Brain disorders (Amsterdam, Netherlands)最新文献

{"title":"ODL-BCI: Optimal deep learning model for brain-computer interface to classify students confusion via hyperparameter tuning","authors":"Md Ochiuddin Miah ,&nbsp;Umme Habiba ,&nbsp;Md Faisal Kabir","doi":"10.1016/j.dscb.2024.100121","DOIUrl":"https://doi.org/10.1016/j.dscb.2024.100121","url":null,"abstract":"<div><p>Brain-computer interface (BCI) research has gained increasing attention in educational contexts, offering the potential to monitor and enhance students’ cognitive states. Real-time classification of students’ confusion levels using electroencephalogram (EEG) data presents a significant challenge in this domain. Since real-time EEG data is dynamic and highly dimensional, current approaches have some limitations for predicting mental states based on this data. This paper introduces an optimal deep learning (DL) model for the BCI, ODL-BCI, optimized through hyperparameter tuning techniques to address the limitations of classifying students’ confusion in real time. Leveraging the “confused student EEG brainwave” dataset, we employ Bayesian optimization to fine-tune hyperparameters of the proposed DL model. The model architecture comprises input and output layers, with several hidden layers whose nodes, activation functions, and learning rates are determined utilizing selected hyperparameters. We evaluate and compare the proposed model with some state-of-the-art methods and standard machine learning (ML) classifiers, including Decision Tree, AdaBoost, Bagging, MLP, Naïve Bayes, Random Forest, SVM, and XG Boost, on the EEG confusion dataset. Our experimental results demonstrate the superiority of the optimized DL model, ODL-BCI. It boosts the accuracy between 4% and 9% over the current approaches, outperforming all other classifiers in the process. The ODL-BCI implementation source codes can be accessed by anyone at <span>https://github.com/MdOchiuddinMiah/ODL-BCI</span><svg><path></path></svg>.</p></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"13 ","pages":"Article 100121"},"PeriodicalIF":0.0,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666459324000064/pdfft?md5=d1e940f4f2575eccdf1f9599afae9b7e&pid=1-s2.0-S2666459324000064-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139738438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroimmunomodulatory properties of laquinimod","authors":"P.G. Amrutha ,&nbsp;Sonyanaik Banoth ,&nbsp;Janardhan Banothu","doi":"10.1016/j.dscb.2024.100119","DOIUrl":"https://doi.org/10.1016/j.dscb.2024.100119","url":null,"abstract":"<div><p>Laquinimod (ABR-215062) is a quinolone-3-carboxamide derivative, which is an orally active immunostimulatory drug molecule and is being developed for multiple sclerosis cases like relapsing-remitting multiple sclerosis (RRMS) and chronic progressive multiple sclerosis (CPMS). Laquinimod may mediate its effects by regulating pro-inflammatory immune responses and interfering with cell trafficking, in addition to possibly acting directly in the central nervous system to prevent demyelination and axonal injury. Nowadays, its benefits are extended further to various other neurodegenerative illnesses. Recently, it was found that laquinimod can exert only minimal effects in the clinical trials for both PPMS and RRMS making it not suitable for the treatment. However, cannot be completely neglected its pharmacological effect for curing disease progression in MS. Modification of the core structure can contribute to a better candidate for the treatment of MS. We have systematically reviewed the literature reported and highlighted the effect of laquinimod therapy not only on multiple sclerosis (MS) patients but also on a variety of other neurodegenerative disorders. Hence, this review can aid the research community in the design and development of novel chemical entities for the effective treatment of neurodegenerative disorders (NDDs).</p></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"13 ","pages":"Article 100119"},"PeriodicalIF":0.0,"publicationDate":"2024-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666459324000040/pdfft?md5=fcaa0d269e8f7fb1fff12efe3ba6f23a&pid=1-s2.0-S2666459324000040-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139749229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Containment of neuroimmune challenge by diosgenin confers amelioration of neurochemical and neurotrophic dysfunctions in ketamine-induced schizophrenia in mice","authors":"Benneth Ben-Azu ,&nbsp;Olusegun G. Adebayo ,&nbsp;Aliance R. Fokoua ,&nbsp;Jackson E. Onuelu ,&nbsp;Jerome N. Asiwe ,&nbsp;Emuesiri G. Moke ,&nbsp;Itivere A. Omogbiya ,&nbsp;Oghenemarho L. Okpara ,&nbsp;Jennifer E. Okoro ,&nbsp;Omadevuaye M. Oghenevwerutevwe ,&nbsp;Christian I. Uruaka","doi":"10.1016/j.dscb.2024.100122","DOIUrl":"https://doi.org/10.1016/j.dscb.2024.100122","url":null,"abstract":"<div><p>Inhibition of neuroinflammation through N-methyl-D-aspartate receptor (NMDAR) regulation can provide normalization of neurochemical homeostasis and neurotrophic support in the pathogenesis of psychiatric disorders with complex symptoms such as schizophrenia. Accordingly, the preventive and reversal effects, and potential mechanisms of diosgenin, a phyto-steroidal sapogenin with anti-inflammatory functions, was evaluated in ketamine (an NMDAR antagonist) model of schizophrenia in mice. Adult male mice were allotted into 5 groups. In the preventive protocol, mice received saline (10 mL/kg), diosgenin (25 and 50 mg/kg) and risperidone (0.5 mg/kg) orally for 14 days, with additional injection of ketamine (20 mg/kg/day/i.p.) from days 8–14. In the reversal protocol, mice took ketamine injection consecutively for 14 days prior to diosgenin and risperidone treatments from days 8–14. Thereafter, schizophrenia-like behavior, therapeutic extrapyramidal adverse effect, neuroimmune, neurochemical and neurotrophic consequences in important brain areas affected in the disorder were assayed. Diosgenin prevented and reversed stereotypy behavior, cognitive impairment, and psychotic-depression relative to ketamine groups. Complementarily, diosgenin prevents and reverses ketamine-induced dopamine and serotonin alterations in the striatum, prefrontal-cortex, and hippocampus relative to ketamine groups. Except for the cortical regions, diosgenin prevented and reversed glutamic acid decarboxylase depletion in these brain regions by ketamine, suggesting improved GABAergic system. Additionally, ketamine-induced elevation of neuroinflammatory markers: myeloperoxidase, tumor necrosis factor-alpha and interleukin-6, were inhibited in the striatum, prefrontal-cortex, and hippocampus. Also, diosgenin improved the levels of neurotrophic factor in the three brain regions in both protocols respectively. Among other mechanisms, the antipsychotic effect of diosgenin might be associated with attenuation of neurochemical and neuroimmune alterations.</p></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"13 ","pages":"Article 100122"},"PeriodicalIF":0.0,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666459324000076/pdfft?md5=918465dbde5e4b168b69f1f8dab86eab&pid=1-s2.0-S2666459324000076-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139726434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropsychopathology of interpersonal dependency in patients with brain damage","authors":"Keagan Duster ,&nbsp;Joseph Barrash ,&nbsp;Kanchna Ramchandran","doi":"10.1016/j.dscb.2024.100120","DOIUrl":"10.1016/j.dscb.2024.100120","url":null,"abstract":"<div><p>Using the Iowa Scales of Personality Change (ISPC), this research investigated the relationship between the following ISPC dimensions of personality disturbance and subscales in the post-acute stage of brain damage: interpersonal dependency (ID), anxiety (ANX), depression (DPRSN), and executive function (EF-subscale). Our sample consisted of 207 adult neurological patients with a history of temporal lobe epilepsy (TLE), stroke, tumor, anoxia, traumatic brain injury (TBI), or herpes simplex encephalitis (HSE). In two studies, we first observed how ID, EF, depression, and anxiety are subject to change prior to brain damage to the post-acute stage. We then evaluated these domains as predictors of ID to inform how they impact quality of life, daily functioning, and behavioral rehabilitation. Results indicate that disturbances in EF and anxiety significantly predicted ID across all categories of brain damage, and that patients with TLE were spared from worsening depression, anxiety, EF, and ID in the long term, after their temporal lobectomy. This contrasts with patients with other sources of brain damage, who significantly deteriorated in these domains. However, the decline in these domains did not reach clinical diagnostic cutoffs (ISPC-Now score ≥ 4 on a defined 7-point scale) in any of these patient groups. This research identifies some of the long-term executive function, affect, and personality determinants of QOL in patients with brain damage, further delineates the comorbidity between these domains in these neurological patients, and indicates that a temporal lobectomy in patients with TLE leaves these domains, which are vital to daily functioning, relatively spared.</p></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"13 ","pages":"Article 100120"},"PeriodicalIF":0.0,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666459324000052/pdfft?md5=43c7b502ed119469ca84c75bcaa5c027&pid=1-s2.0-S2666459324000052-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139878867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COVID-19 vaccine-induced ptosis and ophthalmoparesis: A new rare neurological manifestation","authors":"Umberto Costantino ,&nbsp;Eleonora Torchia ,&nbsp;Giuseppe Granata ,&nbsp;Anna Modoni","doi":"10.1016/j.dscb.2024.100118","DOIUrl":"10.1016/j.dscb.2024.100118","url":null,"abstract":"<div><p>Neuromuscular manifestations of SARS-CoV-2 vaccinations have been reported increasingly over the last years. Specifically, cranial multineuropathies are extremely rare entities and few cases have been reported related to COVID-19, whereas, todate, no case has been observed after vaccine against SARS-CoV-2. Herein we describe a patient who presented ptosis, ophthalmoparesis and a subclinical facial nerve impairment after two weeks from the second dose of AZD1222 (ChAdOx1-S [recombinant]) vaccine.</p></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"13 ","pages":"Article 100118"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666459324000039/pdfft?md5=5d5e939ce3aaab792a3473b9ccad1525&pid=1-s2.0-S2666459324000039-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139638483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-inflammatory and anti-apoptotic effects of Zc3h12d against cerebral ischemia‒reperfusion through the modulation of the NF-κB signaling pathway","authors":"Lijia Peng ,&nbsp;Wenya Bai ,&nbsp;Junjie Li,&nbsp;Li Xiong,&nbsp;Siying Huo,&nbsp;Jianlin Shao","doi":"10.1016/j.dscb.2023.100115","DOIUrl":"10.1016/j.dscb.2023.100115","url":null,"abstract":"<div><h3>Objective</h3><p>Anti-inflammatory and anti-apoptotic therapy is expected to become the focus for attenuating cerebral ischemia‒reperfusion injury (CIRI), but the underlying mechanism needs to be further elucidated. Zc3h12d has been reported to downregulate NF-κB signaling pathway. Nevertheless, no studies have been conducted to investigate whether Zc3h12d is associated with the development of CIRI. The aim of this study was to investigate whether Zc3h12d can ameliorate CIRI and the underlying mechanism.</p></div><div><h3>Methods</h3><p>MCAO/R and OGD/R were performed to mimic CIRI in vitro and in vivo, respectively. The expression levels of Zc3h12d, proinflammatory cytokines, proapoptotic protein, and p-p65 were detected by RT‒qPCR, ELISA or Western blotting assays. Immunofluorescence staining was used to detect the spatial distribution of Zc3h12d and the expression of p-p65 in the nucleus. Apoptotic analyses were performed by TUNEL staining, Nissl staining and flow cytometry. Cell viability was assessed using the CCK-8 assay.</p></div><div><h3>Results</h3><p>CIRI increased Zc3h12d expression and neuronal apoptosis in the brain. Zc3h12d was predominantly located in neurons in the cortex. Overexpression of Zc3h12d can inhibit inflammation and suppress neuronal apoptosis in cells after CIRI. Furthermore, overexpression of Zc3h12d decreased the expression of p-p65 in the nucleus, which was attenuated by TNF-α, a common NF-κB agonist. In addition, overexpression of Zc3h12d can also shorten the half-life of proinflammatory cytokines.</p></div><div><h3>Conclusion</h3><p>Zc3h12d may play a crucial role in inhibiting inflammation and apoptosis after CIRI, and the underlying mechanism may be related to repressing the activation of NF-κB signaling. Targeting Zc3h12d may be a novel strategy for preventing CIRI.</p></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"13 ","pages":"Article 100115"},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666459323000525/pdfft?md5=1bc92e15157ddb25ac0d795d403bc95b&pid=1-s2.0-S2666459323000525-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139540123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of vagus nerve stimulation for children with drug-resistant epilepsy: Retrospective study","authors":"Alireza Zali ,&nbsp;Farhad Mahvelati ,&nbsp;Bijan Herfedoust Biazar ,&nbsp;Fatemeh Sodeifian ,&nbsp;Setareh Akbari ,&nbsp;Meisam Akhlaghdoust","doi":"10.1016/j.dscb.2024.100117","DOIUrl":"https://doi.org/10.1016/j.dscb.2024.100117","url":null,"abstract":"<div><h3>Introduction</h3><p>According to current investigations, there are controversy in our knowledge regarding the safety and efficacy of Vagus Nerve Stimulation (VNS) in children younger than 12 years old. Therefore, we performed this study and aimed to better evaluate the safety and efficacy of VNS in children younger than 12 years.</p></div><div><h3>Method</h3><p>The retrospective study comprised two groups. In the first group, patients (<em>N</em> = 19) underwent VNS implantation procedure and second group, (<em>N</em> = 21) received no VNS implantation. The main study parameters are as follows: (1) Primary outcome evaluated the proportion of cases with &gt;50 % reduction of seizures at the last follow-up. (2) Changes in patients’ status in VNS group after procedure compared to before procedure. (3) Patient's complaints in VNS group compared to control group.</p></div><div><h3>Results</h3><p>Our results demonstrated that there was a significant reduction in the frequency of seizures (per month) in patients 6 months after VNS surgery compared to before VNS surgery (1044.3 ± 1526.7 VS 220.7 ± 421.6; <em>P</em> value = 0.028). 57.9 % of patients underwent VNS showed the response rate of 50 % reduction in seizure frequency. There was significant improvement in memory problem, work/ school limitation, social limitation, and tachycardia 6 months after VNS procedure compared to before VNS procedure in patients. The most common reported side effects were difficulty swallowing (31.5 %) and coughing (31.5 %) followed by stomach discomfort (15.8 %).</p></div><div><h3>Conclusion</h3><p>Considering the significant reduction in the frequency of seizures and improvement of life aspects including in memory problem, work/ school limitation, social limitation, we recommend VNS as an effective treatment modality for drug-resistant epilepsy in children. However, the combination of VNS with other treatment modalities that could improve other aspects of quality such as energy levels, sleep pattern, and feeling management of life is recommended.</p></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"13 ","pages":"Article 100117"},"PeriodicalIF":0.0,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666459324000027/pdfft?md5=a13ea5e1543a697371aae8215478fb17&pid=1-s2.0-S2666459324000027-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139494065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sjögren Larsson syndrome: A case study with unique mutation","authors":"Raidah Albaradie ,&nbsp;Dana Aljamea ,&nbsp;Deeba Noreen Baig ,&nbsp;Shahid Bashir","doi":"10.1016/j.dscb.2024.100116","DOIUrl":"10.1016/j.dscb.2024.100116","url":null,"abstract":"<div><h3>Background</h3><p>Sjogren–Larsson syndrome (SLS) is an autosomal recessive disorder characterized by the triad of ichthyosis, intellectual disability, and spastic quadriplegia or diplegia.</p></div><div><h3>Methods</h3><p>Here, we report the case of a six-year-old female born to consanguineous parents who presented with an abnormal gait, described as tiptoeing, and generalized pruritis. Her symptoms began two years ago and were associated with a delay in expressive language and poor comprehension skills. Her teachers also report that she is delayed compared to her peers. She has a family history of Sjogren–Larsson syndrome (SLS) in her paternal cousin. She was referred to our center due to her presentation and an MRI finding suggestive of leukoencephalopathy. Therefore, a sequence analysis of the ALDH3A2 gene was performed via next-generation sequencing.</p></div><div><h3>Results</h3><p>Genetic testing revealed a unique result that has not been reported yet, which is nucleotide exchange in a homozygous state at position c.844 in exon 6 of the ALDH3A2 gene (c.844A&gt;<em>T</em>).</p></div><div><h3>Conclusions</h3><p>Since this specific mutation has not been well documented in the literature, it is essential to report such cases and hence understand the general implications of such mutations to gain insights into their potential effects.</p></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"13 ","pages":"Article 100116"},"PeriodicalIF":0.0,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666459324000015/pdfft?md5=a2d3b465e7d8cb2c715208aa3a55b645&pid=1-s2.0-S2666459324000015-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139394760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MRI tractographic validation of drug-enhanced hepatic clearance of amyloid-beta and the therapeutic potential for Alzheimer's Disease: A pilot study","authors":"Anindita Bhattacharjee ,&nbsp;Prasun K. Roy","doi":"10.1016/j.dscb.2023.100112","DOIUrl":"10.1016/j.dscb.2023.100112","url":null,"abstract":"<div><p>Alzheimer's disease (AD) may require alternative therapeutic perspectives as current interventions may sometimes be sub-optimal. Amyloid-beta 42 (Aβ₄₂) is mainly eliminated by hepatic clearance which diminishes in AD, hence hepatomodulatory drugs enhancing this clearance may have potentiality for therapeutic implication. Here, we clinically substantiate our systems-biology investigation on repurposed hepatomodulating drugs (metformin, cilostazol and rifampicin) which enhance brain insoluble Aβ₄₂ clearance through liver-bile-faeces route. Through MRI-tractographic analysis, we now formulate a three-segmental basis of brain Aβ₄₂ spread: fronto-thalamic region (segment-1), temporo-occipital region (segment-2), and dorso-cingulate region (segment-3). This segmental pattern is corroborated histopathologically by Braak's stages A, B and C. We further observed that the aforesaid three pharmaceuticals respectively acted on those three segmental regions differentially. We analysed MRI and DTI images of 15 healthy controls (CDR: 0; MMSE: 24–20), and 15 AD patients (CDR: 0.5–1.0; MMSE: 20–26). We found that, tractographically, there is a significant reduction in neuronal integrity in the three aforesaid regions in untreated AD compared to controls. Nevertheless, the three drugs increased neural activation of AD patients in the three corresponding areas. These three drugs act by regulating respectively the genes <em>ABCB11, ABCA1</em> and <em>MDR1.</em> These genes were correspondingly downregulated in the above-mentioned anatomical segments 1, 2 and 3 of Alzheimer's disease. Thus personalized patient-specific hepatomodulative drugs for AD intervention may be explored, as corroborated by the neuroanatomical involvement in AD.</p></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"13 ","pages":"Article 100112"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666459323000495/pdfft?md5=1814225dfa9cb4e3af6459674c599a35&pid=1-s2.0-S2666459323000495-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139394565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of Memantine in slowing cognitive decline in patients with Down syndrome–A systematic review and meta analysis","authors":"Zarmina Islam,&nbsp;Shamas Ghazanfar,&nbsp;Shazil Ahmed Gangat,&nbsp;Wajeeha Bilal Marfani,&nbsp;S.M.Ashraf Jahangeer Al'Saani,&nbsp;Zainab Syyeda Rahmat","doi":"10.1016/j.dscb.2023.100114","DOIUrl":"https://doi.org/10.1016/j.dscb.2023.100114","url":null,"abstract":"<div><h3>Background</h3><p>Memantine, an NMDA antagonist, has shown to be an effective and well-tolerated pharmacological therapy for the reduction of cognitive decline in the general population with Alzheimer's disease. Individuals with Down syndrome (trisomy 21) have higher rates of cognitive decline than the general population in addition to a greatly increased risk for the development of early-onset Alzheimer's disease. The potential efficacy of Memantine as a therapy for cognitive improvement in DS patients is not well understood.</p></div><div><h3>Objective</h3><p>To assess the effectiveness of Memantine in comparison to placebo as a pharmacological therapy for patients with Down syndrome.</p></div><div><h3>Search strategy</h3><p>Multiple databases including Pubmed, CENTRAL, CDSR, and clinicaltrials.gov were searched with terms including “Memantine Hydrochloride” and “Trisomy 21.”</p></div><div><h3>Selection criteria</h3><p>Randomized, double-blind, placebo-controlled trials measuring tolerability, efficacy, and safety of memantine in DS patients were used. Three (3) studies were ultimately included.</p></div><div><h3>Data collection and analysis</h3><p>Standard Mean Difference (SMD), Odds Ratio (OR) and 95 % confidence intervals (CIs) were calculated to assess the significance of intervention.</p></div><div><h3>Main results</h3><p>No statistically significant therapeutic effect was found upon administration of Memantine relative to placebo in DS patients.</p></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"13 ","pages":"Article 100114"},"PeriodicalIF":0.0,"publicationDate":"2023-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666459323000513/pdfft?md5=337daa8e278c98cce4e00f04a31e34c9&pid=1-s2.0-S2666459323000513-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139100918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}