**7. Conclusion**

308 Autoimmune Disorders – Current Concepts and Advances from Bedside to Mechanistic Insights

skeletal muscle relaxants, (Duddy &

Plasmapheresis and IVIg (Dalakas, 2009; Hayashi et al., 1999) -------





Baker, 2009)

Cyclosporine, glucocorticoids and Antithymocyte globulin (Buchwald et al., 2005; Koski & Patterson, 2006)

Pyridostigmine bromide, 3,4- Diaminopyridine, guanidine HCl and immunosuppressive agents (McEvoy et al., 1989; Sanders, 1995)

Glucocorticosteroids, Plasmaoheresis and IVIg (Merchut, 2010)

Glucocorticosteroids, Plasmapheresis and IVIg (Shy, 2007)

Multiple sclerosis=MS; Myasthenia gravis=MG; Guillain-Barre syndrome=GBS; Neuromyelitis optica=NMO; Stiff-Man syndrome =SMS; Paraneoplastic neurological syndromes=PNS; Lambert-Eaton

Table 1. showing the disease mechanisms, current and future therapeutics for neurological

Targeting the immune cell entry is considered to be an ideal approach and based on this concept we noticed a significant blockade of lymphocyte traffic and eventual recovery in EAE mouse model when administered with mucosal addressin cell adhesion molecule (MAdCAM-1) antibody that binds with the integrins on the lymphocyte cell surface. We also developed a combinatorial approach for this model to protect the neurons against glutamate mediated damage with the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/ Kainate receptor antagonist 2,3-dihydroxy -6- nitro-7- sulfamoylbenzo (f)quinoxaline (NBQX), and the N-methyl D-aspartate (NMDA) receptor antagonist GPE(neuro protector glycine-proline-glutamic acid;N-terminal tripeptide of insulin like growth factor ). This combinatorial therapy also helps in reducing the infiltrating immune cells at the site of inflammation in the brain (Kanwar et al, 2004).. We have also patented the treatment of demyelinating diseases by administering GPE (WIPO).In addition, there are

5 SMS

8 NM

9 PN

autoimmune diseases.

Glutamic acid decarboxylase enzyme

Ma2 antibodies

calcium channels

Voltage gated K+ channels and leucine-rich glioma-inactivated

Glycolipid GM1 and myelin associated glycoprotein

myasthenic syndrome=LEMS; Neuromyotonia=NM and Polyneuropathies=PN

1 protein

6 PNS Hu, Yo,Ma1 &

7 LEMS Voltage gated

Further to conclude, the immunosuppressive and anti-inflammatory treatments considered for treating autoimmune diseases pose serious side effects upon long term administration. Hence, it is rather expected, than to hope that emerging therapies based on the advancements made in T and B-cell targeting would definitely complement or if not replace the existing therapies. It is worth mentioning to find many new novel entities that are in clinical trials for MS and other neurological autoimmune diseases. Inspite of these attractive therapeutic strategies strenuous efforts are to be made to identify the best possible candidates for effective disease control benefiting the patient population.
