International Neuropsychiatric Disease Journal
https://journalindj.com/index.php/INDJ
<p style="text-align: justify;"><strong>International Neuropsychiatric Disease Journal (ISSN: <a href="https://nsl.niscpr.res.in/ISSNPROCESS/issnassignedinfo.jsp">2321-7235</a>)</strong> aims to publish high quality papers (<a href="https://journalindj.com/index.php/INDJ/general-guideline-for-authors">Click here for Types of paper</a>) in all areas of ‘Neuropsychiatric Disease related research’. By not excluding papers based on novelty, this journal facilitates the research and wishes to publish papers as long as they are technically correct and scientifically motivated. The journal also encourages the submission of useful reports of negative results. This is a quality controlled, OPEN peer-reviewed, open-access INTERNATIONAL journal.</p>SCIENCEDOMAIN internationalen-USInternational Neuropsychiatric Disease Journal2321-7235Mitigation of Streptozotocin-induced Cortical Neuronal Loss and Nissl Depletion by Dacryodes edulis Alkaloid Fraction in Adult Wistar Rats
https://journalindj.com/index.php/INDJ/article/view/596
<p><strong>Background: </strong>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 <em>Dacryodes edulis</em> on the cytoarchitecture and Nissl substance of STZ-induced diabetic Wistar rats.</p> <p><strong>Methodology:</strong> 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 <em>P</em><0.001 considered statistically significant. The duration of the experiment was 56 days.</p> <p><strong>Results:</strong> 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.</p> <p><strong>Conclusion:</strong> The alkaloid fraction of <em>Dacryodes edulis</em> has the potential to ameliorate cortical and nissl depletion from diabetes.</p>Eru Mba EruChristabel Ojibima FrancisWilliams Afamuefuna NnennaMichael Effiong OkuEric Agim AgabaCharles Effiong AsukwoRaymond Asikpo MbukpaEjiro EderademuJane-Francis Oluoma UdehGlory Udochukwu Kings-Nwachukwu
Copyright (c) 2026 Author(s). The licensee is the journal publisher. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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2026-11-102026-11-10236485610.9734/indj/2026/v23i6596Bipolar I and Bipolar II Disorders in Apparently Healthy Adults: A Critical Review from Population Prevalence to Prevention
https://journalindj.com/index.php/INDJ/article/view/593
<p><strong>Background: </strong>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.</p> <p><strong>Purpose and Scope: </strong>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.</p> <p><strong>Approach: </strong>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.</p> <p><strong>Principal Findings: </strong>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.</p> <p><strong>Implications: </strong>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.</p> <p><strong>Conclusion: </strong>Progress depends on subtype-specific trials, prospective validation of risk states and population studies using clinician-validated diagnoses.</p>Jacques Forwah NdehEmem Samuel EdungBlessing Festus ArimieOdion Judith ErhagbeUkeme Samuel Edung, BosahEzekpeazu-ChikeAdekemi Angelina IbijolaUnakalamba Adaobi SandraAkib AbbaCatherine Chinwendu ObijuruIlevbare Martina OlohirereImmaculata Chiamaka Adindu-NwankwoJane Ulifo FaladeChatt UsainiNsikak Emmanuel EkwereBukunade P. AdenusiEuna Kenechi OnyiaOdiong Okon OdiongIkechukwu Collins NnaomaKaren OkorieAbasiubong Emmanuel AbasiubongNworgu Chizaramekpere IhechukwukwuruMary Ibhade JibiroIbe Chibuike LeonardEjike Emmanuel OgbodoOghenerukevwe Anthony OvadjeBenjamin EssienBassey Okon BasseyOtti Chidiedere JoelEwa Anthony ObiIdiege Idiege OmangAkaba Kingsley OnorideaNnaji Chimuanya JosephImmaculate Ihuoma EkeagbaAbeshi Sylvester Etenikang
Copyright (c) 2026 Author(s). The licensee is the journal publisher. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
https://creativecommons.org/licenses/by/4.0
2026-10-312026-10-3123613310.9734/indj/2026/v23i6593Optogenetics and Light-Gated Ion Channels: Transforming the Study of Neural Circuits and Neurodegenerative Disorders
https://journalindj.com/index.php/INDJ/article/view/595
<p><strong>Background:</strong> 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.</p> <p><strong>Objective:</strong> 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.</p> <p><strong>Discussion:</strong> 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.</p> <p><strong>Conclusion:</strong> 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.</p>Shruti N. SomwanshiOmprasad S. HakePravin F. GawaliDhiraj D. PhutkeRohan K. SalunkeVinay S. Kabra
Copyright (c) 2026 Author(s). The licensee is the journal publisher. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
https://creativecommons.org/licenses/by/4.0
2026-11-092026-11-09236344710.9734/indj/2026/v23i6595