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Małgorzata Kohutnicka, Andrzej Członkowski, Anna Członkowska
Med Sci Monit 1998; 4(6): RA1096-1103
This article is a review of current knowledge concerning the involvement of inflammatory response elements in the development of Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and ischemia. There exists increasing evidence that inflammation may not be only a consequence of the already existing AD pathology but also may by involved in neuronal destruction. Many proteins associated with inflammation have been found within AD lesions. The complement system is one of the most important inflammatory factors that is supposed to play a role in the pathogenesis of AD. Activated glial cells are the most characteristic cellular components associated with pathological features (classical plaques, not diffuse plaques) in AD. It is suggested that microglial cells and astrocytes are sources of various cytokines that may influence the functioning of neurons as well as may contribute to the formation of amyloid plaques, thus play an important role in the pathogenesis of the disease. The suggestion that the inflammatory process is involved in the pathogenesis of AD has also been confirmed by clinical and epidemiological studies. Mechanisms which provoke the cells death in PD remain unknown. It is still a matter of controversy whether immune mechanisms are involved in the pathogenesis of neurodegeneration as the primary event generating a secondary cascade of changes leading to cell death, or their activation is a secondary reaction to the presence of the neurodegenerative process. Markers suggesting the presence of an inflammatory reaction were also observed within the nigrostriatal system of mice with experimental PD. It is possible that factors modifying the course of this experimental model neurodegenerative process may be useful therapeutic agents in the treatment of idiopathic PD. There is increasing evidence suggesting that the inflammatory response plays an important role during CNS ischemic injury. Understanding how leucocytes traffic to the brain injured ischemic tissue has led to the development of potential new treatment interventions of this pathological state.