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DEGENERATIVE DISEASES OF THE NERVOUS SYSTEM
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mutations It must be emphasized, just as it was in Alzheimer disease, that no genetic error relating to synuclein has been found in patients with sporadic Parkinson disease Parkin is a ubiquitin protein ligase that participates in the removal of unnecessary proteins from cells through the proteosomal system (Fig 39-6) Attachment of parkin and ubiquitin to cytosolic proteins is understood to be an obligatory step in the disposal of proteins by proteosomes Mutations in the parkin gene lead either to an inadequacy or misfolding of synuclein, resulting in its accumulation, or to the disruption of disposal of proteins in dopamineproducing cells The importance of the ubiquitination pathway in this disease is further highlighted by the report that parkinsonian features are present in a family with mutations in ubiquitin carboxyterminal hydrolase L1 (UCHL-1) (Table 39-2) These relationships and the processing of synuclein in the cell are illustrated in Fig 39-6 It must be emphasized that some of the notions illustrated are speculative or, more speci cally, are derived largely from the molecular study of familial Parkinson disease and therefore may not apply to the sporadic disease They do, however, accurately describe the pathways involved in the handling of synculein and are therefore likely to be implicated in idiopathic Parkinson disease Several other gene defects are of interest in familial parkinsonism One is a dominantly inherited mutation in the gene Nurr1, whose normal function is to specify the identity of dopaminergic neurons Another is in recessively inherited parkinsonism due to defects in the gene DJ-1, a protein that is essential for the normal neuronal response to oxidative stress Also, a disease-causing mutation in the gene termed PINK, corresponding to Park6, codes for a mitochondrial kinase, therefore implicating this cellular structure in some forms of Parkinson disease (Valente et al) PresumTable 39-4 Drugs commonly used in the treatment of Parkinson disease
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ably, dopaminergic neurons are compromised in some manner by these defects It is hoped that the genetic mutations that give rise to Parkinson disease will expose the molecular pathophysiology of the disease As discussed earlier, several sites are implicated in the familial forms of Parkinson disease, most related to the gene that codes for synuclein, the main component of the Lewy body This conceptually links familial Parkinson disease with Alzheimer disease and possibly with ALS, all potential sequelae of toxic protein aggregation As in the aforementioned diseases, new ndings suggest that soluble forms of the protein may be the toxic agent, rather than the aggregated protein within cells, or that there is an interaction between the mutated proteins and other proteins such as ubiquitin, another major component of the Lewy body The binding of ubiquitin is a step in the degradation of intracellular proteins, and mutant parkin proteins appear to have lost this ability In any case, the current evidence favors a role for the regulation of synuclein in the viability of dopaminergic neurons in the inherited forms of disease, and probably in the sporadic ones as well (Fig 39-6) Treatment Although there is no current treatment that halts or reverses the neuronal degeneration underlying Parkinson disease, methods are now available that afford considerable relief from symptoms Treatment can be medical or surgical, although reliance is placed mainly on drugs, particularly on L-dopa (Table 39-4) The following sections are necessarily detailed in order to give the clinician a full comprehension of the use and side effects and interactions of these drugs L-Dopa and L-Dopa Modifying Drugs At present, L-dihydroxyphenylalanine (L-dopa) is unquestionably the most effective agent
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Carbidopa-L-dopa (Sinemet) Controlled release carbidopa-L-dopa Dopamine agonists Ropinirole
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Reduction of tremor and bradykinesia; less effect on postural dif culties
Nausea, dyskinesias, orthostatic hypotension, hallucinations, confusion
25/100 tid
Up to 50/200 q 4 h
025 mg tid
9 to 24 mg/day
Moderate effects on all aspects; reduced motor uctuations of L-dopa
Orthostatic hypotension, excessive and abrupt sleepiness, confusion, hallucinations
Pramipexole Glutamate agonist Amantadine (Symmetrel)
0125 mg tid 100 mg/day
075 to 3 mg/day 100 mg bid-tid Smoothing of motor uctuations Leg swelling, congestive heart failure, prostatic outlet obstruction, confusion, hallucinations, insomnia Atropinic effects: dry mouth, urinary outlet obstruction, confusion and psychosis As above
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