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[Taurine for Mitochondrial Diseases]. [牛磺酸治疗线粒体疾病]。
Brain and Nerve Pub Date : 2024-10-01 DOI: 10.11477/mf.1416202748
Yoshihide Sunada
{"title":"[Taurine for Mitochondrial Diseases].","authors":"Yoshihide Sunada","doi":"10.11477/mf.1416202748","DOIUrl":"https://doi.org/10.11477/mf.1416202748","url":null,"abstract":"<p><p>Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is characterized by a mitochondrial DNA mutation that leads to defective taurine modification of the leucine tRNA anticodon, with consequent impaired translation of the UUG codon. This defect reduces synthesis of respiratory chain complexes, which causes energy failure. Taurine supplementation improved mitochondrial function in MELAS model cells. A physician-initiated clinical trial reported that high-dose taurine supplementation therapy suppressed stroke-like episodes and improved taurine modification rates in leukocytes.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[A Case of the Anti-aquaporine-4 Antibody-negative Neuromyelitis Optica Spectrum Disorders Associated with Atopic Disease with High Concentration of Anti-IgE Autoantibody and HyperIgEemia]. [一例抗喹诺酮-4 抗体阴性的神经脊髓炎视网膜频谱紊乱伴有高浓度抗 IgE 自身抗体和高 IgE 血症的特应性疾病】。］
Brain and Nerve Pub Date : 2024-10-01 DOI: 10.11477/mf.1416202752
Toshiyuki Sakai, Yuusuke Niwa
{"title":"[A Case of the Anti-aquaporine-4 Antibody-negative Neuromyelitis Optica Spectrum Disorders Associated with Atopic Disease with High Concentration of Anti-IgE Autoantibody and HyperIgEemia].","authors":"Toshiyuki Sakai, Yuusuke Niwa","doi":"10.11477/mf.1416202752","DOIUrl":"https://doi.org/10.11477/mf.1416202752","url":null,"abstract":"<p><p>We report a 70-year-old male patient with the sero-negative neuromyelitis optica spectrum disorders (NMOSD) associated with atopic disease (AD). He was diagnosed with allergic rhinitis at the age of 20. When he was 61 years old, he subacutely developed orthostatic hypotension, bilateral optic neuritis, quadriparesis, urinary retention, and constipation. The laboratory results revealed allergen-specific IgE positivity for cryptomeria japonica and hinoki, hyperIgEemia, and Th (helper T cell) 1 dominance. The serological tests for autoantibodies revealed negative anti-aquaporine 4 antibody, and high concentration of anti-IgE autoantibody (anti-IgE AAb). Cerebrospinal fluid was negative for anti-myelin-oligodendrocyte glycoprotein antibody and glial fibrillary acidic protein antibody. Fluid-attenuated inversion recovery on brain magnetic resonance imaging (MRI) showed high signal intensities in bilateral cerebral deep white matter. T2 weighted image on spine MRI showed longitudinally extensive high signal intensities in the spinal cord, specifically involving C1 vertebral level to conus medullaris. Intravenous methylprednisolone (IVMP) and plasma exchange resulted in partial improvement. Following the onset of NMOSD, he had relapse of NMOSD four times. In each episode, IVMP was to be partially effective with anti-IgE AAb reduction. Anti-IgE AAb may be a reasonable clinical indicator of increased disease activity in the sero-negative NMOSD associated with AD.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Pharmacological Chaperone Therapy for Fabry Disease]. [法布里病的药理伴侣疗法]。
Brain and Nerve Pub Date : 2024-10-01 DOI: 10.11477/mf.1416202749
Masahisa Kobayashi
{"title":"[Pharmacological Chaperone Therapy for Fabry Disease].","authors":"Masahisa Kobayashi","doi":"10.11477/mf.1416202749","DOIUrl":"https://doi.org/10.11477/mf.1416202749","url":null,"abstract":"<p><p>Pharmacological chaperone therapy (PCT) structurally stabilizes mutant enzyme proteins and increases their activity. Although ease of oral administration and effectiveness in patients with central nervous system disorders serve as advantages, PCT is effective only for patients with amenable mutations because its efficacy depends on gene mutations. PCT, which prevents progression of Fabry cardiomyopathy and nephropathy, was approved in Japan in 2018. It is expected that PCT will also be developed for lysosomal diseases that cause central nervous system disorders in the future.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[AMPA Receptors and Neuronal Plasticity]. [AMPA受体与神经元可塑性]。
Brain and Nerve Pub Date : 2024-10-01 DOI: 10.11477/mf.1416202750
Tomoyuki Miyazaki
{"title":"[AMPA Receptors and Neuronal Plasticity].","authors":"Tomoyuki Miyazaki","doi":"10.11477/mf.1416202750","DOIUrl":"https://doi.org/10.11477/mf.1416202750","url":null,"abstract":"<p><p>Interneuronal information transfer occurs at synapses, where AMPA receptors play a key role. With regard to physiological function, synaptic trafficking of AMPA receptors underlies memory, learning and experience. Analysis of animal models of disease and postmortem brains of patients has revealed that abnormal expression and functions of AMPA receptors may trigger various neuropsychiatric disorders. Such findings are currently being used for the development of therapeutic drugs through quantification of AMPA receptors in patients' brains in real-world practice.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Efficacy and Safety of Inebilizumab, an Anti-CD19 Monoclonal Antibody, for the Treatment of Neuromyelitis Optica Spectrum Disorder: Based on the N-MOmentum Trial]. [抗 CD19 单克隆抗体伊奈单抗治疗神经脊髓炎谱系障碍的疗效与安全性：基于 N-MOmentum 试验]。
Brain and Nerve Pub Date : 2024-10-01 DOI: 10.11477/mf.1416202751
Kazuo Fujihara, Hirokazu Sato
{"title":"[Efficacy and Safety of Inebilizumab, an Anti-CD19 Monoclonal Antibody, for the Treatment of Neuromyelitis Optica Spectrum Disorder: Based on the N-MOmentum Trial].","authors":"Kazuo Fujihara, Hirokazu Sato","doi":"10.11477/mf.1416202751","DOIUrl":"https://doi.org/10.11477/mf.1416202751","url":null,"abstract":"<p><p>Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune astrocytopathic disease of the central nervous system characterized by severe optic neuritis and transverse myelitis. The antibody against aquaporin 4 (AQP4), a water channel mainly expressed in astrocytes, is specific to NMOSD and may be detected in >70% of all cases. Inebilizumab is a humanized IgG1 monoclonal antibody against CD19. Anti-AQP4 antibodies are produced by CD19-positive plasmablasts, and inebilizumab administration significantly reduces the number of CD19-positive B cells and has therapeutic effects on NMOSD. The efficacy and safety of inebilizumab have been verified in the N-MOmentum trial, an international double-blind, placebo-controlled phase II/III study, in which Japanese patients also participated. Inebilizumab was approved for the treatment of NMOSD with AQP4-IgG in Japan in March 2021. In this review, we summarize the efficacy and safety of inebilizumab in the treatment of NMOSD and, focus on findings from the primary and additional analyses of the N-MOmentum trial. These results suggest that inebilizumab is effective and safe in preventing the recurrence of NMOSD in populations with different backgrounds and that long-term treatment with inebilizumab is beneficial.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Anti-Amyloid Antibody Therapy for Alzheimer's Disease]. [阿尔茨海默病的抗淀粉样蛋白抗体疗法]。
Brain and Nerve Pub Date : 2024-10-01 DOI: 10.11477/mf.1416202747
Moeko Shinohara, Kenjiro Ono
{"title":"[Anti-Amyloid Antibody Therapy for Alzheimer's Disease].","authors":"Moeko Shinohara, Kenjiro Ono","doi":"10.11477/mf.1416202747","DOIUrl":"https://doi.org/10.11477/mf.1416202747","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is pathologically characterized by deposition of amyloid plaques (comprising amyloid β [Aβ] protein) and neurofibrillary tangles (comprising tau protein), and neuronal death. Aβ monomers aggregate to form oligomers, protofibrils, and mature fibrils. Previously, the mature fibrils and plaques were implicated as contributors to neurotoxicity and neurodegeneration. However, a growing body of evidence proves stronger toxicity of oligomers and protofibrils. Among the many recent phase 3 clinical trials that have investigated the role of anti-Aβ antibodies in AD, some have shown the clinical efficacy of aducanumab, lecanemab, and donanemab in these patients. Lecanemab showed selectivity towards protofibrils over fibrils, and donanemab was specifically directed against Aβ only in brain-specific amyloid plaques. In contrast, other anti-Aβ antibodies did not show efficacy in AD.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Pathomechanism Underlying Intravenous Immunoglobulin Therapy for Chronic Inflammatory Demyelinating Polyneuropathy]. [静脉注射免疫球蛋白治疗慢性炎症性脱髓鞘性多发性神经病的病理机制]。
Brain and Nerve Pub Date : 2024-10-01 DOI: 10.11477/mf.1416202746
Fumitaka Shimizu
{"title":"[Pathomechanism Underlying Intravenous Immunoglobulin Therapy for Chronic Inflammatory Demyelinating Polyneuropathy].","authors":"Fumitaka Shimizu","doi":"10.11477/mf.1416202746","DOIUrl":"https://doi.org/10.11477/mf.1416202746","url":null,"abstract":"<p><p>Considering its proven clinical usefulness and supportive evidence, intravenous immunoglobulin (IVIg) is used as first-line therapy for chronic inflammatory demyelinating polyneuropathy (CIDP) during the acute and chronic stages. However, the pathomechanism underlying IVIg administration for CIDP remains unclear. Autoantibodies, complement, inflammatory cytokines, chemokines, T cells, B cells, macrophages, and the blood-nerve barrier contribute to the onset and progress of CIDP. The mechanisms underlying the actions of IVIg in CIDP include the following: (1)neutralization of pathological autoantibodies by anti-idiotype antibodies, (2)inhibition of the neonatal Fc receptor (FcRn) with a consequent decrease in pathological autoantibodies, (3)neutralization of cytokines, chemokines, and complement, (4)activity modulation of T cells, B cells, and macrophages, and (5) recovery of blood-nerve barrier function. Compared with the management of typical CIDP, IVIg therapy is less effective for management of autoimmune nodopathy associated with anti-neurofascin-155 or contactin-1 IgG4 antibodies because (1)anti-idiotype antibodies associated with IVIg cannot effectively neutralize IgG4 owing to the strong antigen specificity of IgG4 autoantibodies, and (2)complement, T cells, and macrophages play an insignificant role in the pathomechanism of autoimmune nodopathy. Further understanding of the mechanisms underlying IVIg action and effectiveness of molecular targeted therapy, such as use of FcRn or complement inhibitors and the CD20 monoclonal antibody, is warranted to develop novel therapeutic strategies against CIDP.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[B-cell Therapy for Multiple Sclerosis]. [多发性硬化症的 B 细胞疗法]。
Brain and Nerve Pub Date : 2024-10-01 DOI: 10.11477/mf.1416202745
Yusei Miyazaki, Masaaki Niino
{"title":"[B-cell Therapy for Multiple Sclerosis].","authors":"Yusei Miyazaki, Masaaki Niino","doi":"10.11477/mf.1416202745","DOIUrl":"https://doi.org/10.11477/mf.1416202745","url":null,"abstract":"<p><p>B-cell therapy using anti-CD20 antibodies significantly suppresses relapse and is therefore an important treatment option for multiple sclerosis (MS). Based on the production of inflammatory cytokines and enhanced antigen-presenting capacity, B cells trigger MS relapses via activation of pathogenic T cells. Suppression of these abnormal actions of B cells is the primary mechanism underlying relapse prevention using B-cell therapies. Treatments that target B cells are also expected to suppress chronic progression of MS through modulation of B-cell activity within the central nervous system. B-cell therapies based on novel approaches are expected to improve the regulation of acute and chronic MS pathology.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Blood Biomarkers for Alzheimer's Disease: Current Status and Prospects]. [阿尔茨海默病的血液生物标志物：现状与前景]。
Brain and Nerve Pub Date : 2024-09-01 DOI: 10.11477/mf.1416202730
Takeshi Ikeuchi
{"title":"[Blood Biomarkers for Alzheimer's Disease: Current Status and Prospects].","authors":"Takeshi Ikeuchi","doi":"10.11477/mf.1416202730","DOIUrl":"10.11477/mf.1416202730","url":null,"abstract":"<p><p>Blood biomarkers are minimally invasive, are available at a relatively low cost, and are easily accessible; therefore, they are expected to play a pivotal role in the diagnosis of dementia. Measurement of the amyloid-β ratio and phosphorylated tau in plasma has shown high potential for accurate detection of brain pathology in patients with Alzheimer's disease. Studies have investigated blood biomarkers that reflect neurodegeneration and neuroinflammation in patients with dementia. Challenges associated with blood biomarker use include the lack of robustness of the test and the role of confounders that potentially prevent their immediate clinical application. Further real-world studies are warranted to validate the usefulness of blood biomarkers in dementia management. Appropriate recommendations for the use of blood biomarkers for dementia have been published for physicians and investigators, both in Japan and overseas. Considering the versatility of blood biomarkers, they should be cautiously introduced for clinical use.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142300639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Novel Therapeutic Strategies for Alzheimer's Disease]. [阿尔茨海默病的新型治疗策略]。
Brain and Nerve Pub Date : 2024-09-01 DOI: 10.11477/mf.1416202732
Taisuke Tomita
{"title":"[Novel Therapeutic Strategies for Alzheimer's Disease].","authors":"Taisuke Tomita","doi":"10.11477/mf.1416202732","DOIUrl":"10.11477/mf.1416202732","url":null,"abstract":"<p><p>The molecular pathogenesis of Alzheimer's disease (AD) has been elucidated through the biochemical analysis of senile plaques, neurofibrillary tangles, and pathological features of the brains of patients with AD. Genetic analysis, initiated with familial AD investigation, has revealed that Aβ aggregation and accumulation are crucial processes in AD pathogenesis. The success of lecanemab against aggregated Aβ is the result of these efforts. Meanwhile, research on tau as a causative molecule in AD and various other tauopathies is advancing gradually. Furthermore, genetic analysis has revealed that the inflammatory response of glial cells modifies AD pathophysiology; a novel therapeutic strategy for inflammation control is thus currently under consideration. This article summarizes the latest discoveries related to these new therapeutic strategies for AD.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142300645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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