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Autoimmune Research Studies

Autoimmune Research Studies

The following is a list of Autoimmune Disease research studies:

1.  www.AARDA.org

2.  López-Armada, M. J., Riveiro-Naveira, R. R., Vaamonde-García, C., & Valcárcel-Ares, M. N. (2013). Mitochondrial dysfunction and the inflammatory response. Mitochondrion, 13(2), 106-118. Abstract conclusion: Inflammation has been linked to multiple degenerative and acute diseases as well as the aging process. Moreover, mitochondrial alterations play a central role in these processes. Mitochondria have an important role in pro-inflammatory signaling; similarly, pro-inflammatory mediators may also alter mitochondrial function. Both of these processes increase mitochondrial oxidative stress, promoting a vicious inflammatory cycle. Additionally, damage-associated molecular patterns derived from mitochondria could contribute to inflammasome formation and caspase-1 activation, while alterations in mitochondrial autophagy may cause inflammation. Strategies aimed at controlling excessive oxidative stress within mitochondria may represent both preventive and therapeutic interventions in inflammation.

3.  Gironi M, Borgiani B, Mariani E, Cursano C, Mendozzi L, Cavarretta R, et al. Oxidative stress is differentially present in multiple sclerosis courses, early evident, and unrelated to treatment. J Immunol Res. 2014;2014:961863. Abstract conclusion: We found lower antioxidant agents and higher anti-oxLDL antibodies in MS, and the highest antibody titers occurred in the benign form. We suggest that natural anti-oxLDL antibodies can be protective against MS, saving blood brain barrier integrity. Our findings also suggest that milder MS is associated with a distinct oxidative stress pattern, which may provide a useful biomarker of disease prognosis.

4.  Miller E, Walczak A, Saluk J, Ponczek MB, Majsterek I. Oxidative modification of patient’s plasma proteins and its role in pathogenesis of multiple sclerosis. Clin Biochem. 2012;45:26–30. Abstract conclusion: Oxidative stress plays an important role in multiple sclerosis (MS). The present study was designed to evaluate the modifications of plasma proteins by estimation markers of oxidative/nitrosative stress: carbonyl groups and 3-nitrotyrosines (3-NT) levels in relapsing-remitting (RR) (n=10) and secondary progressive (SP) (n=10) clinical course of multiple sclerosis. Moreover, we estimated the level of uric acid (UA) in plasma of MS patients. Compared to controls (n=10), the levels of carbonyl groups in plasma proteins were elevated (P<0.0001) as well in RRMS as in SPMS. The highest concentration of 3-NT was observed in plasma proteins obtained from SPMS patients (P<0.0005). The level of uric acid in plasma was significantly lower in RRMS (P<0.0001) than SPMS. This is the first report which presented differences between SPMS and RRMS patients in 3-NT and protein carbonyl groups in plasma proteins.

5.  Gonsette RE. Neurodegeneration in multiple sclerosis: the role of oxidative stress and excitotoxicity. J Neurol Sci. 2008;274:48–53. Abstract conclusion: In multiple sclerosis (MS) disability results from neuronal and axonal loss, the hallmark of neurodegenerative diseases (ND). Neurodegeneration is initiated by microglia activation and mediated by oxidative stress and excitotoxicity. The same sequence of events has been consistently observed in MS. However, microglia activation correlates with a marked cell infiltration in MS but not in ND. In both pathological states, peroxynitrite is the common initiating factor of oxidative stress and excitotoxicity and is thus a potential interesting therapeutic target. Oxidative stress leads to multiple lipid and protein damages via peroxidation and nitration processes. The pathomechanisms of excitotoxicity are complex involving glutamate overload, ionic channel dysfunction, calcium overload, mitochondriopathy, proteolytic enzyme production and activation of apoptotic pathways. The inflammatory component in MS is important for the design of therapeutic strategies. Inflammation not only causes axonal and neuronal loss but it also initiates the degenerative cascade in the early stage of MS. Potent anti-inflammatory agents are now available and it is not unreasonable to think that an early blockade of inflammatory processes might also block associated degenerative mechanisms and delay disability progression. The development of neuroprotective drugs is more problematic. Indeed, given the multiple and parallel mechanisms involved in neurodegeneration, modulation of a single specific pathway will likely yield a partial benefit if any.

6.  Fischer MT, Sharma R, Lim JL, Haider L, Frischer JM, Drexhage J, et al. NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury. Brain. 2012;135:886–99. Abstract conclusion: Mitochondrial injury can be triggered by reactive oxygen and nitric oxide species, and we recently provided evidence for oxidative damage of oligodendrocytes and dystrophic axons in early stages of active multiple sclerosis lesions. In this study, we identified potential sources of reactive oxygen and nitrogen species through gene expression in carefully staged and dissected lesion areas and by immunohistochemical analysis of protein expression. Genome-wide microarrays confirmed mitochondrial injury in active multiple sclerosis lesions, which may serve as an important source of reactive oxygen species. In addition, we found differences in the gene expression levels of various nicotinamide adenine dinucleotide phosphate oxidase subunits between initial multiple sclerosis lesions and control white matter. These results were confirmed at the protein level by means of immunohistochemistry, showing upregulation of the subunits gp91phox, p22phox, p47phox, nicotinamide adenine dinucleotide phosphate oxidase 1 and nicotinamide adenine dinucleotide phosphate oxidase organizer 1 in activated microglia in classical active as well as slowly expanding lesions. The subunits gp91phox and p22phox were constitutively expressed in microglia and were upregulated in the initial lesion. In contrast, p47phox, nicotinamide adenine dinucleotide phosphate oxidase 1 and nicotinamide adenine dinucleotide phosphate oxidase organizer 1 expression were more restricted to the zone of initial damage or to lesions from patients with acute or early relapsing/remitting multiple sclerosis. Double labelling showed co-expression of the nicotinamide adenine dinucleotide phosphate oxidase subunits in activated microglia and infiltrated macrophages, suggesting the assembly of functional complexes. Our data suggest that the inflammation-associated oxidative burst in activated microglia and macrophages plays an important role in demyelination and free radical-mediated tissue injury in the pathogenesis of multiple sclerosis.

7.  Andrews, H. E., Nichols, P. P., Bates, D., & Turnbull, D. M. (2005). Mitochondrial dysfunction plays a key role in progressive axonal loss in multiple sclerosis. Medical hypotheses, 64(4), 669-677. Abstract conclusion: The actual cause of cell death could be due to a number of mechanisms related to mitochondrial dysfunction including failure of ionic homeostasis, calcium influx, mitochondrial mediated cell death or impaired axonal transport. Whatever the cause of axonal loss our hypothesis is that mitochondria are central to this process. We explore steps to test this hypothesis and discuss the possible therapeutic approaches which target the mitochondrial mechanisms that may contribute to chronic axonal loss.

8.  Witte, M. E., Mahad, D. J., Lassmann, H., & van Horssen, J. (2014). Mitochondrial dysfunction contributes to neurodegeneration in multiple sclerosis. Trends in molecular medicine, 20(3), 179-187. Abstract conclusion: This review provides a comprehensive overview on the current knowledge regarding mitochondrial dysfunction in MS. Importantly, more insight into the cause and consequences of impaired mitochondrial function provide a basis for mitochondrial-targeted medicine to combat progressive MS.

9.  Perl, A., Nagy, G., Gergely, P., Puskas, F., Qian, Y., & Banki, K. (2004). Apoptosis and mitochondrial dysfunction in lymphocytes of patients with systemic lupus erythematosus. In Autoimmunity (pp. 87-114). Humana Press. Abstract conclusion: Oxidative stress affects signaling through the T-cell receptor as well as the activity of redox-sensitive caspases. ATP depletion may be responsible for diminished activation-induced apoptosis and sensitize lupus T cells to necrosis. Mitochondrial dysfunction is identified as a key mechanism in the pathogenesis of SLE.

 
 
 

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