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List, Here are two sites that suggest the possibility of infectious
diseases in Parkinson's. I know that much research took place in this
area in prior years, but that this was before the advanced techniques of=20
PCR testing. And I hope the first article does not deter anyone from
taking deprenyl, the third article provides a little more support as
to it's benefits.

                                      Linda Forrest's Mom =20
Title=20
     Neuroprotective therapy for Parkinson's disease.=20
Author=20
     Koller WC=20
Address=20
     Department of Neurology, University of Kansas Medical Center,
Kansas City 66160-7314, USA.=20
Source=20
     Exp Neurol, 144(1):24-8 1997 Mar=20
Abstract=20
     The concept of neuroprotection relates to the fact that
intervention may be able to interfere with the pathogenesis of
     neuronal cell death. Neuroprotective therapy may make it possible
to delay disease progression or prevent the disease
     altogether. The pathophysiological mechanism of cell death in
Parkinson's disease is unknown; however, hypotheses
     have been developed. The discovery that the toxin MPTP can cause
Parkinson's disease both in humans and in animals
     strengthened the hypothesis that either exogenous or endogenous
toxins may be involved in the mechanism of cell death
     in Parkinson's disease. The mechanism of MPTP toxicity has been
elucidated, lending several possible mechanisms for
     therapeutic intervention in Parkinson's disease. Current data
suggest that oxidative stress may play a prominent role in
     the pathogenesis of Parkinson's disease. It is possible that the
generation of free radicals leads to neuronal cell death.
     There is also evidence that mitochondrial damage may play a role in
the pathogenesis of Parkinson's disease. Other
     theories of possible pathogenesis include excitotoxicity,
disturbances of calcium homeostasis, immunological mechanisms,
     and infectious etiologies. The first agent to be tested as a
candidate for neuroprotection was the MAO-B inhibitor
     deprenyl. Evidence is reviewed for and against the theory that this
drug is neuroprotective.=20
Language=20
     Eng=20
Unique Identifier=20
     97271196=20



MESH Headings=20
     Animal; Antiparkinson Agents (TU); Human; Infection (CO);
Mitochondria (PH); Neuroprotective Agents (*TU);
     Oxidative Stress; Parkinson Disease (*DT/ET); Parkinson Disease,
Symptomatic (CI); Selegiline (TU);
     1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (PO)=20



Publication Type=20
     JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL=20
ISSN=20
     0014-4886=20
Country of Publication=20
     UNITED STATES=20


                                      http://www.medscape.com
                                Medscape is produced by Medscape, Inc.
              All material on this server Copyright =A9 1994, 1995, 1996,
1997 by the publishers involved.


Title=20
     Pharmacological options for the management of dyskinesias.=20
Author=20
     Shale H; Tanner C=20
Address=20
     Parkinson's Institute, Sunnyvale, California, USA.
[log in to unmask]
Source=20
     Drugs, 52(6):849-60 1996 Dec=20
Abstract=20
     Dyskinesias are abnormal involuntary movements characterised by an
excessive amount of movement. Typically, these
     movements are choreiform in nature. They may be caused by systemic,
metabolic, endocrinologic, structural, vascular,
     infectious or inherited degenerative conditions, or be toxin- or
drug-induced. With many non-drug-induced dyskinesias,
     treatment of the underlying condition may be sufficient to
eliminate the movements, although temporary treatment may be
     required to control the movements if they are severe. Drug-induced
dyskinesias often resolve when the offending drug is
     discontinued. A notable exception is tardive dyskinesia, which is
caused by exposure to dopamine receptor blocking
     drugs, the majority of which are antipsychotic agents. Tardive
dyskinesias will persist, or may even develop after the
     causative agent has been stopped and may not spontaneously remit.
Another commonly encountered form of
     drug-induced dyskinesia is seen in patients with Parkinson's
disease who are receiving levodopa. Medications which
     deplete dopamine are most successful in treating choreiform
dyskinesias, although anticholinergics, GABAergics,
     serotonergics, and calcium channel blocking agents have been
reportedly beneficial in some cases. Treatment of
     levodopa-induced dyskinesias requires manipulation of the patient's
antiparkinsonian drug regimen.=20
Language=20
     Eng=20
Unique Identifier=20
     97116067=20



MESH Headings=20
     Adrenergic Uptake Inhibitors*; Anti-Dyskinesia Agents*; Chorea*;
Dyskinesia, Drug-Induced*; Human; Huntington's
     Disease*; Risk Factors*=20



Publication Type=20
     JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL=20
ISSN=20
     0012-6667=20
Country of Publication=20
     NEW ZEALAND=20


                                      http://www.medscape.com
                                Medscape is produced by Medscape, Inc.
              All material on this server Copyright =A9 1994, 1995, 1996,
1997 by the publishers involved.



Title=20
     Deprenyl in the treatment of Parkinson's disease: clinical effects
and speculations on mechanism of action.=20
Author=20
     Olanow CW=20
Address=20
     Mount Sinai School of Medicine, New York, NY, USA.=20
Source=20
     J Neural Transm Suppl, 48():75-84 1996=20
Abstract=20
     Selegiline is a relatively selective inhibitor of monoamine oxidase
type B that has been used in Parkinson's disease as an
     adjunct to levodopa and as putative neuroprotective therapy.
Clinical trials demonstrate that selegiline slows the rate of
     disease progression and delays the appearance of disability
necessitating levodopa. However, confounding symptomatic
     effects have made it difficult to ascertain the presence of any
direct neuroprotective effect. Laboratory studies
     demonstrate that selegiline protects dopaminergic neurons through a
mechanism that does not involve MAO-B inhibition.
     Recent studies suggest that neuroprotection in laboratory models
may be related to the capacity of selegiline to
     up-regulate a series of anti-oxidant and anti-apoptotic molecules
which promote cell survival. Further delineation of the
     precise mechanism whereby selegiline induces this effect may permit
for the development of enhanced neuroprotective
     benefits in PD patients.=20
Language=20
     Eng=20
Unique Identifier=20
     97142237=20



MESH Headings=20
     Antioxidants (ME); Apoptosis (DE); Clinical Trials; Dopamine (ME);
Double-Blind Method; Drug Therapy,
     Combination; Human; Levodopa (AD/TU); Monoamine Oxidase Inhibitors
(PD/TU); Multicenter Studies;
     Neuroprotective Agents (AD/PD/*TU); Nootropic Agents (AD/PD/*TU);
Oxidative Stress; Parkinson Disease
     (*DT); Parkinson Disease, Symptomatic (DT/ET); Prospective Studies;
Randomized Controlled Trials; Selegiline
     (AD/PD/*TU); 1-Methyl-4-phenylpyridinium (TO)=20



Publication Type=20
     JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL=20
ISSN=20
     0303-6995=20
Country of Publication=20
     AUSTRIA=20


                                      http://www.medscape.com
                                Medscape is produced by Medscape, Inc.
              All material on this server Copyright =A9 1994, 1995, 1996,
1997 by the publishers involved.