Nicotine can protect the brain from Parkinson's disease, research suggests

ScienceDaily (Aug. 1, 2011) — If you've ever wondered if nicotine offered society any benefit, a new study published in The FASEB Journal offers a surprising answer. Nicotine can protect the brain against Parkinson's disease, the research suggests, and the discovery of how nicotine does this may lead to entirely new types of treatments for the disease.

"This study raises the hope for a possible neuroprotective treatment of patients at an early step of the disease or even before at a stage where the disease has not been diagnosed according to motor criteria," said Patrick P. Michel, co-author of the study from the Institut du Cerveau et de la Moelle Épinière, Hôpital de la Salpêtrière, in Paris, France.

To make this discovery, scientists used mice genetically engineered without a specific nicotine receptor (the alpha-7 subtype) and mice with a functional receptor. Using tissue from mouse embryos, researchers prepared brain cultures using conditions that favor the slowly progressing loss of dopamine neurons, a hallmark of the disease. The scientists found that nicotine had the potential to rescue dopamine neurons in cultures from normal mice, but not in cultures from mice without the nicotine receptor. These findings suggest that it may be feasible to develop novel therapies for Parkinson's disease that target nicotine receptors, particularly the alpha-7 nicotine receptor.

"If you're a smoker, don't get too excited," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Even if smoking protects you from Parkinson's, you might not live long enough to develop the disease because smoking greatly increases the risk for deadly cancers and cardiovascular diseases. But now, we should be able find non-toxic ways to hit the same target."

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Federation of American Societies for Experimental Biology, via EurekAlert!, a service of AAAS.

Journal Reference:

D. Toulorge, S. Guerreiro, A. Hild, U. Maskos, E. C. Hirsch, P. P. Michel. Neuroprotection of midbrain dopamine neurons by nicotine is gated by cytoplasmic Ca2. The FASEB Journal, 2011; 25 (8): 2563 DOI: 10.1096/fj.11-182824

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REM sleep behavior disorder is a risk factor for Parkinson's disease

ScienceDaily (July 29, 2011) — Patients suffering REM sleep behaviour disorders dream nightmares in which they are attacked and pursued, with the particularity that they express them by screaming, crying, punching and kicking while sleeping. Lancet Neurology has published the third consecutive work in five years about the relationship between this disorder and Parkinson's disease.

The first work showed in 2006 that 45% of patients who suffer this sleep disorder develop Parkinson's disease and other neurodegenerative diseases caused by a lack of dopamine in the brain. The second article discovered that neuroimaging tests that measure dopamine in the brain, such as the brain SPECT, are useful to identify patients with REM sleep disorders with increased risk of developing a neurodegenerative diseases such as Parkinson's disease.

The new study applied brain SPECT to conclude that the levels of dopamine in the brain are quickly lowering over the years in patients with REM sleep behaviour disorder. This neuroimaging technique becomes the first tool to detect the disease progression at an early stage. The first author of the three articles is Dr. Àlex Iranzo, doctor from the Neurology Service at the Hospital Clínic of Barcelona, researcher at the Biomedical Research Institute of August Pi i Sunyer (IDIBAPS) and member of the Multidisciplinary Sleep Disorders Unit , and the senior authors were to Dr. Joan Santamaria and Dr. Eduard Tolosa, from the same institution.

The study involved comparing for three years the evolution of brain SPECT in 20 patients with REM disorder and 20 healthy controls. The neuroimaging technique measures the presence of dopamine in the substantia nigra, a part of the brain associated with learning and harmony of body movements. In Parkinson's disease a deficiency of dopamine in the substantia nigra causes tremor, stiffness and movement slowness in patients. Results show that after 3 years of monitoring the production of dopamine in the control group was reduced by 8% due to age, while the group of REM sleep disorder patients experienced a reduction of 20%. Once the 3 year follow-up ended, 3 of 20 patients in the REM sleep disorder group had developed Parkinson's disease and their dopamine reduction was around 30%.

The three works led by the IDIBAPS -- Hospital Clínic of Barcelona team conclude that more efforts are needed to create neuroprotective drugs that prevent the progression from REM sleep behavior disorders to Parkinson's disease. For the first time scientists have a technique, brain SPECT, to evaluate whether these drugs are effective. Authors of the study suggest that, to be considered effective, a neuroprotective drug should significantly prevent the dopamine concentration from dropping in these patients.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by IDIBAPS - Institut d'Investigacions Biomèdiques August Pi i Sunyer.

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Increased risk of Parkinson's disease in methamphetamine users, study finds

ScienceDaily (July 26, 2011) — People who abused methamphetamine or other amphetamine-like stimulants were more likely to develop Parkinson's disease than those who did not, in a new study from the Centre for Addiction and Mental Health (CAMH).

The researchers examined almost 300,000 hospital records from California covering 16 years. Patients admitted to hospital for methamphetamine or amphetamine-use disorders had a 76 per cent higher risk of developing Parkinson's disease compared to those with no disorder.

Globally, methamphetamine and similar stimulants are the second most commonly used class of illicit drugs.

"This study provides evidence of this association for the first time, even though it has been suspected for 30 years," said lead researcher Dr. Russell Callaghan, a scientist with CAMH. Parkinson's disease is caused by a deficiency in the brain's ability to produce a chemical called dopamine. Because animal studies have shown that methamphetamine damages dopamine-producing areas in the brain, scientists have worried that the same might happen in humans.

It has been a challenge to establish this link, because Parkinson's disease develops in middle and old age, and it is necessary to track a large number of people with methamphetamine addiction over a long time span.

The CAMH team took an innovative approach by examining hospital records from California -- a state in which methamphetamine use is prevalent -- from 1990 up to 2005. In total, 40,472 people, at least 30 years of age, had been hospitalized due to a methamphetamine- or amphetamine-use disorder during this period.

These patients were compared to two groups: 207,831 people admitted for appendicitis with no diagnosis of any type of addiction, and 35,335 diagnosed with cocaine use disorders. A diagnosis of Parkinson's disease was identified from hospital records or death certificates. Only the methamphetamine group had an increased risk of developing Parkinson's disease.

While the appendicitis group served as a comparison to the general population, the cocaine group was selected for two reasons. Because cocaine is another type of stimulant that affects dopamine, this group could be used to determine whether the risk was specific to methamphetamine stimulants. Cocaine users also served as a control group to account for the health effects or lifestyle factors associated with dependence on an illicit drug.

"It is important for the public to know that our findings do not apply to patients who take amphetamines for medical purposes, such as attention deficit hyperactivity disorder (ADHD), since these patients use much lower doses of amphetamines than those taken by patients in our study," said Dr. Stephen Kish, a CAMH scientist and co-author.

To put the study findings into numbers, if 10,000 people with methamphetamine dependence were followed over 10 years, 21 would develop Parkinson's, compared with 12 people out of 10,000 from the general population. "It is also possible that our findings may underestimate the risk because in California, methamphetamine users may have had less access to health-care insurance and consequently to medical care," said Dr. Callaghan.

The current project is significant because it is one of the few studies examining the long-term association between methamphetamine use and the development of a major brain disorder. "Given that methamphetamine and other amphetamine stimulants are the second most widely used illicit drugs in the world, the current study will help us anticipate the full long-term medical consequences of such problematic drug use," said Dr. Callaghan.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Centre for Addiction and Mental Health, via EurekAlert!, a service of AAAS.

Journal Reference:

Russell C. Callaghan, James K. Cunningham, Jenna Sykes, Stephen J. Kish. Increased risk of Parkinson's disease in individuals hospitalized with conditions related to the use of methamphetamine or other amphetamine-type drugs. Drug and Alcohol Dependence, 2011; DOI: 10.1016/j.drugalcdep.2011.06.013

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Parkinson's Patients Get No Benefit From Antidepressants Sertraline Or Mirtazapine, But Have More Side Effects

Editor's Choice
Academic Journal
Main Category: Parkinson's Disease
Also Included In: Depression;  Psychology / Psychiatry
Article Date: 19 Jul 2011 - 15:00 PDT window.fbAsyncInit = function() { FB.init({ appId: 'aa16a4bf93f23f07eb33109d5f1134d3', status: true, cookie: true, xfbml: true, channelUrl: 'http://www.medicalnewstoday.com/scripts/facebooklike.html'}); }; (function() { var e = document.createElement('script'); e.async = true; e.src = document.location.protocol + '//connect.facebook.net/en_US/all.js'; document.getElementById('fb-root').appendChild(e); }()); email to a friend   printer friendly   opinions  

Two antidepressants prescribed often for individuals with Parkinson's disease - sertraline or mirtazapine - were found to have no benefits for such patients. In fact, they also experienced unpleasant side effects., according to the results of the HTA-SADD trial published in The Lancet. The article was written by Professor Sube Banerjee and team, Institute of Psychiatry, King's College London, UK.

The trial involved 325 patients from nine different centers in England. They all had either possible Alzheimer's disease, depression which had lasted at least 4 weeks, or a dementia-related depression above a certain score. Any patient who was a suicide risk, contraindicated for the drugs, was already on antidepressants, or was at the time already taking part in another trial, was ineligible for this study.

They were randomly selected into one of three groups: Sertraline group - 150mg per day - 107 patientsMirtazapine group - 45 mg per day - 107 patientsControl group - placebo - 111 patientsThe researchers were focusing (primary outcome) on how much depression might be reduced after 13 weeks of treatment. They all also received standard care.

At 13 weeks there were no differences in the depression scores among the three groups, not even at 39 weeks.

26% of those on the placebo group experienced adverse reactions, compared to 43% in the sertraline group and 41% in the mirtazapine group. By week 39 five participants had died in each group.

The researchers concluded:

"The two classes of antidepressants most likely to be prescribed for depression in Alzheimer's disease are no more effective than placebo. In our study, there were more adverse reactions in individuals treated with antidepressants than there were with placebo. Clinicians and investigators need to reframe the way they think about the treatment of people with Alzheimer's disease who are depressed, and reconsider routine prescription of antidepressants."

Dr Henry Brodaty, Brain and Ageing Research Program and Primary Dementia Collaborative Research Centre, University of New South Wales, Sydney, Australia, concluded in a Comment in the same journal:

"The HTA-SADD trial has underscored the need for clinicians to think about creative alternatives to drug treatment for management of depression in people with dementia, and to use evidence-based techniques and partnerships with family carers."

"Sertraline or mirtazapine for depression in dementia (HTA-SADD): a randomised, multicentre, double-blind, placebo-controlled trial"
Prof Sube Banerjee MD, Jennifer Hellier MSc, Michael Dewey PhD, Renee Romeo PhD, Clive Ballard MD, Robert Baldwin MD, Peter Bentham MRCPsych, Chris Fox MD, Clive Holmes PhD, Cornelius Katona MD, Martin Knapp PhD, Claire Lawton FRCPsych, James Lindesay DM, Gill Livingston MD, Niall McCrae PhD, Esme Moniz-Cook PhD, Joanna Murray MA, Shirley Nurock MSc, Martin Orrell PhD, John O'Brien DM, Michaela Poppe PhD, Alan Thomas PhD, Rebecca Walwyn PhD, Kenneth Wilson MD, Alistair Burns MD

The Lancet, Early Online Publication, 18 July 2011 doi:10.1016/S0140-6736(11)60830-1

Written by Christian Nordqvist
Copyright: Medical News Today
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