nigra pars compacta and accumulation of Lewy bodies. Parkinson’s disease is traditionally known to be associated with motor symptoms; however, it is also associated with non-motor symptoms like pain which may precede motor symptoms by more than a decade. Therapy for Parkinson’s disease primarily involves the use of levodopa which is linked to polyneuropathy and predominantly targets motor symptoms neglecting the non-motor symptoms cold hypersensitivity. The aim of the study was to investigate the effect of Cannabidiol (CBD) and Tetrahydrocannabinol (THC) on Cold Hypersensitivity in reserpine induced Parkinson’s disease in mice. Forty-two (42) mice were randomly divided in to seven groups of six mice each. Group I was the control group that were administered distilled water (10 ml/kg). Group II received reserpine (0.5 mg/kg), Group III received reserpine (0.5 mg/kg) and Cannabidiol (CBD) (30 mg/kg), Group IV received reserpine (0.5 mg/kg) and CBD (60 mg/kg), Group V received reserpine (0.5 mg/kg) and; Tetrahydrocannabinol (THC) (4 mg/kg), Group VI received reserpine (0.5 mg/kg) and; Tetrahydrocannabinol(THC) (6 mg/kg) and Group VII received reserpine (0.5 mg/kg) and; CBD (60 mg/kg) +THC (6 mg/kg). All administration were carried out intraperitoneally for three weeks. Cold pain threshold increased significantly (P < 0.05) in reserpine (0.5 mg/kg) + CBD (60 mg/kg) and reserpine (0.5 mg/kg) + THC (6 mg/kg) groups. Malonaldehyde (MDA) concentration decreased significantly in the reserpine (0.5 mg/kg) + CBD (30 mg/kg), reserpine (0.5mg/kg) + THC (4mg/kg) and reserpine (0.5 mg/kg) + CBD (60 mg/kg) +THC (6 mg/kg) treatment groups respectively. Superoxide dismutase (SOD) concentration increased significantly (P < 0.05) in reserpine (0.5 mg/kg) + CBD (60 mg/kg), reserpine (0.5 mg/kg) + THC (6 mg/kg) and reserpine (0.5 mg/kg) + CBD (60 mg/kg) +THC (6 mg/kg). Reduced glutathione level (GSH) increased significantly (p < 0.05) in reserpine (0.5 mg/kg) + THC (6 mg/kg) and reserpine (0.5 mg/kg) + CBD (60 mg/kg) + THC (6 mg/kg) groups. In conclusion, CBD and THC were able to improve cold pain threshold and at the same time decreasing MDA concentration and increasing SOD activity and GSH concentration.

Aims:Major depressive disorder (MDD) is a common psychiatric disorder, and objective measures that can support clinical assessment are increasingly being investigated. Electroencephalography (EEG) provides a non-invasive and relatively low-cost approach for examining brain activity and has shown potential for EEG-based MDD classification. This study investigated whether short resting-state EEG segments could distinguish individuals with MDD from healthy controls (HC) using two compact deep learning architectures: a Lightweight 1D Convolutional Neural Network (Light 1D-CNN) and a CNN-MiniTransformer. Materials and Methods: The study included 112 resting-state EEG recordings from 56 individuals with MDD and 56 HC. Ninety-two recordings were used for model development and internal evaluation, while 20 independent recordings were reserved for external validation. Nineteen-channel eyes-closed EEG recordings were standardized to 125 Hz and divided into non-overlapping 1-s segments. Channel-ablation analysis was performed to examine spatial EEG importance. Results: On the internal test set, the Light 1D-CNN achieved 96.43% accuracy, a 96.39% F1-score, and an AUROC of 0.9941, while the CNN-MiniTransformer achieved 95.26%, 95.31%, and 0.9906, respectively. On external validation, the Light 1D-CNN achieved 93.72% accuracy and an AUROC of 0.9785, whereas the CNN-MiniTransformer achieved 94.65% accuracy and an AUROC of 0.9872. P4 was the most influential channel in both global and MDD-specific analyses, with Fz and F4 also showing strong contributions. The parietal region showed the highest importance, followed by the frontal region. Conclusion: Both compact deep learning models showed strong performance for MDD–HC classification using short resting-state EEG segments and maintained high performance on independently held-out recordings. Similar channel-importance patterns across the two architectures also provide an interpretable basis for further investigation of spatial EEG characteristics associated with MDD.

Aims: Consumer neuroscience increasingly integrates neurophysiological measurement with self-report methods, yet a comprehensive quantitative synthesis across different neurophysiological modalities within a common meta-analytic framework has remained limited. This meta-analysis systematically evaluates the association between EEG, eye-tracking, galvanic skin response (GSR), and multimodal measures and consumer outcomes (purchase intention, brand attitude, advertisement evaluation, and preference) reported in empirical studies published between 2010 and 2024. Materials and Methods: Following PRISMA 2020 guidelines, 3,109 records were screened, resulting in 22 primary studies included in the final analysis. Effect sizes were synthesized in two independent pools (standardized mean differences and Fisher z-transformed correlations) using random-effects models (REML with Knapp-Hartung adjustment). Results: The pooled effect sizes were moderate and statistically significant (SMD: d = 0.47, 95% CI [0.18, 0.75]; correlation: r ≈ 0.33, 95% CI [0.07, 0.61]), with high heterogeneity observed across studies (I² = 77.3%–84.1%). None of the tested moderators reached statistical significance after FDR correction. Publication bias was detected in the SMD pool, but corrected estimates remained significant. Conclusion: Neurophysiological measures provide meaningful but context-dependent insights into consumer behavior, functioning as complementary rather than universal predictors whose explanatory value varies depending on stimulus characteristics, measurement modality, and experimental design.

Living beings bring more order to the world, and are required by the second law of thermodynamics, to simultaneously produce more disorder through metabolic heat dissipation. Consciousness in living beings produces even more order, enhancing survival and reproduction, and incurs an entropy debt that must be paid separately, and non-metabolically, through heat dissipation produced by Landauer’s principle: the erasure of information within the "explanatory gap" of the hard problem. Consciousness is assumed to depend on the properties of tryptophan in microtubules and their ability to dissipate heat through superradiation as required by Landauer. After the post-mortem decomposition of microtubules, consciousness will have no mechanism for the necessary heat discharge, which would violate Landauer’s principle and thus the second law. Any actual such  survival would imply life-before-death to be solipsism. The aim is to distinguish near-death experiences and out-of-body experiences from life-after-death in biophysical terms, and to explain how they might arise as a result of natural forces. It is hypothesized that near-death and out-of-body experiences, and their vivid nature, arise from the disinhibition of microtubular consciousness after electroencephalographic brain activity has stopped, but while microtubular Tryptophan continues to be activated by ultraviolet photons. These are hypothesized to be transmitted to the brain primarily via light falling on the retina or skin, carried to the brain through mitochondria and microtubules acting as optical waveguides. Additionally, bioluminescent ultra-weak photon emissions accompany membrane depolarization at the moment of death. It is hypothesized that the relativistic transactional interpretation of quantum mechanics could explain the entanglement of this photonic microtubular input, as potentialities, with environmental photons in order to account for rare, veridical near-death extraocular perceptions. Veridical Auditory near-death and out-of-body experiences require a coordinated stimulation of Heschl’s gyrus by ambient sound, which might be accomplished by adiabatic mechanical propulsion of axonal solitons along the Auditory nerve, or possibly transcranial perception of low frequency sound waves.Ultimately, the approach of death can be accompanied by a pseudo-solipsism of "added time" that could seem like an eternity for the deceased person even as microtubular stimulation decreases.

Electronic cigarettes (e-cigarettes) have achieved global adoption, with an estimated 82 million users worldwide and disproportionate uptake among adolescents. Despite marketing as a safer tobacco alternative, e-cigarette aerosols contain neurotoxic constituents including nicotine, flavoring agents, carbonyl compounds, and heavy metals. This review maps empirical evidence on CNS effects of e-cigarette exposure across biological model types. A systematic scoping review was conducted per the Arksey and O'Malley framework and reported per PRISMA-ScR guidelines. PubMed and Scopus were searched in January 2026 for studies from 2015 to 2026 examining quantifiable CNS outcomes following e-cigarette exposure in human, animal, or in vitro models. Data were extracted across eight domains and synthesized narratively. Seventy-four studies met inclusion criteria: 49 animal in vivo (66.2%), 17 human (23.0%), and 8 in vitro (10.8%), spanning 14 countries. Seven CNS outcome domains were identified: neuroinflammation and oxidative stress, blood-brain barrier (BBB) integrity, cognitive and behavioral outcomes, neuroimaging and pharmacokinetics, neurotransmitter systems and electrophysiology, developmental neurotoxicology, and other outcomes. Neuroinflammation and BBB disruption showed high directional consistency. Cognitive impairment, hippocampal volume reductions, and reward circuit reorganization were consistently observed. Developmental studies identified epigenomic reprogramming and disrupted GABAergic interneuron migration. Non-nicotine constituents were independently implicated in CNS toxicity. E-cigarette exposure is associated with a consistent and biologically plausible pattern of CNS harm. The developing brain represents a priority risk population. Current evidence does not support the neurological safety of e-cigarettes; regulatory frameworks should mandate CNS-specific toxicity assessment for electronic nicotine delivery systems.

Aim: Several reports have shown environmental neuron toxins such as aluminium to accumulate in the brain, potentially triggering neurodegenerative disorders. Adansonia digitata (Baobab) has been reported to possess beneficial properties. This study, assessed the neuroprotective properties of aqueous fruit pulp extract of Adansonia digitata (AEAD) on aluminum chloride (AlCl3) – induced memory dysfunctions and hippocampal changes in Wistar rats. The neuroprotective effects of AEAD were assessed with the Morris water maze for learning and memory, oxidative stress biomarkers glutathione (GSH), superoxide dismutase (SOD), and Malondialdehyde (MDA), and histopathological changes on the hippocampal CA3 region using histological techniques. Materials and Methods: Thirty male Wistar rats (110 and 150 g) were divided into six groups at random (n=5). The Control group, the animals in Group 1 received 2 ml/ kg distilled water. Group 2 received 100 mg/kg of AlCl3. Ascorbic acid at a dose of 595 mg/kg was given to Group 3. 100 mg/kg AlCl3 and different concentrations of the AEAD (500 mg/kg and 1500 mg/kg, respectively) were given to groups 4 and 5. Group 6 received 595 mg/kg of ascorbic acid and 100 mg/kg of AlCl3. Results: The latency time spent to locate the escape platform in the Morris water maze test was observed with remarkable (P<0.05) improvement in the AEAD treatments compared with the AlCl3- treated group. There was a notable increase in MDA levels and a reduction in SOD and GSH activities in the AlCl3-treated group in relation to the AEAD-treated groups. Histopathological examination of the CA3 hippocampal region treated with AlCl3 revealed neurodegenerative changes, whereas, administration of AEAD ameliorated AlCl3-induced neuronal damages in rats at doses 500mg/kg and 1500mg/kg when compared with the AlCl3-treated group. Conclusion: Aqueous fruit pulp extract of Adansonia digitata demonstrated a possible neuroprotection against aluminium chloride-induced memory deficit and CA3 hippocampal neurotoxicity.

Aim: Lack of sleep has been linked in studies to increased beta-amyloid levels, oxidative stress, and memory impairments. Furthermore, sleep is known to help clear toxins that accumulate in the brain. This study investigated the restorative potentials of recovery sleep on total sleep deprivationinduced memory impairment, oxidative stress, stress response and changes in beta amyloid plaques in the hippocampus of adult male Wistar rats. Materials and Methods: Twenty-four male Wistar rats weighing between 150 and 200 g were divided into four groups. Group I remained in their home cages, while Groups II, III, and IV underwent sleep deprivation for 5 days. Groups III and IV then had recovery periods of 7 and 21 days, respectively. Spatial learning and memory was measured using the Novel Object Recognition test. The rats were euthanized with ketamine, oxidative stress was analyzed using hippocampal tissue homogenate and beta-amyloid plaques in the CA1 and CA3 regions using Congo red stain. Results: Comparing the sleep-deprived group to the sleep-recovered group, the discrimination ratio increased significantly (p < 0.0001). Sleep recovery also decreased levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and malonaldehyde (MDA) and corticosterone (p < 0.01). Additionally, extracellular amyloid-beta expression in the CA1 and CA3 regions of the sleep recovery groups was significantly reduced (p < 0.0001 and p < 0.01). Conclusion: Recovery sleep was found to improve memory and decrease beta amyloid expression and oxidative stress in the CA1 and CA3 areas of the hippocampus. 

Aim: Autism Spectrum Disorder (ASD) involves complex alterations in brain structure that persist across the lifespan. While structural brain alterations are known in children, the persistence of these neuroanatomical differences into adulthood remains less understood. This study examines the neuroanatomical basis of ASD in adulthood, specifically investigating how cortical thickness (CT) and structural similarity networks (SSN) are organized within the social brain network. Materials and Methods: T1-weighted MRI data were obtained for 24 adults with ASD and 24 neurotypical (NT) controls (ages 18–30) from the OpenNeuro dataset (ds002522). Image preprocessing was performed using the recon-all pipeline in FreeSurfer. We investigated CT and SSN at both: (1) the whole-brain, and (2) a hypothesis-driven level targeting 14 specific social brain network regions. CT was assessed using vertex-wise surface-based morphometry, while SSN were constructed using the Morphometric INverse Divergence (MIND) method. MIND quantifies morphological similarities based on the divergence of regional distributions for thickness, volume, surface area, mean curvature, and sulcal depth. Results: The SSN analysis revealed significantly increased nodal connectivity strength in the ASD group within the right posterior insula (pFDR=0.04) and the orbital part of the right inferior frontal gyrus (pFDR = 0.04). ROI-based CT comparisons and whole-brain SSN analyses showed no significant group differences. Conclusion: Our findings reveal a neuroanatomical signature in adults with ASD, characterized by localized structural hyper-connectivity within the inferior frontal gyrus and the insula. These results highlight that adult ASD is defined by persistent structural anomalies, manifesting as atypically high structural similarity within key social brain nodes rather than widespread, global network disruptions.