ABSTRACT
Alzheimer's disease [AD], a neurodegenerative disorder associated with advanced age, is the most common cause of dementia globally. AD is characterised by cognitive dysfunction, deposition of amyloid plaques, neurofibrillary tangles and neuro-inflammation. Inflammation of the brain is a key pathological hallmark of AD. Thus, clinical and immunopathological evidence of AD could be potentially supported by inflammatory mediators, including cytokines, chemokines, the complement system, acute phase proteins and oxidative mediators. In particular, oxidative mediators may actively contribute to the progression of AD and on-going inflammation in the brain. This review provides an overview of the functions and activities of inflammatory mediators in AD. An improved understanding of in?ammatory processes and their role in AD is needed to improve therapeutic research aims in the field of AD and similar diseases
ABSTRACT
Multiple sclerosis [MS] is an autoimmune disease of the central nervous system [CNS]. The major pathological outcomes of the disease are the loss of blood-brain barrier [BBB] integrity and the development of reactive astrogliosis and MS plaque. For the disease to occur, the non-resident cells must enter into the immune-privileged CNS through a breach in the relatively impermeable BBB. It has been demonstrated that matrix metalloproteinases [MMPs] play an important role in the immunopathogenesis of MS, in part through the disruption of the BBB and the recruitment of inflammatory cells into the CNS. Moreover, MMPs can also enhance the cleavage of myelin basic protein [MBP] and the demyelination process. Regarding the growing data on the roles of MMPs and their tissue inhibitors [TIMPs] in the pathogenesis of MS, this review discusses the role of different types of MMPs, including MMP-2, -3, -7, -9, -12 and -25, in the immunopathogenesis and treatment of MS
ABSTRACT
Multiple sclerosis [MS] is the most common inflammatory disease of the CNS. Experimental autoimmune encephalomyelitis [EAE] is a widely used model for MS. In the present research, our aim was to test the therapeutic efficacy of Calcium [Ca] in an experimental model of MS. In this study the experiment was done on C57BL/6 mice. EAE was induced using 200 micro g of the MOG[35-55] peptide emulsified in CFA and injected subcutaneously on day 0 over two flank areas. In addition, 250 ng of pertussis toxin was injected on days 0 and 2. In the treatment group, 30 mg/kg Ca was administered intraperitoneally four times at regular 48 hour intervals. The mice were sacrificed 21 days after EAE induction and blood samples were taken from their hearts. The brains of mice were removed for histological analysis and their isolated splenocytes were cultured. Our results showed that treatment with Ca caused a significant reduction in the severity of the EAE. Histological analysis indicated that there was no plaque in brain sections of Ca treated group of mice whereas 4 +/- 1 plaques were detected in brain sections of controls. The density of mononuclear infiltration in the CNS of Ca treated mice was lower than in controls. The serum level of Nitric Oxide in the treatment group was lower than in the control group but was not significant. Moreover, the levels of IFN- gamma in cell culture supernatant of splenocytes in treated mice were significantly lower than in the control group. The data indicates that Ca intervention can effectively attenuate EAE progression