Parkinson’s Disease: Effect of Deep Brain Stimuation on Driving

Priv. Doz. Dr. Carsten Buhmann Department of Neurology University Medical Center Hamburg-Eppendorf, Hamburg, Interview with:
Priv. Doz. Dr. Carsten Buhmann
Department of Neurology
University Medical Center Hamburg-Eppendorf
Hamburg, Germany. What are the main findings of the study?

Answer: Deep brain stimulation (DBS) of the subthalamic nucleus (STN) has no negative but rather a beneficial effect on driving in patients with Parkinsons´s disease (PD). Driving not only was superior in even more clinically affected PD patients with DBS compared with PD patients without DBS but also patients with DBS drove better with stimulation than with levodopa.

This might reflect favorable driving-relevant nonmotor effects due to STN-DBS.
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Parkinson’s Disease: ApoA1 may be a Protection Marker

Alice Chen-Plotkin, MD Assistant Professor Department of Neurology University of Pennsylvania School of Medicine Interview with Alice Chen-Plotkin, MD
Assistant Professor
Department of Neurology
University of Pennsylvania School of Medicine What are the main findings of the study?

Answer: Parkinson’s disease (PD) is an incurable neurodegenerative disease.  Many neurons die, but the neurons that make dopamine (dopaminergic neurons) are particularly vulnerable.  We think that the disease actually starts well before the time when people show clinical symptoms.  We were therefore interested in finding proteins from the blood that correlated with better or worse dopaminergic neuron integrity.  Since it’s hard to access the dopaminergic neurons directly, we looked at a tracer that labels the ends of the dopaminergic neurons in people who do not have Parkinson’s disease but are at high risk for developing it, and we also looked at the age at onset of PD in people who are already symptomatic.  Screening just under 100 different proteins from the blood, we found that higher plasma levels of apolipoprotein A1 (ApoA1) were correlated with better tracer uptake in the people who did not yet have PD, and with older ages at onset in the people who already had PD.  These data suggest that plasma ApoA1 may be a marker for PD risk, with higher levels being relatively protective.

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Parkinson’s disease and exposure to Pesticides eInterview with Dr. Emanuele Cereda

Nutrition and Dietetics Service, Fondazione IRCCS Policlinico San Matteo
Viale Golgi 19, 27100 Pavia, Italy What are the main findings of the study?

Dr. Cereda: A large analysis of more than 100 studies shows that exposure to pesticides, or bug and weed killers, and solvents is likely associated with a higher risk of developing Parkinson’s disease. Were any of the findings unexpected?

Dr. Cereda: In first instance I can say no as in every day clinical practice we frequently see patients reporting such exposure. Accordingly, it appears quite obvious to look at these exposures as risk factors. Unfortunately, from an epidemiologic point of view this is not enough! That’s why we did this study. Amazing rather than surprising was the fact that commonly the sources of funding in the studies we retrieved and included in meta-analysis were health or health-related institutions, private foundations (mainly Parkinosn’s disease foundations), or government or para-government companies. No study acknowledged the involvement of any chemicals manufacturer!
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Degenerative Disease Research: Structural basis of kynurenine 3-monooxygenase inhibition eInterview: Professor Nigel S. Scrutton ScD FRSC FSB

Director Manchester Institute of Biotechnology
EPSRC Established Career Fellow |Faculty of Life Sciences | Manchester Institute of Biotechnology | University of Manchester | Manchester | M1 7DN | UK | What are the main findings of your study?

Dr. Scrutton: A major breakthrough has been made by our team of researchers seeking treatments for degenerative illnesses such as Parkinson’s Disease.

We have detailed how an enzyme in the brain interacts with a drug-like lead compound directed against Huntington’s Disease (but also with major implications for Alzheimer’s and Parkinson’s diseases) to inhibit its activity. The work – which solved the molecular structure of a crucial brain enzyme called kynurenine 3-monooxygenase – opens the door to effective treatment for neurodegenerative diseases such as Huntington’s, Alzheimer’s and Parkinson’s. The main findings not only describe the molecular details of the enzyme, but also how it interacts with a lead drug compound that inhibits the natural activity of the enzyme.
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