International Neuropsychiatric Disease Journal

Mitigation of Streptozotocin-induced Cortical Neuronal Loss and Nissl Depletion by Dacryodes edulis Alkaloid Fraction in Adult Wistar Rats

2026-11-10T12:47:30+00:00

Background: Diabetes-associated alterations in cortical structure and Nissl substance provide a basis for evaluating the potential protective effects of plant-derived compounds. This study evaluated the potential neuroprotective effect of the alkaloid fraction of Dacryodes edulis on the cytoarchitecture and Nissl substance of STZ-induced diabetic Wistar rats.

Methodology: Twenty-five (25) adult male Wistar rats (130–250 g) were divided into five groups, A–E (n = 5 per group). Group A (control) received rat chow and water. Diabetes was induced in groups B–D by administering 60 mg/kg body weight of streptozotocin (STZ) for 14 days. Groups C and D received 200 mg/kg and 100 mg/kg of alkaloids, respectively, while group E received 50 mg/kg of metformin. The animals were euthanised by intraperitoneal injection of 0.5% ketamine and their brains were excised and fixed in 10% buffered formal saline. The cytoarchitecture of the cerebral cortex was assessed using the haematoxylin and eosin (H&E) staining technique. Nissl substance was assessed histochemically using the cresyl fast violet (CFV) staining technique. Data were analysed using the Statistical Package for the Social Sciences (SPSS), version 25 for Windows. Mean body weight was analysed using one-way ANOVA and Tukey’s test, with P<0.001 considered statistically significant. The duration of the experiment was 56 days.

Results: Group C (STZ + high dose) had the highest percentage change in body weight (32.48%) whereas group D (STZ + low dose) had the lowest (7.12%). Histologically, group A, C and E showed normal neuron with prominent nucleoli while group B and D showed the neuron surrounded by vacuole. Using the cresyl fast violet staining, normal control (group A) was deeply stained, diabetic group (group B) was sparsely stained whereas the treatment groups (C-E) were moderately stained.

Conclusion: The alkaloid fraction of Dacryodes edulis has the potential to ameliorate cortical and nissl depletion from diabetes.

Hippocampal Neurohistology Following Prolonged Tenofovir Disoproxil Fumarate, Lamivudine, Dolutegravir (TLD) Use and Quercetin Supplementation in Adult Male Wistar Rats

2026-11-12T11:32:31+00:00

Background: Prolonged exposure to some anti-retroviral agents may induce neuronal alterations, changes in synaptic plasticity, mitochondrial dysfunction, and oxidative stress, although findings remain inconsistent and the underlying mechanisms are not fully understood. This study aimed to determine the potential effects of quercetin on dolutegravir/lamivudine/tenofovir disoproxil fumarate (TLD)-induced histological, immunohistochemical, and biochemical changes in the hippocampus of adult male Wistar rats.

Methodology: Thirty adult male Wistar rats were randomly divided into six groups of five rats each (n = 5). Group A (control) was given distilled water, Group B was given 25 mg/kg of quercetin, Group C was given 24 mg/kg of TLD, Group D received quercetin and TLD for seven days after which TLD alone continued until the end of the experiment, Group E received quercetin and TLD throughout the experiment, and Group F received quercetin and TLD for seven days after which quercetin alone was continued till the end of the experiment. Treatments were administered orally once daily for 30 days. At the end of treatment, the animals were euthanised with ketamine (100 mg/kg, i.p.), the hippocampi were processed for oxidative stress markers, and histological (H&E) and immunohistochemical (GFAP) analyses were conducted. Data were analysed using GraphPad Prism, version 10. One-way analysis of variance (ANOVA) and Tukey's test were performed and p < 0.05 was considered statistically significant.

Results: Treatment with dolutegravir-containing combination therapy (TLD) was associated with extensive architectural deformation with pyknotic neuronal cells and obliterated neurons in the hippocampus. MDA levels increased significantly, alongside significant reductions in GSH levels and antioxidant enzyme (SOD and CAT) activities compared with the other treatment groups (p < 0.05).

Conclusion: Treatment with quercetin was associated with restoration of neuronal histopathological features, increased levels of the antioxidants SOD, GSH and CAT, and reduced MDA levels in the hippocampus.

Bipolar I and Bipolar II Disorders in Apparently Healthy Adults: A Critical Review from Population Prevalence to Prevention

2026-11-01T02:29:08+00:00

Background: Bipolar I disorder and bipolar II disorder are recurrent mood disorders that usually begin in late adolescence or early adulthood, carry excess mortality from suicide and cardiovascular disease, and are often missed because the presenting complaint is depression. Many adults who meet criteria in population surveys have never received a bipolar diagnosis, so the boundary between apparent health and illness is a central but neglected issue.

Purpose and Scope: This critical narrative review examines both disorders from the perspective of adults who appear healthy when encountered in surveys, primary care or screening. It appraises evidence on prevalence, aetiology, clinical features, diagnostic criteria, pathophysiology, management and prevention, asking throughout whether conclusions drawn from bipolar I disorder transfer legitimately to bipolar II disorder.

Approach: Peer-reviewed literature published from January 2000 to August 2026 was identified through structured searches of biomedical and multidisciplinary indexes, citation tracking and authoritative classification and guideline documents, and was appraised qualitatively for design, measurement validity, subtype disaggregation and consistency.

Principal Findings: Community prevalence estimates vary several-fold, largely because lay-administered interviews and self-report screeners detect hypomania poorly and criteria have shifted between classification editions. Under-recognition and diagnostic delay are substantial, especially for bipolar II disorder, although over-diagnosis also occurs. Familial and polygenic liability is the strongest established risk factor, whereas most environmental exposures rest on observational and frequently low-quality meta-analytic evidence. Bipolar II disorder is not a mild variant: its depressive burden, chronicity and suicide risk approach those of bipolar I disorder. Mechanistic models involving reward sensitivity, circadian instability, immune activation and neuroprogression remain largely correlational. Lithium and several antipsychotics have the strongest maintenance evidence, but randomised evidence specific to bipolar II disorder is sparse and of very low certainty.

Implications: Prevention is at present secondary and tertiary rather than primary. Structured enquiry about hypomania in adults presenting with depression, cautious antidepressant use, attention to sleep, substances and the postpartum period, and early specialised care are better supported than population screening.

Conclusion: Progress depends on subtype-specific trials, prospective validation of risk states and population studies using clinician-validated diagnoses.

Optogenetics and Light-Gated Ion Channels: Transforming the Study of Neural Circuits and Neurodegenerative Disorders

2026-11-09T11:32:36+00:00

Background: Optogenetics combines genetic targeting with light-sensitive proteins to manipulate cellular activity with high temporal precision. It has become an important method for investigating neural circuits and mechanisms relevant to neurodegenerative disorders.

Objective: This narrative review examines the molecular basis of light-gated ion channels and related opsins, their contribution to causal circuit analysis, disease-oriented applications, and barriers to clinical translation. Methods: Topic-focused searches of the literature were used to identify foundational experimental studies and selected peer-reviewed reviews on microbial opsins, neural-circuit research, neurodegenerative disorders and translational considerations. This was not a systematic review; no exhaustive screening, formal risk-of-bias assessment or meta-analysis was undertaken.

Discussion: Excitatory and inhibitory opsins enable researchers to test how defined neuronal populations and activity patterns influence memory, movement and pathological network dynamics. Alzheimer’s disease research has examined memory-associated circuits and gamma-frequency activity, while Parkinson’s disease studies have clarified contributions of basal-ganglia pathways to motor behaviours. Evidence is less extensive and more heterogeneous for Huntington’s disease, amyotrophic lateral sclerosis and multiple sclerosis. Findings from cellular and animal models support mechanistic investigation but do not establish clinical efficacy. Direct therapeutic translation faces challenges involving gene delivery, cell specificity, optical access, device compatibility, immune responses and long-term safety. Indirect translation—using circuit knowledge to inform established neuromodulation or other interventions—may be more feasible for some disorders.

Conclusion: Optogenetics is best regarded as a powerful research platform and a source of therapeutic hypotheses, rather than an established treatment for most neurodegenerative diseases. Progress will depend on reproducible disease-relevant outcomes, rigorous safety assessment and clinically meaningful evaluation.