Marsteller, H. B. (1988). The first American case of myasthenia gravis. Archives of neurology, 45(2), 185-187. (LANDMARK)https://jamanetwork.com/journals/jamaneurology/fullarticle/587278
This reference describes the first case of Myasthenia Gravis in Indian Chief Opechankanough who died in 1644. The account described him to have weakness and needing assistance holding up his eyelids.
Crignon, C. (2017). How Animals may help understand men. Thomas Willis’s Anatomy of the Brain (1664) & Two Discourses Concerning the Soules of Brutes (1672). (LANDMARK)https://quod.lib.umich.edu/e/eebo/A66518.0001.001?rgn=main;view=fulltext
This account is from Thomas Willis to first to describe the disease of myasthenia gravis. He discusses multiple brain and neurological disorders that affect the human body. His description of myasthenia gravis talks about muscular weakness in patients with the disease.
Wilks, S. (1877). On Cerebritis, Hysteria, and Bulbar Paralysis, as Illustrative of Arrest of Function of the Cerebrospinal Centres. Guy’s Hosp, 22, 7-55. https://books.google.com/books?hl=en&lr=&id=siOQbiF8fikC&oi=fnd&pg=PR1&dq=related:FConfyeyRmMJ:scholar.google.com/&ots=ibbK-uom0L&sig=WG6Odd7Uuvs9Wp_nVOV0hZXVaCA#v=onepage&q&f=false
This describes the first modern account of myasthenia gravis by Samuel Wilks in France. Wilks described paralysis in those with the disorder in his characterization.
Shaw, L. E. (1890). A Case of Bulbar Paralysis Without Structural Changes in the Medulla, Brain 13, 96-99.https://books.google.com/books?id=jbNjDwAAQBAJ&pg=PT220&lpg=PT220&dq=Shaw,+L.+E.:+A+Case+of+Bulbar+Paralysis+Without+Structural+Changes+in+the+Medulla+,+Brain+13:96-99,+1890&source=bl&ots=BAu32AYWcq&sig=ACfU3U2c2sE7N9mEEOZlZJA0XNsbPWmevg&hl=en&sa=X&ved=2ahUKEwiAod_Crun9AhWnEVkFHRxFBSwQ6AF6BAgGEAM#v=onepage&q=Shaw%2C%20L.%20E.%3A%20A%20Case%20of%20Bulbar%20Paralysis%20Without%20Structural%20Changes%20in%20the%20Medulla%20%2C%20Brain%2013%3A96-99%2C%201890&f=false
This book contains one of the first case studies describing the disease myasthenia gravis. The case report talked about how the individual with the disease experienced nerve loss in the medulla of the brain. This case of bulbar paralysis was cited to have nerve loss but the structure of the medulla did not change.
Jolly, F. (1895). Ueber myasthenia gravis pseudoparalytica. Berl Klin Wschr, 32, 1-7.(LANDMARK) https://www.acpjournals.org/action/showTocPdf?issue=6&volume=52&journalCode=aim&area=production
This case study report contains two case studies of myasthenia gravis in England they were. Here the disorder was then named “myasthenia gravis pseudo-paralytica”. The case reports described those with the disorder to have decreased muscle tone and weakness.
BUZZARD, E. F. (1906). The clinical history and post-mortem examination of five cases of myasthenia gravis. Brain, 28(3-4), 438-483. https://ia600708.us.archive.org/view_archive.php?archive=/22/items/crossref-pre-1909-scholarly-works/10.1093%252Fbrain%252F18.2-3.457.zip&file=10.1093%252Fbrain%252F28.3-4.438.pdf
This case reports the findings of Edward Buzzard at the National Hospital in Queens Square of patients with Myasthenia Gravis. He explained the accumulation of lymphocytes in the muscles and thymus of patients with myasthenia gravis. This indicated that the disorder may be affecting the lymphatic system of patients.
Bell, E. T. (1917). Tumors of the thymus in myasthenia gravis. The Journal of Nervous and Mental Disease, 45(2), 130-143.(LANDMARK)https://journals.lww.com/jonmd/Citation/1917/02000/TUMORS_OF_THE_THYMUS_IN_MYASTHENIA_GRAVIS.2.aspx
This paper describes a study looking at patients with myasthenia gravis in Germany. Bell found through multiple papers and cases that the thymus was abnormal in patients with the disorder. The phenomenon of thymus tumors and the abnormal finding was found in over half of the patients with myasthenia gravis.
Haberer, H. V., & Von Haberer, H. (1918). Zur klinischen Bedeutung der Thymusdrüse. Arch. klin. Chir, 109, 193-243.(LANDMARK)https://books.google.com/books?hl=en&lr=&id=mnQ4AQAAMAAJ&oi=fnd&pg=PA193&ots=MXWi6JEfoW&sig=Svo0yusI_rXYSvNbyEVJm2YI32o#v=onepage&q&f=false
This book describes the cases where partial removal of the thymus was used in treating those with myasthenia gravis. The highlight of the procedure was a 27-year-old man who had undergone the procedure and saw great improvement. The cases also talked about the surgical hazards and how those with the disorder had increased risks of having surgery and being under anesthesia.
Edgeworth, H. (1930). A report of progress on the use of ephedrine in a case of myasthenia gravis. Journal of the American Medical Association, 94(15), 1136-1136. https://jamanetwork.com/journals/jama/article-abstract/235110
This article discusses the use of ephedrine to treat myasthenia gravis. The patient took the drug for menstrual symptoms and had reduced weakness. The drug was then thought to stimulate the nervous system and began being prescribed to those with myasthenia gravis.
Walker, M. B. (1935). Case showing the effect of Prostigmin on myasthenia gravis.(LANDMARK) https://journals.sagepub.com/doi/10.1177/003591573502800633
This paper describes the work of Dr. Mary Walker who injected myasthenia gravis patients with prostigmine. This injection greatly reduced the symptoms of paralysis in the patients she visited.
Norris, E. H. (1936). The thymoma and thymic hyperplasia in myasthenia gravis with observations on the general pathology. The American Journal of Cancer, 27(3), 421-433.https://aacrjournals.org/amjcancer/article/27/3/421/679273/The-Thymoma-and-Thymic-Hyperplasia-in-Myasthenia
This paper describes the finding of Norris with there being thymic hyperplasia found in patients that had necroscopy. This proposed the idea that removal of the thymus can be a possible treatment for those with myasthenia gravis.
Zaimis, E. J. (1951). The action of decamethonium on normal and denervated mammalian muscle. The Journal of Physiology, 112(1-2), 176.https://physoc.onlinelibrary.wiley.com/doi/10.1113/jphysiol.1951.sp004518
This study helped explain how acetylcholine receptors are involved in the mechanism of muscular contraction. It was found that decamethonium can produce a neuromuscular blockage in the tissue of mammals.
Mackay, R. I. (1951). Congenital myasthenia gravis. Archives of Disease in Childhood, 26(128), 289.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1988397/?page=1
This case study discusses the need to investigate the presence of congenital myasthenia gravis further. The case presented in a hospital in Salford is a unique case because the disorder is more seen in early childhood. This case highlighted the need to add congenital myasthenia gravis to textbooks since the cases were now seen to present earlier in development.
Churchill-Davidson, H. C., & Richardson, A. T. (1953). Neuromuscular transmission in myasthenia gravis. The Journal of Physiology, 122(2), 252.(LANDMARK) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1366112/
This study compared the effects of normal muscular tissue to those with myasthenia gravis when exposed to decamethonium. They found through the chemical excitation that there was a difference in the transmission to the muscles. This study suggested a new mechanism by which myasthenia gravis affects muscular contraction through acetylcholine receptors.
TURNER J. W. (1959). Myasthenia gravis. British medical journal, 1(5124), 778–779. https://doi.org/10.1136/bmj.1.5124.778 (LANDMARK) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1992998/?page=1
This article examines the effectiveness of using neostigmine to treat patients with myasthenia gravis. The treatment potentials of the drug can help improve weakness after infection, before an increase in activity, or after receiving a thymectomy.
STERN, G. M., HALL, J. M., & ROBINSON, D. C. (1964). NEONATAL MYASTHENIA GRAVIS. British medical journal, 2(5404), 284–286. https://doi.org/10.1136/bmj.2.5404.284 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1815576/
This study describes the presentation of neonatal myasthenia gravis in two cases bringing light to the increasing prevalence in younger individuals compared to previous diagnoses of the disease occurring later in life. The use of immunofluorescence was able to analyze the serum to find there were no antibodies to normal muscle in both the mother and child.
Warrier, C. B., & Pillai, T. D. (1967). Familial myasthenia gravis. British medical journal, 3(5569), 839–840. https://doi.org/10.1136/bmj.3.5569.839https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1842611/
This article was able to highlight the genetic basis of myasthenia gravis in families. Utilizing case studies, pedigree charts helped show the rare inheritance of the disease with only a few generations having more than one affected by the disorder.
Patrick, J., & Lindstrom, J. (1973). Autoimmune response to acetylcholine receptor. Science, 180(4088), 871-872. (LANDMARK)https://www.science.org/doi/epdf/10.1126/science.180.4088.871?adobe_mc=MCMID%3D50757547858844446241803403673976370587%7CMCORGID%3D242B6472541199F70A4C98A6%2540AdobeOrg%7CTS%3D1679322271
This article indicated that the malfunction of the acetylcholine receptors will result in an autoimmune response. This response resulted in muscle paralysis because the depolarization of the muscles is blocked. This provided insight into the mechanism by which myasthenia gravis cause paralysis and opens the door to a potential treatment target.
Rosenberg, R. N., & Campbell, J. (1973). Myasthenia gravis. California medicine, 118(1), 18–23.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1454990/
This article discussed the presentation and diagnosis of patients with myasthenia gravis. The article provided insight into the metabolism of acetylcholine and suggested how competition with the transmitter increases acetylcholine transferase. This results in less acetylcholine at the next receptor and muscular dysfunction occurs as a result.
Toyka, K. V., Brachman, D. B., Pestronk, A., & Kao, I. (1975). Myasthenia gravis: passive transfer from man to mouse. Science, 190(4212), 397-399. (LANDMARK)https://www.science.org/doi/10.1126/science.1179220
This paper first identified that it was a circulating factor in the immune system that cause myasthenia gravis to develop. When mice were injected with the serum containing immunoglobulin of myasthenia patients resulted in mice developing the disorder.
Haas L. (1976). Myasthenia Gravis. Proceedings of the Royal Society of Medicine, 69(12), 879.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1864779/
This article discussed a case in which a drug regimen can help provide some relief for patients instead of undergoing a thymectomy. For the particular patient neostigmine was prescribed along with codeine phosphate. The codeine was used to help with the patient’s abdominal pain. This highlighted one of the many treatment combinations that were used in patients with myasthenia gravis.
Drachman, D. B., Angus, C. W., Adams, R. N., Michelson, J. D., & Hoffman, G. J. (1978). Myasthenic antibodies cross-link acetylcholine receptors to accelerate degradation. New England Journal of Medicine, 298(20), 1116-1122.https://www.nejm.org/doi/10.1056/NEJM197805182982004?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
This article was able to build on the previously established idea that the autoimmune response of myasthenia gravis degrades acetylcholine receptors. Patients with myasthenia gravis were found to need specific antibodies to be able to degrade the receptors. When these receptors crosslink with one, the speed of degradation can occur with specifically myasthenic IgG and Fab.
Smit, L. M. E., & Earth, P. G. (1980). Arthrogryposis multiplex congenita due to congenital myasthenia. Developmental Medicine & Child Neurology, 22(3), 371-374.https://onlinelibrary.wiley.com/doi/10.1111/j.1469-8749.1980.tb03718.x
This article provided insight into arthrogryposis multiplex congenital which results from decreased fetal movement. Here it was proven that myasthenia gravis can cause this condition. This link provided more information about the conditions that can be caused by myasthenia gravis which influenced the diagnosis of the disorder.
Tzartos, S. J., & Lindstrom, J. M. (1980). Monoclonal antibodies used to probe acetylcholine receptor structure: localization of the main immunogenic region and detection of similarities between subunits. Proceedings of the National Academy of Sciences, 77(2), 755-759. (LANDMARK) https://www.pnas.org/doi/abs/10.1073/pnas.77.2.755
This paper identifies the monoclonal immunogenic regions for the acetylcholine receptor. This was done using monoclonal antibodies for the alpha and beta subunits of the receptor.
Sahashi, K., Engel, A. G., Lambert, E. H., & Howard Jr, F. M. (1980). Ultrastructural localization of the terminal and lytic ninth complement component (C9) at the motor end-plate in myasthenia gravis. Journal of Neuropathology & Experimental Neurology, 39(2), 160-172.https://academic.oup.com/jnen/article/39/2/160/2613146?login=true
This article provides an explanation of what occurs at the post-synaptic region when the acetylcholine receptor is deficient. Specifically, abundance C9 at the motor end-plate, when lacking the structural integrity that is present in those with myasthenia gravis, ends up with an increase in space between the junctions. This helps explain the impact acetylcholine receptors have on neuromuscular function.
Tindall, R. S., Phillips, J. T., Rollins, J. A., Wells, L. I. E. S. E. L. O. T. T. E., & Hall, K. (1993). A clinical therapeutic trial of cyclosporine in myasthenia gravis. Annals of the New York Academy of Sciences, 681, 539-551. https://nyaspubs.onlinelibrary.wiley.com/doi/epdf/10.1111/j.1749-6632.1993.tb22937.x
This clinical trial discussed a new drug cyclosporine proven effective in autoimmune disorder treatment for myasthenia gravis by blocking T-cell dependent function which myasthenia gravis requires. This new treatment could be used instead of corticosteroids for patients which over time can become toxic in patients.
Deschenes, M. R., Maresh, C. M., & Kraemer, W. J. (1994). The neuromuscular junction: Structure, function, and its role in the excitation of muscle. The Journal of Strength & Conditioning Research, 8(2), 103-109. https://journals.lww.com/nsca-jscr/Abstract/1994/05000/The_Neuromuscular_Junction__Structure,_Function,.8.aspx#:~:text=The%20neuromuscular%20junction%20plays%20a,in%20a%20muscle%20fiber%20action.
This paper helped explain the mechanism of muscle excitation. The paper described how molecules travels across the synapse in signaling.
Moiola, L., Karachunski, P., Protti, M. P., Howard, J. F., & Conti-Tronconi, B. M. (1994). Epitopes on the beta subunit of human muscle acetylcholine receptor recognized by CD4+ cells of myasthenia gravis patients and healthy subjects. The Journal of clinical investigation, 93(3), 1020-1028. (LANDMARK) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC294026/
This paper identified the epitopes of the acetylcholine peptides that are recognized by CD4+ lymphocyte cytes. This discovery helped further explain the pathogenesis of myasthenia gravis and identified potential treatment targets.
Engel, A. G., Ohno, K., Milone, M., Wang, H. L., Nakano, S., Bouzat, C., … & Sine, S. M. (1996). New mutations in acetylcholine receptor subunit genes reveal heterogeneity in the slow-channel congenital myasthenic syndrome. Human molecular genetics, 5(9), 1217-1227.https://pubmed.ncbi.nlm.nih.gov/8872460/
This paper helped identify the mechanism of myasthenia gravis. Specifically discussing how the alpha-1 malfunctions and acetylcholine is not taken up.
Green, W. N., & Wanamaker, C. P. (1998). Formation of the nicotinic acetylcholine receptor binding sites. Journal of Neuroscience, 18(15), 5555-5564. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6793068/#:~:text=Nicotinic%20acetylcholine%20receptors%20(AChRs)%20are,with%20%CE%B3%20and%20%CE%B4%20subunits.
This paper discussed the mechanism by which acetylcholine receptors are formed. This formation is important for signaling muscular contraction.
Nichols, P., Croxen, R., Vincent, A., Rutter, R., Hutchinson, M., Newsom‐Davis, J., & Beeson, D. (1999). Mutation of the acetylcholine receptor ε‐subunit promoter in congenital myasthenic syndrome. Annals of Neurology: Official Journal of the American Neurological Association and the Child Neurology Society, 45(4), 439-443. (LANDMARK)https://onlinelibrary.wiley.com/doi/pdf/10.1002/1531-8249%28199904%2945%3A4%3C439%3A%3AAID-ANA4%3E3.0.CO%3B2-W
This article helped identify one of the mutations in the acetylcholine receptor that can result in myasthenia gravis. This point mutation in the ε‐subunit promoter results in congenital myasthenia gravis developing.
Ohno, K., Tsujino, A., Brengman, J. M., Harper, C. M., Bajzer, Z., Udd, B., … & Engel, A. G. (2001). Choline acetyltransferase mutations cause myasthenic syndrome associated with episodic apnea in humans. Proceedings of the National Academy of Sciences, 98(4), 2017-2022.https://www.pnas.org/doi/full/10.1073/pnas.98.4.2017
This article analyzes mutations in choline acetyltransferase. These mutations impact the function of the enzyme and result in congenital myasthenic syndrome. These mutations can be potential treatment and diagnostic targets for those with myasthenia gravis.
Brejc, K., van Dijk, W. J., Klaassen, R. V., Schuurmans, M., van Der Oost, J., Smit, A. B., & Sixma, T. K. (2001). Crystal structure of an ACh-binding protein reveals the ligand-binding domain of nicotinic receptors. Nature, 411(6835), 269-276.https://www.nature.com/articles/35077011
This paper used the ACh-binding protein to identify the ligand-binding domain. This identification helped understand how acetylcholine and other ligands bind to the receptor.
Wang, X. B., Kakoulidou, M., Qiu, Q., Giscombe, R., Huang, D., Pirskanen, R., & Lefvert, A. K. (2002). CDS1 and promoter single nucleotide polymorphisms of the CTLA-4 gene in human myasthenia gravis. Genes & Immunity, 3(1), 46-49. https://www.nature.com/articles/6363816
This paper highlighted single nucleotide polymorphisms that could be a genetic link to the development of myasthenia gravis. Specifically in the CTLA-4 gene, which is a T lymphocyte protein, the promoter and first exon of the gene had certain polymorphisms that lead to thymoma. The +49 base pair was shown to lead to the development of myasthenia gravis which would help determine the genetic cause of the disorder.
Karlin, A. (2002). Emerging structure of the nicotinic acetylcholine receptors. Nature Reviews Neuroscience, 3(2), 102-114. https://ftp.rush.edu/users/molebio/Bob_Eisenberg/CV%20on%20moleobio-Bob_Eisenberg/__Fragments%20and%20Ideas/Bubbles/Bubbles%20References/karlin%20stucture%20paper-20021.pdf.
This paper highlighted key features of acetylcholine receptors. This understanding is important for healthy neuromuscular transmission.
Lowe, J. B., & Marth, J. D. (2003). A genetic approach to mammalian glycan function. Annual review of biochemistry, 72(1), 643-691.https://www.annualreviews.org/doi/abs/10.1146/annurev.biochem.72.121801.161809
This paper looks at the role mutation play in the mechanism of glycan function. This pathway is important to understand the impacts of myasthenia gravis.
Chou, K. C. (2004). Insights from modelling the 3D structure of the extracellular domain of α7 nicotinic acetylcholine receptor. Biochemical and biophysical research communications, 319(2), 433-438. https://www.sciencedirect.com/science/article/pii/S0006291X04009684
This paper identifies the α7 acetylcholine receptor domain. This is important for understanding the mechanism of neuromuscular signaling.
Dajas-Bailador, F., & Wonnacott, S. (2004). Nicotinic acetylcholine receptors and the regulation of neuronal signalling. Trends in pharmacological sciences, 25(6), 317-324. https://pubmed.ncbi.nlm.nih.gov/15165747/
This paper laid out the mechanism of how acetylcholine works in neurotransmission. This paper also highlighted regulatory aspects that can be targeted in drug design.
Giraud, M., Taubert, R., Vandiedonck, C., Ke, X., Lévi-Strauss, M., Pagani, F., … & Garchon, H. J. (2007). An IRF8-binding promoter variant and AIRE control CHRNA1 promiscuous expression in thymus. Nature, 448(7156), 934-937.https://www.nature.com/articles/nature06066
This paper highlighted and advanced the understanding of the regulation of acetylcholine receptors. It was found that the CHRNA1 gene that encodes the α-subunit of the receptor is regulated by IRF8 and AIRE which also regulate the auto-antigen signaling in the thymus. Misregulation was found in those with myasthenia gravis which provides insight into the mechanism of the disorder and identifies potential treatment targets.
Huijbers, M. G., Lipka, A. F., Plomp, J. J., Niks, E. H., Van Der Maarel, S. M., & Verschuuren, J. J. (2014). Pathogenic immune mechanisms at the neuromuscular synapse: the role of specific antibody‐binding epitopes in myasthenia gravis. Journal of internal medicine, 275(1), 12-26.(LANDMARK) https://onlinelibrary.wiley.com/doi/10.1111/joim.12163
This paper was able to identify the role of autoantibody-binding epitopes play in the pathogenesis of myasthenia gravis. Being able to map these epitomes on the gene can identify locations for potential treatments.
Olsen, J. A., Balle, T., Gajhede, M., Ahring, P. K., & Kastrup, J. S. (2014). Molecular recognition of the neurotransmitter acetylcholine by an acetylcholine binding protein reveals determinants of binding to nicotinic acetylcholine receptors. PloS one, 9(3), e91232. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0091232
This paper identified the molecular interactions necessary for acetylcholine to bind to the receptor. This binding opens the ion channel of the receptor.
Xu, S., Zhang, T., Kompella, S. N., Yan, M., Lu, A., Wang, Y., … & Wang, C. (2015). Conotoxin αD-GeXXA utilizes a novel strategy to antagonize nicotinic acetylcholine receptors. Scientific Reports, 5(1), 14261. https://www.nature.com/articles/srep14261
This paper revolutionized the possible basis to design drugs that target nicotinic acetylcholine receptors. GeXXA-CTD plays an antagonistic role by allosterically inhibiting the binding site of the receptors to opening.
Ha, J. C., & Richman, D. P. (2015). Myasthenia gravis and related disorders: Pathology and molecular pathogenesis. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1852(4), 651-657. https://www.sciencedirect.com/science/article/pii/S0925443914003640
This paper analyzed the muscle endplate function in those with myasthenia gravis. They found that membrane attack complex causes damage to the endplates.
Bauché, S., O’regan, S., Azuma, Y., Laffargue, F., McMacken, G., Sternberg, D., … & Nicole, S. (2016). Impaired presynaptic high-affinity choline transporter causes a congenital myasthenic syndrome with episodic apnea. The American Journal of Human Genetics, 99(3), 753-761.https://pubmed.ncbi.nlm.nih.gov/27569547/
This paper discussed how myasthenia gravis affects the diaphragm. When the diaphragm is paralyzed by the disorder, patients are unable to breath.
Noridomi, K., Watanabe, G., Hansen, M. N., Han, G. W., & Chen, L. (2017). Structural insights into the molecular mechanisms of myasthenia gravis and their therapeutic implications. Elife, 6, e23043.(LANDMARK) https://elifesciences.org/articles/23043
This paper helped identify the mechanism by which myasthenia gravis develops. Specifically how the immune response degrades acetylcholine receptors.
Dalakas, M. C. (2019). Immunotherapy in myasthenia gravis in the era of biologics. Nature Reviews Neurology, 15(2), 113-124.https://www.nature.com/articles/s41582-018-0110-z
Since the disease’s first discovery, treatment has been a challenge since there has not yet been an effective combination of treatments that widely work in patients. This is due to the complexity if the disorder highlighting the need to develop more specific treatments and immunotherapies instead of continuing to look at general therapeutics.
Omar, A., Marwaha, K., & Bollu, P. C. (2020). Physiology, neuromuscular junction. In StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK470413/.
This paper describes the function of neuromuscular junctions. These junctions are important for signaling muscular contractions.
O’Connor, L., Westerberg, E., & Punga, A. R. (2020). Myasthenia gravis and physical exercise: a novel paradigm. Frontiers in Neurology, 11, 675.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7403401/
This paper looked at exercise and its association with myasthenia gravid symptoms. They found that the increase in exercise increases the severity of the symptoms.
Matta, J. A., Gu, S., Davini, W. B., & Bredt, D. S. (2021). Nicotinic acetylcholine receptor redux: Discovery of accessories opens therapeutic vistas. Science, 373(6556), eabg6539. (LANDMARK) https://www.science.org/doi/10.1126/science.abg6539
Acetylcholine receptors have long been studied and it has been known for a while their malfunction is a major player in the pathogenesis of myasthenia gravis. The discovery of the auxiliary subunits and chaperone proteins that regulate the receptors opens the door to a new area of possible therapeutics to help treat those with myasthenia gravis.
Australia, H. (2021). Neuromuscular system. https://www.healthdirect.gov.au/neuromuscular-system. This paper identified the organs and structure of the nervous system. This function is present in individuals without myasthenia gravis.
Oh, S., Mao, X., Manfredo-Vieira, S., Lee, J., Patel, D., Choi, E. J., … & Payne, A. S. (2023). Precision targeting of autoantigen-specific B cells in muscle-specific tyrosine kinase myasthenia gravis with chimeric autoantibody receptor T cells. Nature Biotechnology, 1-10.https://www.nature.com/articles/s41587-022-01637-z
This paper discusses a new drug that can be used to help treat those with myasthenia gravis. This new treatment avoids the chronic immunosuppression that previous treatments cause by using MuSK-CAART to treat those with myasthenia gravis by targeting the autoantibody for MuSK.
Verdier, J., Fayet, O. M., Hemery, E., Truffault, F., Pinzón, N., Demeret, S., … & Le Panse, R. (2023). Single-cell mass cytometry on peripheral cells in Myasthenia Gravis identifies dysregulation of innate immune cells. Frontiers in Immunology, 14.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9922723/
This paper contributes further to the understanding of the immune response and development of myasthenia gravis. They suggest that the inflammation in the thymus prevents the proper differentiation of γδ T cells. They explained how these cells are likely involved in autoimmunity which helps develop the pathway of the disorder.
Stergiou, C., Williams, R., Fleming, J. R., Zouvelou, V., Ninou, E., Andreetta, F., … & Tzartos, S. (2023). Immunological and Structural Characterization of Titin Main Immunogenic Region; I110 Domain Is the Target of Titin Antibodies in Myasthenia Gravis. Biomedicines, 11(2), 449.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9952892/
This paper was able to identify the I110 domain as a target of titin antibodies. Titin antibodies join other identified autoantigens that target the neuromuscular junction and result in the development of myasthenia gravis. This identification will help further studies to improve the diagnostics and treatment for individuals that have titin autoimmunity.
Clinical overview of MG. Myasthenia Gravis Foundation of America. (n.d.). Retrieved April 26, 2023, from https://myasthenia.org/Professionals/Clinical-Overview-of-MG#:~:text=The%20prevalence%20of%20myasthenia%20gravis,cases%20in%20the%20United%20States .
This source provides an overview as well as statistics on myasthenia gravis. The cases and prevalence in the United States is included.
