![]() It has been suggested that cerebrospinal fluid (CSF) NfL levels are increased in ALS patients compared to patients with other neurodegenerative diseases, and phosphorylation of Nfs is indicative of the pathogenesis of some neurodegenerative diseases. One of the known factors of the histopathological mechanisms of ALS includes alteration of axonal transport and protein aggregation. Nfs are composed of at least three polypeptide subunits such as neurofilament light chain (NfL, 68 kDa), neurofilament medium chain (NfM, 150 kDa) and neurofilament heavy chain (NfH, 200 kDa). Neurofilament proteins (Nfs) are target in large myelinated neurons. Neurofilament heavy chain proteins might be a promising biomarker in the disease progression of ALS. We also discussed potential biomarkers in ALS, potential compounds for the treatment of ALS, possible uses of stem cell therapy in ALS, and immunotherapy for the treatment of ALS. We discussed several outcomes of these potential neurotrophic factors for the treatments of ALS. Thus, neurotrophic factors have been the focus in clinical trials to restore the deficits of the motoneurons in ALS. However, the pool target of different trophic factors might have neuroprotection for the motoneurons. Riluzole, an inhibitor of glutamate release, is the only compound clinically used in patients suffering from ALS. To the best of our knowledge, there are no potential drugs for the treatments of ALS. Thus, the spatiotemporal organization of the motoneurons makes it difficult to find efficient procedures for the treatment of this disease. Motoneurons are considered a key factor in ALS the survival of these neurons depends on their targets, skeletal muscle and myelinated Schwann cells surrounding the peripheral axons. Another possible primary mechanism could be related to the toxin itself of the mutant SOD1. Unbalanced glutamate uptake may be critical for ALS disease, as a dramatic loss of glutamate transporters has been found in the ALS motor cortex. ![]() There are several hypotheses suggesting that neuronal death may be caused by oxidative stress, a deficit in trophic factors, chronic inflammation, and possibly glutamate-induced excitoxicity ]. The molecular mechanisms of neuronal death are unknown for ALS. Thus, ALS might be caused or induced through several factors, both genetic and environmental. Another cause of ALS includes mutations in valosin-containing protein (VCP) gene and C9ORF72 gene in chromosome 9. There is also evidence that a failure to degrade ubiquitin-dependent protein can lead to the pathogenesis of ALS. There are other forms of ALS that have been found linked to other chromosomes ]. The disease is linked to a genetic defect on chromosome 21q, and chromosome 9q34. It is estimated that 10% of cases are inherited and 20% caused by mutations in superoxide dismutase 1 gene (SOD1), and the remaining cases present mutations of other known and unknown genes. Familial ALS (fALS) is similar to sporadic ALS. Kassis received a post-doctoral research fellowship from American University of Beirut, Beirut, Lebanon a fellowship from the Interdepartmental Program in Cardiothoracic, Pulmonary and Critical Care from Bridgeport/Yale Health System, Bridgeport, CT and a Plastic Surgery Fellowship from Vanderbilt University Medical Center, Nashville, TN.Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder caused by loss of cortical, brainstem and spinal motoneurons ], which occurs in both forms familial and sporadic ALS. He completed his general surgery internship and his residency at Yale University Medical Center, New Haven, CT, where he served as a chief resident in General Surgery. ![]() Kassis received a Bachelor of Science from American University of Beirut, Beirut, Lebanon, and his medical degree from American University as well. His recently published articles include: Comparative Antimicrobial Activity of Commercial Wound-Care Solutions on Bacterial and Fungal Biofilms, Annals of Plastic Surgery Applied Bioengineering in Tissue Reconstruction, Replacement, and Regeneration, Tissue Engineering Characteristics of Patients With Injury Secondary to Smoking on Home Oxygen Therapy Transferred Intubated to a Burn Center, Journal of the American College of Surgeons.ĭr. Kassis’s research interests include migraine surgery, nerve surgery, breast reinnervation, burn surgery, platelet rich plasma/aesthetic surgery, lymphedema, and biofilms. Kassis is certified by the American Board of General Surgery.ĭr. His clinical areas of expertise include cosmetic plastic surgery, acute and reconstructive burn surgery, and chronic headache. Kassis joined our surgical faculty as an Assistant Professor in the Department of Plastic Surgery after completing a Plastic Surgery Fellowship at Vanderbilt University Medical Center, Nashville, TN.
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