Developmental Neurobiology最新文献

{"title":"Cannabis Oil Protects Against Valproic Acid–Induced Autism Spectrum Disorder by Reducing Oxidative Stress","authors":"Faiza Ali,&nbsp;Adeeb Shehzad,&nbsp;Raheem Shahzad,&nbsp;Salman Khan,&nbsp;Luay Rashan,&nbsp;Muhammad Taha","doi":"10.1002/dneu.22969","DOIUrl":"https://doi.org/10.1002/dneu.22969","url":null,"abstract":"<div>\u0000 \u0000 <p>Autism spectrum disorder (ASD) is characterized by persistent problems in speech, social interaction, restricted and repetitive behavior patterns, lack of interest, and intellectual disabilities. Currently, there is no effective treatment available for the core symptoms of ASD. Among various treatments, herbal pharmacological treatments have shown promising results with fewer side effects, especially cannabidiol (CBD) treatment for the core symptoms and co-morbidities of ASD. The current study was performed to explore the therapeutic potential of CBD oil supplementation against the valproic acid (VPA)-induced autism mouse model. The autism mouse model was developed by exposing albino BALB/c mouse fetuses to VPA (600 mg/kg) on gestational day 13. On postnatal day (PND)-21, the male pups from both control and diseased groups were further divided into the following treatment groups: (I) control saline group, (II) VPA-exposed group, (III) VPA + CBD oil (100 mg/kg/day/orally) group, and (IV) standard group of VPA + risperidone (RISP) (0.5 mg/kg/day/orally) for 3 consecutive weeks. VPA mice displayed autistic behaviors upon delivery, such as increased anxiety levels, delayed response to painful stimuli, and impaired social interaction. VPA mice also showed depletion of glutathione and other antioxidant levels. CBD oil improved these dysfunctions, as seen through biochemical analysis and morphological staining of the hippocampal region, prefrontal cortex, and Purkinje cells. These findings showed that CBD oil treatment significantly improved behavioral abnormalities and lowered the oxidative stress in the autistic mouse model by acting as an antioxidant.</p>\u0000 </div>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mature and Juvenile Neuromuscular Plasticity in Response to Unloading","authors":"Michael R. Deschenes,&nbsp;Max Rackley,&nbsp;Sophie Fernandez,&nbsp;Megan Heidebrecht","doi":"10.1002/dneu.22966","DOIUrl":"https://doi.org/10.1002/dneu.22966","url":null,"abstract":"<p>The neuromuscular junction (NMJ) is the synapse that enables the requisite electrical communication between the motor nervous system and the myofibers that respond to such electrical stimulation with movement and force development. Changes in an NMJ's normal activity pattern have been demonstrated to remodel both the synapse and the myofibers that comprise the NMJ. Significant amounts of research have been devoted to the study of aging on the neuromuscular system. Far less, however, has been focused on revealing the effects of reduced activity on the NMJ and myofibers comprising juvenile neuromuscular systems. In the present investigation, the consequences of decreased activity imposed by muscle unloading (UL) via hindlimb suspension for 2 weeks (a period known to induce muscle remodeling) were examined in both young adult, that is, mature (8 mo), and juvenile (3 mo) neuromuscular systems. In total, 4 treatment groups comprised of 10 animals (Juvenile-Control, Juvenile-Unloaded, Mature-Control, and Mature-Unloaded) were studied. Immunofluorescent procedures, coupled with confocal microscopy, were used to quantify remodeling of both the pre- and postsynaptic features of NMJs, as well as assessing the myofiber profiles of the soleus muscles housing the NMJs of interest. Results of ANOVA procedures revealed that there were significant (<i>p</i> &lt; 0.05) main effects for both treatment, whereby UL consistently led to expanded size of the NMJ, and Age where expanded NMJ dimensions were consistently linked with mature compared to juvenile neuromuscular systems. Moreover, only sporadically was interaction between the main effects of Age and Treatment noted. Importantly, one variable that remained impressively resistant to the effects of both Age and Treatment was the critical parameter of pre- to postsynaptic coupling suggesting stability in effective communication at the NMJ throughout the lifespan and despite changes in activity patterns. The data presented here suggest that further inquiry must be performed regarding disuse-related plasticity of the neuromuscular system in adolescent individuals as those individuals regularly suffer injuries resulting in periods of muscle UL.</p>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dneu.22966","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct Developmental Programs Displayed by the Xenopus Tadpole Accessory Optic System and Retinotectal Projection","authors":"Uwemedimo G. Udoh,&nbsp;Kaiyuan Zheng,&nbsp;John R. Bruno,&nbsp;Jasper E. Hunt,&nbsp;Kara G. Pratt","doi":"10.1002/dneu.22968","DOIUrl":"https://doi.org/10.1002/dneu.22968","url":null,"abstract":"<div>\u0000 \u0000 <p>The retinotectal projection, the direct synapse between retinal ganglion cells (RGCs) of the eye and tectal neurons of the optic tectum, is a major component of the amphibian visual system. A model of circuit formation, this projection has been studied in detail. There are, however, other retinorecipient targets that also comprise the amphibian visual system such as the pretectum and ventral midbrain tegmentum. Understanding how these other components of the visual system form and function will lead to a more comprehensive understanding of how the visual system, as a whole, assembles and functions. Toward this aim, here we describe the functional development of the <i>Xenopus</i> tadpole accessory optic system (AOS), a direct synaptic connection between RGC axons and the basal optic nucleus of the midbrain tegmentum. The AOS is highly conserved across vertebrates. It functions as the sensory side of the optokinetic and optomotor reflexes, compensatory eye and body movements, respectively, that stabilize the visual scene as the organism moves through it. Using an isolated brain preparation and whole-cell electrophysiological approaches, we compared the development of the AOS and retinotectal projection. We found that these two retinofugal projections display distinct developmental programs, which appear to mirror their different functions. Retinotectal synapses moved through a dynamic phase of previously described NMDA receptor-dependent refinement, a process that is known to sharpen the retinotopic map and thereby visual acuity. In contrast, the AOS synapse appeared more stable and activity independent across development, indicative of a hardwired circuit, built to support reflexive optic behaviors.</p>\u0000 </div>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated Serum Histamine N-Methyltransferase Levels Are Associated With the Pathophysiology of Major Depressive Disorder: A Case–Control Study","authors":"Mariya Akter,&nbsp;Dibbo Protim Ghosh,&nbsp;Toha Tasnem,&nbsp;Tanvir Ahmed,&nbsp;Md. Aminul Haque,&nbsp;Md. Siddiqul Islam,&nbsp;Md. Rabiul Islam","doi":"10.1002/dneu.22967","DOIUrl":"https://doi.org/10.1002/dneu.22967","url":null,"abstract":"<div>\u0000 \u0000 <p>Major depressive disorder (MDD) is a common neuropsychiatric disorder with persistent low mood, feelings of weakness, and a lack of interestin daily tasks. Histamine N-methyltransferase (HNMT) protein is involved in the inactivation process of histamine in human physiology. Here, we aimed to assess the role of HNMT in the pathophysiology and development of MDD. This case–control study included 56 MDD patients and 32 healthy controls (HCs) by matching age, sex, body mass index (BMI), and other sociodemographic characteristics. A clinical psychiatrist assessed the MDD patients and HCs according to the DSM-5 criteria. We used the Ham-D scale in evaluating the severity of depressive symptoms. We used ELISA kits to estimate serum HNMT levels. We observed elevated serum HNMT concentration in MDD patients (29.25 ± 5.34 pg/ml) compared with HCs (23.13 ± 2.10 pg/ml). Serum HNMT levels and Ham-D scores are positively correlated with each other in MDD patients (<i>r</i> = 0.632, <i>p</i> &lt; 0.001). Also, the receiver operating characteristic curve analysis illustrated a significant diagnostic value for HNMT with the area under the curve (AUC = 0.916) at <i>p</i> &lt; 0.001. The promising findings from this study anticipate that the elevated serum levels of HNMT may be associated with the pathophysiology and mechanism of MDD. We recommend further interventional studies to produce more precise and accurate results on this biomarker in depression.</p>\u0000 </div>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143897030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Rare Syndrome Aicardi–Goutières 4: A Case Report and Literature Review","authors":"Hilal Aydin,&nbsp;Hilmi Bolat","doi":"10.1002/dneu.22965","DOIUrl":"https://doi.org/10.1002/dneu.22965","url":null,"abstract":"<p>Aicardi–Goutières syndrome (AGS) is a genetically heterogeneous type of interferonopathy resulting from defects in the processing or sensing of nucleic acids. The AGS phenotype encompasses a broad range of neurological and non-neurological findings. It presents with a congenital or subacute onset, manifesting as microcephaly, spasticity, dystonia, seizures, cortical blindness, and psychomotor retardation in the first year of life. The radiological and laboratory findings of AGS are generally accompanied by intracranial calcification, white matter abnormalities, cerebral atrophy, and cerebrospinal fluid lymphocytic pleocytosis. A case diagnosed as AGS type 4 among patients presenting to the Balikesir University Medical Faculty pediatric neurology clinic, Türkiye, between August 1, 2024, and February 1, 2025, and undergoing genetic testing was included in the study. The patient exhibited a coarse facial appearance, a low ear line, scoliosis, contractures in the upper and lower extremities, hyperactive deep tendon reflexes, an equivocal Babinski response, and upper and lower extremity muscle strength of 3/5. The patient was started on levetiracetam at 20 mg/kg in two doses for epilepsy. Whole exome sequencing revealed a homozygous pathogenic variant in <i>RNASEH2A</i>. Parental genetic analyses for the targeted variant were heterozygous. In conclusion, the diagnosis of AGS relies on clinical characteristics and genetic testing. Basic neurological characteristics include developmental delay, dystonia, microcephaly, brain calcification, and leukodystrophy. Although data concerning genotype-phenotype in AGS type 4 have been reported in the literature, these are still limited.</p>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dneu.22965","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143861457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal Treadmill Exercise and Zinc Supplementation Alleviate Prenatal Stress–Induced Cognitive Deficits and Restore Neurological Biomarkers in Offspring: A Study on Male Rats Aged 30 and 90 Days","authors":"Sina Fatehfar,&nbsp;Parsa Sameei,&nbsp;Naseh Abdollahzade,&nbsp;Leila Chodari,&nbsp;Ehsan Saboory,&nbsp;Shiva Roshan-Milani","doi":"10.1002/dneu.22964","DOIUrl":"https://doi.org/10.1002/dneu.22964","url":null,"abstract":"<div>\u0000 \u0000 <p>The detrimental effects of prenatal stress (PS) on offspring's neurological and behavioral outcomes are well documented. However, strategies to mitigate these effects are underexplored. This study examines whether prenatal zinc supplementation and treadmill exercise can modulate PS-induced cognitive impairments and neurobiological markers in young and adult male rat offspring, leveraging the established neuroprotective potential of both physical activity and zinc. Pregnant rats were divided into five groups: control, stress, stress + exercise, stress + zinc, and stress + exercise + zinc, with all rats except the control group subjected to restraint stress (gestational days 15–19). Pregnant rats in the exercise groups underwent forced exercise, whereas those in the zinc groups received oral zinc sulfate throughout the pregnancy. At postnatal days 30 and 90, the cognitive function of male offspring was evaluated using the Morris water maze (MWM) test, and the hippocampal gene expression levels of caspase-3, brain-derived neurotrophic factor (BDNF), and glial fibrillary acidic protein (GFAP) were measured using reverse transcription–polymerase chain reaction (RT-PCR). PS impaired cognitive functions, increased caspase-3 expression, and decreased BDNF and GFAP expression levels in adult rats. Prenatal exercise was found to mitigate PS-induced cognitive deficits primarily through enhancing GFAP expression, whereas prenatal zinc improved PS-induced cognitive impairments mainly through reduced caspase-3 and increased BDNF expression. The combined effect of exercise and zinc was not additive on cognitive functions and biomarkers. Physical activity may alleviate PS-induced cognitive deficits by modulating astrocytic factors, whereas zinc may exert its effects by inhibiting apoptosis via a BDNF-dependent pathway. Further targeted research is necessary to confirm these relationships.</p>\u0000 </div>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143793649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Azilsartan Confers Protection Against Kainic Acid–Induced Hippocampal Neuron Damage by Upregulating Sirt3/Sod2 Pathway","authors":"Hui-hui Lv,&nbsp;Mao-ying Xia","doi":"10.1002/dneu.22962","DOIUrl":"https://doi.org/10.1002/dneu.22962","url":null,"abstract":"<div>\u0000 \u0000 <p>Epilepsy refers to a diverse group of neurological pathologies, coupled with a significant worldwide impact. Azilsartan, an angiotensin receptor blocker, is broadly applied as an antihypertensive medication. Considering that the neuroprotective potential of Azilsartan has been newly documented, our work was committed to characterizing the association of Azilsartan with epilepsy and its possible mechanism. First, mice hippocampal neuron (HT-22) cells were exposed to kainic acid (KA) with or without Azilsartan treatment. Cell Counting Kit 8 (CCK8) method assessed the viability of KA-treated HT-22 cells. Flow cytometry assay was employed to detect cellular apoptotic capacity. DCF-DA fluorescent staining, JC-1 probe, and related assay kits were used to estimate mitochondrial oxidative stress. Western blotting examined the expression of Sirtuin 3 (Sirt3), superoxide dismutase 2 (Sod2), and apoptosis-related proteins. Additionally, Sirt3 was silenced to analyze whether the protective effect of Azilsartan on KA-induced damage of HT-22 cell damage was achieved by regulating Sirt3. Results indicated that KA intervention concentration-dependently triggered the viability loss, apoptosis, and mitochondrial damage in HT-22 cells. Azilsartan treatment protected against KA-induced HT-22 cell injury by elevating the viability, reducing the apoptosis, and attenuating mitochondrial damage. Besides, Azilsartan administration activated Sirt3 and Sod2 expression in KA-stimulated HT-22 cells, and Sirt3 depletion partially blocked the impacts of Azilsartan on Sirt3/Sod2 pathway, mitochondrial damage, viability, and apoptosis in HT-22 cells exposed to KA. Collectively, Azilsartan might act as a neuroprotective agent in treating epilepsy through the activation of Sirt3/Sod2 pathway.</p>\u0000 </div>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cordycepin Ameliorates Kainic Acid-Induced HT22 Cell Neurotoxicity by Activating GPR120-Mediated Mitophagy","authors":"Yongzhi San,&nbsp;Minghua Wang","doi":"10.1002/dneu.22961","DOIUrl":"https://doi.org/10.1002/dneu.22961","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Mitophagy is important for normal neural activity. Epilepsy is intimately linked to neurotoxicity due to mitochondrial dysfunction. Cordycepin (Cor) has been shown to exert neuroprotective effects. This study aims to investigate whether Cor could mitigate neurotoxicity in epilepsy by modulating mitophagy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In vitro, kainic acid (KA) was utilized to induce cytotoxicity in HT22 cell. Cell viability was assessed using the CCK-8 assay, while cell damage was evaluated through an LDH kit. Flow cytometry was used to assess apoptosis. The expressions of G protein-coupled receptor 120 (GPR120), apoptosis, and mitophagy-related proteins were analyzed by western blot. Inflammatory factors and oxidative stress levels were examined by kits. DCFH-DA staining was applied to observe cellular reactive oxygen species (ROS) levels. The three-dimensional coordinates of GPR120 were retrieved from the PDB database, and molecular docking was performed using AutoDock. Immunofluorescence staining was used to observe mitophagy level.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Cor significantly attenuated KA-induced HT22 cell viability injury and inflammation, while suppressing ROS and oxidative stress levels. Notably, Cor ameliorated the decrease of mitophagy level observed in HT22 cells treated with KA. GPR120 expression was upregulated following KA treatment and further elevated after adding Cor. Cor could bind to GPR120. Interference with GPR120 reversed the ameliorative effects of Cor on KA-induced mitophagy and cytotoxicity in HT22 cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Overall, Cor significantly alleviated KA-induced HT22 cell neurotoxic damage and oxidative stress. This protective effect may be mediated through GPR120-regulated mitophagy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143489729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Mechanism Behind the Therapeutic Role of Alpha-Tocopherol in Mitigating Hypobaric Hypoxia–Induced Eye Defect in Drosophila melanogaster","authors":"Seekha Naik,&nbsp;Smruti Sudha Biswal,&nbsp;Monalisa Mishra","doi":"10.1002/dneu.22963","DOIUrl":"https://doi.org/10.1002/dneu.22963","url":null,"abstract":"<div>\u0000 \u0000 <p>Hypoxia, or low oxygen levels, is linked to several pathological disorders, including retinopathies. Retina being a metabolically active tissue, low oxygen levels resulted in retinal degradation. The developmental perspective of hypobaric hypoxia (HBH)-induced eye development remains elusive. <i>Drosophila</i> is used as our model organism to investigate the impact of HBH on eye development and alpha-tocopherol as a potential inhibitor. To induce the hypoxic condition, we exposed the <i>Drosophila</i> to hypobaric pressure (120 mbar). Hypoxia induces eye defects in different developmental stages of <i>Drosophila</i> as revealed by histological staining. Biochemical estimation disclosed the presence of reactive oxygen species (ROS) during hypoxia, which led to cellular injury and DNA damage. Quantitative PCR reveals the upregulation of <i>Puf</i>, <i>Wge</i>, and <i>Twr</i> genes and the downregulation of <i>Rh1</i> and <i>Rh6</i> involved in eye development. All these defects are brought back to normal levels after treatment with alpha-tocopherol. This research provides a foundation for understanding ocular developmental problems caused by oxygen deprivation and alpha-tocopherol as a crucial therapeutic approach to the treatment of HBH.</p>\u0000 </div>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143481425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Neurodiversity Framework in Medicine: On the Spectrum","authors":"Raul Miranda-Ojeda,&nbsp;Anuksha Wickramasinghe,&nbsp;Georgios Ntolkeras,&nbsp;Isabel Castanho,&nbsp;Walid Yassin","doi":"10.1002/dneu.22960","DOIUrl":"10.1002/dneu.22960","url":null,"abstract":"<div>\u0000 \u0000 <p>The term “neurodiversity” refers to the natural heterogeneity in human neurological functioning, which includes neurodevelopmental differences and other mental health conditions (e.g., autism spectrum disorder [ASD], attention-deficit hyperactivity disorder [ADHD], dyslexia, bipolar disorder, schizophrenia, and depression). This new viewpoint has significant consequences for the future of medicine, specifically in psychiatry, neurology, and neurodevelopmental medicine, as it undermines established notions of these conditions as disorders/diseases that may be healed or corrected. The neurodiversity approach, on the other hand, acknowledges these divergences as natural variations, calling for tailored support and interventions that accommodate individual needs. Neurodiversity could impact current medical perspectives by supporting a shift from pathology to identity. Rather than focusing on the difficulties associated with a specific ailment, the neurodiversity approach stresses the strengths and distinct perspectives that come with neurodivergent identities. This shift has significant consequences for research and therapy by fostering the development of innovative treatments aimed at increasing quality of life and improving functional results. This new perspective advocates including neurodivergent people in all sectors of society, including research, clinical practice, and policymaking, by recognizing, accepting, and integrating natural variances in brain functioning. In this article, we review the development of the neurodiversity movement and propose “The Neurodiversity Framework in Medicine,” which challenges traditional views by recognizing neurological differences as natural variations, advocating for inclusive, person-centered approaches in healthcare.</p>\u0000 </div>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}