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| 1 | A mutation in the dimerization domain of filamin c causes a novel type of autosomal-dominant myofibrillar myopathy显示文摘 | Vorgerd M van der Ven PFM Bruchertseifer V | 2005 | Am J Hum Genet2005，7，： | 1 |
| 2 | Therapeutic options in other metabolic myopa thies显示文摘 | Vorgerd M | 2008 | Neurothera Deuties2008，5，4： | 1 |
| 3 | Effects of progesterone on T-type-Ca^(2+)-channel expression in Purkinje cells显示文摘Plasticity of cerebellar Purkinje cells(PC)is influenced by progeste rone via the classical progeste rone receptors PR-A and PR-B by stimulating dendritogenesis,spinogenesis,and synaptogenesis in these cells.Dissociated PC cultures were used to analyze progeste rone effects at a molecular level on the voltage-gated T-type-Ca^(2+)-channels Ca_(v)3.1,Ca_(v)3.2,and Ca_(v)3.3 as they helped determine neuronal plasticity by regulating Ca^(2+)-influx in neuronal cells.The results showed direct effects of progesterone on the mRNA expression of T-type-Ca^(2+)-channels,as well as on the protein kinases A and C being involved in downstream signaling pathways that play an important role in neuronal plasticity.For the mRNA expression studies of T-type-Ca^(2+)-channels and protein kinases of the signaling cascade,laser microdissection and purified PC cultures of diffe rent maturation stages were used.Immunohistochemical staining was also performed to characte rize the localization of T-type-Ca^(2+)-channels in PC.Expe rimental progesterone treatment was performed on the purified PC culture for 24 and 48 hours.Our results show that progesterone increases the expression of Ca_(v)3.1 and Ca_(v)3.3 and associated protein kinases A and Cin PC at the mRNA level within 48 hours after treatment at latest.These effects extend the current knowledge of the function of progesterone in the central nervous system and provide an explanatory approach for its influence on neuronal plasticity. | Annika Eickhoff Jonas Tjaden Sarah Stahlke Matthias Vorgerd Verena Theis Veronika Matschke Carsten Theiss | 2022 | Neural Regeneration Research2022，17，11： | 1 |
| 4 | Idebenone in patients with Friedreich ataxia显示文摘 | Scho Is L Vorgerd M Schillings M | 2001 | Neurosci Lett2001，306，： | 1 |
| 5 | Insulin resistance and impaired insulin secretion due to phosphofructo-1-kinase-deficiency in humans显示文摘 | Ristow M Vorgerd M | 1999 | J Mol Med1999，77，1： | 1 |
| 6 | Metabolic and mitochondrial myopathies显示文摘 | Vorgerd M Deschauer M | | 0，，03： | 1 |
| 7 | Molecular analysis of the AGL gene:heterogeneity of mutations in patients with glycogen storage disease type Ⅲ from Germany,Canada,Afghanistan,Iran,and Turkey显示文摘 | Endo Y Horinishi A Vorgerd M | 2006 | J Hum Genet2006，51，11： | 1 |
| 8 | Assessment of postexcitatory inhibition in patients with focal dystonia显示文摘 | Schwenkreis P Vorgerd M Malin JP | 1999 | Acta Neurol Scand1999，100，4： | 1 |
| 9 | Rippling muscle disease:variable phenotype in a family with five afflicted members显示文摘 | Jacobi C Ruscheweyh R Vorgerd M | 2010 | Muscle Nerve2010，41，1： | 1 |
| 10 | A mutation in the dimerization domain of filamin C causes a novel type of auto- somal dominant myofibrillar nyopathy 显示文摘 | Vorgerd M van der Ven PFM Bruchertseifer V | 2005 | Am J Hum Genet2005，77，： | 1 |
| 11 | Therapeutic options in other metabolic myopa- thies显示文摘 | Vorgerd M | 2008 | Neurotherapeutics2008，5，4： | 1 |
| 12 | Idebenone in patients with friedreich ataxia显示文摘 | Sch(o)ls L Vorgerd M Schillings M | 2001 | Neurosci Lett2001，306，： | 1 |
| 13 | Variable reduction of caveolin-3 in patients with LGMD2B/MM显示文摘 | Walter MC Braun C Vorgerd M | 2003 | J Neurol2003，250，： | 1 |
| 14 | Metabolic and mitochondrial myopathies 显示文摘 | Vorgerd M Deschauer M | 2013 | Z Rheumatol2013，72，： | 1 |
| 15 | Molecular analysis of the AGL gene: heterogeneity of mutations in patients with glycogen storage disease type Ⅲ from Germany, Canada, Afghanistan, Iran, and Turkey显示文摘 | Endo Y Rorinishi A Vorgerd M | 2006 | J Hum Genet2006，51，11： | 1 |
| 16 | 免疫介导的波纹肌肉病 | Schulte- Mattler W.J. Kley R.A. Rothenfu.er- Korber E. M. Vorgerd 张玉龙 | 2005 | 世界核心医学期刊文摘(神经病学分册)2005，0，6： | 0 |
| 17 | ANO5-related muscle diseases:From clinics and genetics to pathology and research strategies显示文摘Anoctamin-5(ANO5)is a multi-pass membrane protein localized to the sarcolemma and the sarcoplasmic reticulum.Mutations were linked to rare autosomal recessive muscle diseases.Here,we summarize the clinical spectrum,imaging data and molecular research findings as well as results of animal modeling,which significantly moved forward the understanding of mechanisms underlying ANO5-related muscle diseases.Given that precise histological information on inflammatory processes taking place in patient-derived muscle are still lacking,an(immuno)histological study on biopsies derived from six ANO5-patients was performed showing focal accumulation of necrotic fibers,mild fiber-size variances and myophagocytosis.In addition,MRI data of four ANO5-patients(including a 10-year follow-up in one patient)are presented and discussed in the context of previously published MRI-findings.Hence,data presented in this article combining a review of the literature with own myopathological findings address scientific trends and open questions on ANO5-related muscle diseases,which would be of significant interest for a wide neuromuscular diseases community.To conclude,a clear genotypeephenotype correlation does not exist,and ANO5-related muscle disorders might represent the next entity of a clinical continuum with varying degree of muscle cell pathologies.In addition,results of pre-clinical studies allowed the definition of suitable cell and animal models characterized by certain histological and functional pathologies resembling the human phenotype.These models might serve as suitable systems for testing of interventional concepts in future. | Jon Christiansen Anne-Katrin Guttsches Ulrike Schara-Schmidt Matthias Vorgerd Christoph Heute Corinna Preusse Werner Stenzel Andreas Roos | 2022 | Genes & Diseases2022，9，6： | 0 |
| 18 | Unraveling the gut-brain axis:the impact of steroid hormones and nutrition on Parkinson's disease显示文摘This comprehensive review explores the intricate relationship between nutrition,the gut microbiome,steroid hormones,and Parkinson's disease within the context of the gut-brain axis.The gut-brain axis plays a pivotal role in neurodegenerative diseases like Parkinson's disease,encompassing diverse components such as the gut microbiota,immune system,metabolism,and neural pathways.The gut microbiome,profoundly influenced by dietary factors,emerges as a key player.Nutrition during the first 1000 days of life shapes the gut microbiota composition,influencing immune responses and impacting both child development and adult health.High-fat,high-sugar diets can disrupt this delicate balance,contributing to inflammation and immune dysfunction.Exploring nutritional strategies,the Mediterranean diet's anti-inflammatory and antioxidant properties show promise in reducing Parkinson's disease risk.Microbiome-targeted dietary approaches and the ketogenic diet hold the potential in improving brain disorders.Beyond nutrition,emerging research uncovers potential interactions between steroid hormones,nutrition,and Parkinson's disease.Progesterone,with its anti-inflammatory properties and presence in the nervous system,offers a novel option for Parkinson's disease therapy.Its ability to enhance neuroprotection within the enteric nervous system presents exciting prospects.The review addresses the hypothesis thatα-synuclein aggregates originate from the gut and may enter the brain via the vagus nerve.Gastrointestinal symptoms preceding motor symptoms support this hypothesis.Dysfunctional gut-brain signaling during gut dysbiosis contributes to inflammation and neurotransmitter imbalances,emphasizing the potential of microbiota-based interventions.In summary,this review uncovers the complex web of interactions between nutrition,the gut microbiome,steroid hormones,and Parkinson's disease within the gut-brain axis framework.Understanding these connections not only offers novel therapeutic insights but also illuminates the origins of neurodegenerative diseases such as Parkinson's disease. | Paula Maria Neufeld Ralf A.Nettersheim Veronika Matschke Matthias Vorgerd Sarah Stahlke Carsten Theiss | 2024 | Neural Regeneration Research2024，19，10： | 0 |
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