Dm Disease-A-Month最新文献

{"title":"The role and benefits of ketogenic diet in modulating inflammation in multiple sclerosis: A systematic review and meta-analysis.","authors":"Nalla Jaipal Reddy, Neo Zhong Yi Benjamin, Pannala Harsha Reddy, Andy Thai, Hamza Muntasir Al Rawashdeh, Chiranjeevee Saravanan, Priyadarshi Prajjwal, Yogesh Tekuru, Pugazhendi Inban, Jobby John","doi":"10.1016/j.disamonth.2025.102013","DOIUrl":"https://doi.org/10.1016/j.disamonth.2025.102013","url":null,"abstract":"<p><strong>Background: </strong>The ketogenic diet, known for its anti-inflammatory and neuroprotective effects, has gained attention as a potential therapeutic approach for modulating inflammation and improving clinical outcomes in Multiple Sclerosis patients.</p><p><strong>Objectives: </strong>To systematically evaluate and synthesize clinical and preclinical evidence on the ketogenic diet's role in modulating inflammation in Multiple Sclerosis patients and quantitatively assess its effects on inflammation.</p><p><strong>Results: </strong>The meta-analysis revealed significant effects of the KD on inflammatory markers in MS patients. At 3 months, Leptin levels decreased significantly (mean difference: -2.63 ng/mL, 95 % CI: -3.03 to -2.24, p < 0.00001), and Adiponectin levels increased (mean difference: -1.78 mcg/mL, 95 % CI: -2.26 to -1.29, p < 0.00001). At 6 months, Leptin again decreased (mean difference: -2.18 ng/mL, 95 % CI: -2.92 to -1.43, p < 0.00001), and Adiponectin increased (mean difference: -1.65 mcg/mL, 95 % CI: -1.93 to -1.36, p < 0.00001). However, Neurofilament Light Chain (NfL) showed no significant change (mean difference: -0.10, 95 % CI: -0.61 to 0.40, p > 0.05), suggesting stable neurodegeneration biomarkers. The overall results suggest that the ketogenic diet reduces Leptin, increases Adiponectin, but does not worsen neurodegeneration, highlighting its anti-inflammatory effects.</p><p><strong>Conclusion: </strong>The ketogenic diet shows promise in improving inflammation, fatigue, depression, and quality of life in MS patients. While neurodegenerative biomarkers like NfL remain stable, deeper ketosis may enhance neuroprotection. Further long-term studies are needed to confirm these effects.</p>","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"102013"},"PeriodicalIF":4.3,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145259900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Foreword for Schizophrenia and psychosis in children and adolescents: An inspiring journey of scientific progress and the rich influences of history and religion","authors":"Jerrold B. Leikin MD FACP, FACEP, FAACT, FACMT, FACOEM, FASAM","doi":"10.1016/j.disamonth.2025.101982","DOIUrl":"10.1016/j.disamonth.2025.101982","url":null,"abstract":"","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":"71 10","pages":"Article 101982"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144977574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"C2: Editorial Board","authors":"","doi":"10.1016/S0011-5029(25)00171-3","DOIUrl":"10.1016/S0011-5029(25)00171-3","url":null,"abstract":"","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":"71 10","pages":"Article 102017"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145247907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Information for Readers","authors":"","doi":"10.1016/S0011-5029(25)00173-7","DOIUrl":"10.1016/S0011-5029(25)00173-7","url":null,"abstract":"","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":"71 10","pages":"Article 102019"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145247981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Schizophrenia and psychosis in children and adolescents: An inspiring journey of scientific progress and the rich influences of history and religion","authors":"Donald E․ Greydanus MD, DrHC ,&nbsp;Muhammad Waqar Azeem MD ,&nbsp;Ahsan Nazeer MD","doi":"10.1016/j.disamonth.2025.101983","DOIUrl":"10.1016/j.disamonth.2025.101983","url":null,"abstract":"&lt;div&gt;&lt;div&gt;The human brain begins &lt;em&gt;in utero&lt;/em&gt; through neurulation, during which the neural plate develops into the neural tube. Through a complex journey of remarkable neurological intricacy, the central nervous system (CNS) forms with billions of neurons and trillions of connections. This extraordinary process is filled with dangers, including genetic abnormalities (from both maternal and paternal sources), maternal injuries such as infections, substance use, immunological conditions, and other factors. It is somewhere during this development of cerebral functions that a vulnerability to schizophrenia arises. The evolutionary origins still remain elusive to this day. Clinically recognized about 130 years ago, the history of schizophrenia spans thousands of years, with conceptualization evolving from linking the condition to supernatural invasions to understanding it as a complex brain disorder, as defined by the American Psychiatric Association’s 2013 DSM-5 criteria.&lt;/div&gt;&lt;div&gt;The typical age range for presentation and diagnosis is usually between 15 and 30 years of age; presentations in older and younger age groups are also identified. Diagnostic definitions can vary; in this discussion, presentation of schizophrenia prior to 18 years of age is called pediatric schizophrenia (or EOS: early-onset schizophrenia) and COS: childhood-onset schizophrenia (very early-onset schizophrenia or VEOS) with onset prior to 13 years of age.&lt;/div&gt;&lt;div&gt;Concepts of pediatric schizophrenia are considered that include historical perspectives, epidemiology, diagnosis, etiology, co-morbid conditions, differential diagnoses, evaluation principles, and concepts of management (i.e., psychopharmacology, psychotherapy, ECT and psychosocial support).&lt;/div&gt;&lt;div&gt;Clinicians evaluating a child or adolescent with features suggestive of psychosis must keep in mind the numerous medical and psychological conditions that can serve as differential diagnoses and co-morbid conditions. These disorders are discussed in this treatise. The younger the child, the more likely there is another disorder simulating schizophrenia, such as epilepsy, infection, inborn errors of metabolism, porphyria, immunologic conditions, genetic (epigenetic) aberrations, and numerous others. Before treating this young person for schizophrenia, one must have the back-up or support of a comprehensive testing protocol (i.e., laboratory studies, neuroimaging results, genetic analyses, etc.). Always screen for suicidality as suicide is a persistent peril for individuals with psychosis.&lt;/div&gt;&lt;div&gt;As one provides psychopharmacologic products (i.e., mostly dopamine receptor antagonists) for this psychiatric problem, the medical and psychiatric health of the child or adolescent must be known in detail. The potential side effects (i.e., neurologic, extrapyramidal, metabolic, cardiac, others) of these current agents are disturbing to these young individuals and are reviewed along with management principles. Clozapin","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":"71 10","pages":"Article 101983"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144977569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Title Page","authors":"","doi":"10.1016/S0011-5029(25)00172-5","DOIUrl":"10.1016/S0011-5029(25)00172-5","url":null,"abstract":"","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":"71 10","pages":"Article 102018"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145247908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple sclerosis updates and the safety and efficacy of Bruton tyrosine kinase inhibitors in it: A systematic review.","authors":"Priyadarshi Prajjwal, Prachi Vikrambhai Patel, Zeel Vishnubhai Patel, Pugazhendi Inban, Divyakshi Patel, Priya Mahato, Laiba Shamim, Nathan Joseph Silva Godinho, Yogesh Tekuru","doi":"10.1016/j.disamonth.2025.102012","DOIUrl":"https://doi.org/10.1016/j.disamonth.2025.102012","url":null,"abstract":"<p><strong>Background: </strong>Multiple sclerosis (MS) is a chronic neurodegenerative and autoimmune disease characterized by CNS inflammation and demyelination. Although current disease-modifying therapies (DMTs) can reduce peripheral immune responses, their impact on CNS-compartmentalized inflammation remains limited. Bruton Tyrosine Kinase inhibitors (BTKis) have emerged as promising oral agents targeting both B cells and microglia.</p><p><strong>Objective: </strong>To evaluate the safety profiles and effectiveness of two BTK inhibitors- Tolebrutinib and Evobrutinib in the management of relapsing multiple sclerosis.</p><p><strong>Methods: </strong>A literature search was conducted using PubMed, Embase, and Scopus for randomized controlled trials published between 2020 and 2024. Studies comparing Evobrutinib and Tolebrutinib in MS patients were screened and evaluated based on predetermined inclusion and exclusion criteria. Four relevant RCTs were matched and examined in more detail.</p><p><strong>Results: </strong>On MRI, both BTK inhibitors showed decreases in gadolinium-enhancing lesions; Tolebrutinib demonstrated dose-dependent efficacy in reducing new Gd-enhancing lesions and T2 lesion counts, with optimal effects at 60 mg daily. Evobrutinib showed dose-dependent decreases in serum neurofilament light (NfL) levels and relapse rates, with twice-daily dosing providing greater BTK inhibition and clinical benefit. Nasopharyngitis, temporary increases in liver enzymes, and mild gastrointestinal symptoms were among the frequent side effects for both agents. The included studies did not report any direct clinical comparisons of CNS penetration or microglial modulation.</p><p><strong>Conclusion: </strong>With good safety and efficacy profiles in treating relapsing multiple sclerosis, both of the BTKis (Evobrutinib and Tolebrutinib) show promise. Both have promise as oral treatments of the future, but Tolebrutinib might have better effects on the central nervous system. To confirm long-term results and determine their role in progressive MS, more phase III trials are necessary.</p>","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"102012"},"PeriodicalIF":4.3,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Danon disease: From genetic origins and molecular defects to therapeutic advances.","authors":"Rishabh Chaudhary, Alpana Singh","doi":"10.1016/j.disamonth.2025.102015","DOIUrl":"https://doi.org/10.1016/j.disamonth.2025.102015","url":null,"abstract":"<p><p>Danon disease (DD) represents a rare and complex X-linked disorder, characterized by hypertrophic cardiomyopathy, skeletal muscle deterioration, and cognitive deficits. At its core, the disease stems from mutations in the LAMP2 (lysosome-associated membrane protein 2) gene, which result in a critical deficiency of LAMP-2, particularly the LAMP-2B isoform. This loss destabilizes normal autophagic clearance, leading to the buildup of dysfunctional autophagic vacuoles that ultimately disrupt cellular homeostasis. Although accurately modeling the full range of DD symptoms remains challenging, patient-specific induced pluripotent stem cells and innovative LAMP-2-deficient animal models have provided valuable insights into the disease's molecular and cellular basis. Recent research points decisively to mitochondrial dysfunction and fragmentation as pivotal contributors to disease progression, shifting our understanding of DD beyond lysosomal defects alone. These mechanistic revelations have inspired new therapeutic directions, with gene therapy emerging as a particularly promising candidate based on encouraging preclinical results and ongoing clinical studies. Moving forward, a deeper integration of molecular insights with therapeutic innovation will be essential to developing effective strategies that address the multifaceted pathology of DD and improve outcomes for affected individuals. In this review, we provide a comprehensive analysis of DD, focusing on its genetic and molecular underpinnings, particularly the role of LAMP-2 deficiency in disrupting autophagy and mitochondrial integrity. We critically evaluate experimental models that have advanced our understanding of DD pathogenesis. Additionally, we discuss emerging therapeutic strategies, with an emphasis on gene therapy and other innovative approaches aimed at restoring cellular homeostasis and mitigating cardiomyopathy and neuromuscular symptoms.</p>","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"102015"},"PeriodicalIF":4.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145082445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Foreword danon disease: From genetic origins and molecular defects to therapeutic advances.","authors":"Jerrold B Leikin","doi":"10.1016/j.disamonth.2025.102014","DOIUrl":"https://doi.org/10.1016/j.disamonth.2025.102014","url":null,"abstract":"","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"102014"},"PeriodicalIF":4.3,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145066299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Foreword: Role of Bruton tyrosine kinase inhibitors and ketogenic diet for inflammatory modulation in multiple sclerosis.","authors":"","doi":"10.1016/j.disamonth.2025.102011","DOIUrl":"https://doi.org/10.1016/j.disamonth.2025.102011","url":null,"abstract":"","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"102011"},"PeriodicalIF":4.3,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145034462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}