| Neurodegenerative disorders such as Alzheimer's disease (AD) and Amyotrophic Lateral Sclerosis (ALS) have now greatly attracted many interests in neuroscience research. The most striking pathological changes of these diseases are characterized by progressive neuronal loss and degeneration in specific brain regions. ALS is a devastating syndrome which produces selective upper and lower motoneuron death, leading to paralysis, while AD frequently results in marked degeneration of cholinergic neurons in basal forebrain. The specific mechanism for this selective vulnerability still remains undefined though many efforts have been made. Recently, the findings of antibody in serum and cerebral spinal fluid of patients with AD and ALS could recognize and destroy specific neurons, and the presence of immunoglobulins in brain and spinal cord of AD and ALS have suggested a link between antibody and the pathogenesis of these disease. These observation have raised the question of whether antibody might directly initiate the process of neuronal death and through which mechanism the antibody trigger the action.Cytokines such as certain interleukins (ILs), Tumor necrosis factor (TNF) and Interferon (IFN) have been implicated in the pathophysiology of several immune-mediated CNS disorders. Of these cytokines, IL-1 and IL-6 appear to play a particularly important role in the pathogenesis of various neurological disorders. For years, great efforts have been mainly focused on studying the alteration of classical transmitters and their synthesis in the CNS suffered these diseases. The work on the involvement of cytokines in neurodegeneration has been just in its early stage. Upto date, little is known regarding the involvement of cytokine (IL-1, 6) and low-affinity NGF receptor (LNGFR) in specific antibody mediated neurodegeneration. Therefore we investigated the mechanism of antibody mediated neuronal injury and its relationship to expression of IL-1, 6...
|
PDF Full Text Request