Parkinson s disease pathophysiology

Kish, S.J. Shannak, K. and Homykiewicz, O. Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson s disease. Pathophysiologic and clinical implications. N Engl J Med 318 876-880, 1988. 

Colosimo C, De Michele M. Motor fluctuations in Parkinson s disease pathophysiology and treatment. Eur J Neurol 1999 6(1) 1-21. 

Emerging evidence suggests that dysfunction of the ubiquitin-proteasome system may be part of the pathophysiology of sporadic Parkinson s disease, especially... 

Moore DJ, West AB, Dawson VL et al (2005) Molecular pathophysiology of Parkinson s disease. Annu Rev Neurosci 28 57-87... 

Furthermore, the presence of CB1 in the structures and pathways associated with the pathophysiology of Tourette s syndrome, and especially the functional link between CB1 and Di, D2, also argues that the endocannabinoid system may have some involvement in this disorder as well (Consroe, 1998). In addition, it has been suggested that activation of CB1 receptors, also owing to their link with the dopaminergic system, may reduce dyskinesia produced by L-DOPA in patients with Parkinson s disease (Brotsie, 1998). 

Parkinson s disease 253-4, 298 pathophysiology of iron in humans 228 absorption disorders 211-20 acquired and genetic disorders 207 deficiency... 

Moore, R. Y. Organization of midbrain dopamine systems and the pathophysiology of Parkinson s disease. Parkinsonism Relat. Disord. 9(Suppl 2) S65-S71,2003. 

Lashuel, H. A., Petre, B. M., Wall, J., Simon, M., Nowak, R. J., Walz, T., and Lansbury, P. T., Jr. (2002). Alpha-synuclein, especially the Parkinson s disease-associated mutants, forms pore-like annular and tubular protofibrils./. Mol. Biol. 322,1089-1102. LeVine, H. (1993). Thioflavine T interaction with synthetic Alzheimer s disease beta-amyloid peptides Detection of amyloid aggregation in solution. Protein Sci. 2, 404—410. Lin, H., Bhatia, R., and Lai, R. (2001). Amyloid beta protein forms ion channels Implications for Alzheimer s disease pathophysiology. FASEB J. 15, 2433-2444. Lorenzo, A., and Yankner, B. A. (1994). Beta-amyloid neurotoxicity requires fibril formation and is inhibited by Congo red. Proc. Natl. Acad. Sci. USA 91, 12243-12247. Luhrs, T., Ritter, C., Adrian, M., Riek-Loher, D., Bohrmann, B., Dobeli, H., Schubert, D., and Riek, R. (2005). 3D structure of Alzheimer s amyl o id-( be la) (1—12) fibrils. Proc. Natl. Acad. Sci. USA 102, 17342-17347. 

As dopamine deficiency of the nigrostriatal tract, resulting in an overactivity of cholinergic interneurons, is considered to be the fundamental pathophysiological mechanism for Parkinson s disease two approaches for pharmacological intervention seem rational. 

Obeso, J.A., Rodriguez-Oroz, M.C., Rodriquez, M., Lanciego, J.L., Artieda, J., Gonzalo, N. (2000) Pathophysiology of the basal ganglia in Parkinson s disease. Trends Neurosci 23, S8-S19. 

Wichmann T, DeLong MR. Pathophysiology of Parkinson s disease the MPTP primate model of the human disorder. Ann N YAcad Sci. 2003 991 199-213. 

Because of the instability of peroxynitrite under physiological conditions, the detection of 3-nitrotyrosine (NC>2-Tyr) has become a biochemical marker for the presence of peroxynitrite in pathophysiological processes. The biological significance of tyrosine nitration is a subject of great interest, because extensive evidence supports the formation of nitrotyrosine in vivo in diverse pathological conditions such as heart diseases, chronic inflammation and autoimmune diseases, cancer, Parkinson s disease, Alzheimer s disease, multiple sclerosis, amyotrophic lateral sclerosis, and ischemia-reperfusion injury [11]. 

Briefly outline the epidemiology, pathophysiology and clinical features of Parkinson s disease. 

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