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Talk to focus on tobacco

More Americans die each year from lung cancer than breast, prostate and colorectal cancers combined, according to a news release from Integris Health.

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November is Lung Cancer Awareness Month. to spread the word to Oklahoma City’s Hispanic population, Dr. Jose Acosta will deliver a presentation about the harmful effects of tobacco, including second- and third-hand smoke. the presentation is co-sponsored by the Integris Hispanic Initiative and the Latino M-Power program. it will be from 6:30 to 7:30 p.m. Nov. 10 in the cancer center conference room at Integris Southwest Medical Center, 4301 S Western Ave.

For more information or to register, call 951-2277. Press 2 for Spanish.

Experts to discuss Parkinson’s

National and local experts will share information about Parkinson’s disease at “The Victory Summit” this month in Tulsa. the summit is a collaboration between the Davis Phinney Foundation, the American Parkinson Disease Association and the Parkinson Foundation of Oklahoma, among others.

Guests will learn about the latest research into the disease, which affects the body’s motor system. Victims suffer tremors, stiffness, slowness of movement and impaired balance or a lack of coordination. the disease is progressive. there is no cure.

The summit will include interactive sessions on exercise, speech therapy and other activities that may help with symptoms, according to a news release.

Dale and Glenda Alexander, of Oklahoma City, will be honored as “Local Heroes” for their leadership in the Parkinson’s community. Dale Alexander was diagnosed with the disease in 2002. Since then, he and his wife have raised $300,000 for support groups as co-chairmen of the annual “Tee it Up for Parkinson’s” golf tournament.

The summit will be from 9 a.m. to 3:30 p.m. Nov. 12, at the Tulsa Convention Center, 100 Civic Center, Tulsa. the event is free, but advance registration is required. go to davisphinneyfoundation.org for details.

Hospital to host charity sale

The volunteer auxiliary at Integris Canadian Valley Hospital invites everyone to attend a Gift Gallery Holiday Bazaar.

“The two-day event will feature jewelry, home and holiday decorations, OU and OSU items, gift sets, gourmet foods, infant and toddler attire, stocking stuffers and much more,” according to a news release.

All proceeds will benefit the auxiliary’s charitable projects, including the creation of homemade comfort items.

“Many members … stitch or knit baby caps and blankets for newborns at the hospital,” the release notes, “or make quilts and hand crocheted crosses for patients facing illness or injury. the hospital has more than 120 volunteers whose main objective is to ease the stress of being ill or having a loved one hospitalized.”

Sales will last from 7 a.m. to 6 p.m. Nov. 17 and from 7 a.m. to noon Nov. 18. the bazaar will be held in Conference Room A/B at the hospital, 1201 Health Center Pkwy., Yukon.

Look like a fireman

Ever wondered how you’d look with a mustache? Now’s the time to find out. the Oklahoma City Barons hockey team and Integris Men’s Health University encourage you to grow a mustache (or don a fake one if you’re female) to celebrate Movember.

What’s Movember? It’s a men’s health movement that started in Australia in 2003 and has grown into a worldwide effort to raise awareness and funds for cancers that affect men. Since 2009, more than $45 million has been raised.

Locally, anyone wearing a real or fake mustache will get $4 off admission to any Barons home game in November. the deal only applies to tickets purchased at the box office; game dates are Nov. 11, 12, 18 and 19.

The Barons also will offer a donation site at movember.com to raise money for men’s cancer awareness.

A “Best Mustache Contest” will be held at the Nov. 19 game.

For participation details, go to okcbarons.com. to learn more about the prizes and rules, go to integrisok.com/movember-integris.

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BIOTIE THERAPIES CORP. ?????STOCK EXCHANGE RELEASE ??????7 April 2011, at 9.00 a.m.??

?

Biotie announces start of Phase 2b trial of SYN115 in Parkinson’s disease

Turku, Finland, April 7th 2011- Biotie Therapies Corp., a development stage company focused on diseases of the central nervous system, today announced? the start of a Phase 2b trial evaluating SYN115 in Parkinson’s Disease (PD). Results from the study are expected in the first half of 2013.

SYN115 is an orally bioavailable potent and selective adenosine A2a receptor antagonist. Adenosine A2a inhibition has been shown in preclinical studies to reverse motor deficits and enhance the effect of current PD therapies, e.g. levodopa and dopamine agonists, without inducing troublesome dyskinesia (involuntary movements). in addition, SYN115 also displays activity in preclinical models on non-motor symptoms of PD including depression, cognition and anxiety.

The Phase 2b trial is a randomized, double-blind, placebo-controlled study that will evaluate four doses of SYN115 versus placebo as adjunctive therapy in 400 levodopa-treated PD patients with end of dose wearing off.? in these patients, treatment with levodopa is insufficient to control PD symptoms until their next dose, resulting in an ‘off’ period when symptoms reappear. The aim of the Phase 2b study is to determine the efficacy and safety of SYN115 in reducing the mean time spent in the ‘off’ state over a 12 week treatment period. The trial will also assess the impact of SYN115 on various measures of motor symptom severity, dyskinesia and non-motor symptoms.??

?”SYN115 is the lead product coming from our recent acquisition of Synosia and we are very pleased to advance this promising candidate into late-stage clinical development,” said Timo Veromaa, President and Chief Executive Officer of Biotie. “Despite the availability of treatments for Parkinson’s Disease, there remains a significant unmet medical need for therapies with an alternative mechanism of action and SYN115 could be the first drug with a novel mechanism of action in PD for a generation.”

Biotie has granted UCB Pharma S.A. a license for exclusive, worldwide rights to SYN115. UCB will be responsible for Phase 3 development and commercialization.

In Turku, 7 April 2011

Biotie Therapies Corp.

Timo Veromaa President and CEO

For further information, please contact:

Dr. Stephen Bandak, Chief Medical Officertel. +1?650?296 0946 (Pacific Daylight Time)email: :mailto:

Virve Nurmi, Investor Relations Managertel. +358 2 274 8900, e-mail: :mailto:

Distribution: NASDAQ OMX Helsinki LtdMain Media

About SYN115

SYN115 is an orally bioavailable, potent and selective adenosine A2a receptor antagonist, which enters the brain and modulates regions associated with motor and non-motor function. Biotie obtained development and commercialization rights to SYN115 from Roche in 2007 for selected diseases of the central nervous system and has an option to rights for development in all indications.

About Parkinson’s disease

Parkinson’s disease is the second most common neurodegenerative disorder, after Alzheimer’s disease. It affects about one percent of people ages 65-69, rising to up to three percent of people who are 80 years and older. The symptoms of Parkinson’s disease result from decreased dopamine production in regions of the brain controlling movement.?

About Biotie

Biotie is a specialized drug development company focused on the development of drugs for neurodegenerative and psychiatric disorders (Parkinson’s disease, Alzheimer’s disease and other cognitive disorders, bipolar disorder, and alcohol and drug dependence) and inflammatory diseases (rheumatoid arthritis, psoriasis, chronic obstructive pulmonary disease and others). It has several innovative small molecule and biological drug candidates at different stages of clinical development. Biotie’s products address diseases with high unmet medical need and significant market potential.

Partnerships with top/tier pharmaceutical partners are in place for several programs ?as well as a strategic collaboration with UCB Pharma S.A. Biotie’s most advanced product, nalmefene for alcohol dependence, is currently in Phase 3 clinical development by licensing partner H. Lundbeck A/S.

Biotie shares are listed on NASDAQ OMX Helsinki ltd.

This announcement is distributed by Thomson Reuters on behalf of Thomson Reuters clients.The owner of this announcement warrants that:(i) the releases contained herein are protected by copyright and other applicable laws; and(ii) they are solely responsible for the content, accuracy and originality of theinformation contained therein.Source: Biotie Therapies Oyj via Thomson Reuters ONEHUG#1504261

Adults With ADHD Symptoms have Tripled Risk of Dementia later, Study Finds

Jan. 20, 2011 — Adults with symptoms of ADHD, or attention deficit hyperactivity disorder, are more than three times as likely as other adults to develop a form of dementia later in life, according to new research from Argentina.

”We found a higher risk of dementia with Lewy bodies in patients with preceding adult ADHD symptoms,” write the researchers from Hospital Italiano Buenos Aires. The study is published in the European Journal of Neurology.

Lewy body dementia (LBD) affects about 1.3 million people in the U.S., according to the Lewy Body Dementia Association. Lewy bodies is the name given to the abnormal protein deposits that disrupt the brain’s normal functioning.

The symptoms include cognitive impairment, like the more well-known dementia, Alzheimer’s disease. however, in the Lewy body form, patients can also have visual hallucinations, fluctuation in cognition — sometimes appearing fine, other times not — and motor abnormalities similar to those in Parkinson’s disease patients.

But a U.S.-based expert cautions that the study found an association between ADHD symptoms and the dementia, not cause and effect. “It may be that both of these disorders are linked to some other risk factor that is common for both,” says James B. Leverenz, MD, chair of the Lewy Body Dementia Association’s scientific advisory council and professor of neurology and psychiatry and behavioral sciences at the University of Washington, Seattle. He reviewed the study for WebMD.

ADHD and Dementia: The Study

Led by Angel Golimstok at the Hospital Italiano Buenos Aires, researchers evaluated 360 patients with dementia — 109 had LBD and 251 had Alzheimer’s — comparing them with 149 healthy people matched by sex, education, and age.

Then they looked at how often ADHD symptoms had been reported earlier. in patients who were too impaired to answer, they got information from an informant who had known the patient for at least 10 years and had information from a close relative who knew the patient in childhood. The researchers say that since this method has not been validated, they refer to the patients as having ADHD symptoms, rather than being diagnosed with ADHD.

•  47.8% of those with LBD had previous ADHD symptoms.
• 15.2% of those with Alzheimer’s disease had previous ADHD symptoms.
• 15.1% of those in the healthy group did.

Why the link? “It is believed that the same neurotransmitter pathway problems are involved in the development of both conditions, so our research set out to test the theory that adult ADHD often precedes [Lewy body dementia],” Golimstok says in a news release.

The researchers believe their study is the first to look at the link between ADHD symptoms and dementia.

In ADHD, often diagnosed in childhood, people have problems paying attention and can act impulsively. Symptoms can persist into adulthood.

“Our hypothesis is that ADHD could be the clinical result of the first step in these pathway disorders, and after a long time, this problem degenerates to a more severe pathology with structural changes in the brain, as Lewy Body Dementia is,” Golimstok writes in an email interview with WebMD.

“A question to answer in the very near future is, Could available ADHD treatment prevent the conversion to a degenerative disease such as Lewy Body Dementia?” Golimstok writes.

Posted on: Friday, 7 January 2011, 18:40 CST

New findings could lead to new treatments for the 95 percent of Parkinson’s cases with no known cause

Just 5 percent of Parkinson’s disease cases can be explained by genetic mutation, while the rest have no known cause. but a new discovery by researchers at the University of Texas Health Science Center may begin to explain why the vast majority of Parkinson’s patients develop the progressive neurodegenerative disease.

This week in the Journal of Neuroscience, the researchers demystified a process that leads to the death of brain cells – or neurons – in Parkinson’s patients. When researchers blocked the process, the neurons survived.

The findings could lead to an effective treatment to slow the progression of Parkinson’s disease, rather than simply address symptoms that include tremors, slowed movement, muscle stiffness and impaired balance. further studies could lead to a diagnostic test that could screen for Parkinson’s years before symptoms develop, said Syed Z. Imam, Ph.D., adjunct assistant professor at the UT Health Science Center.

Parkinson’s disease, which usually is not diagnosed until age 60 or later, affects an estimated half-million people in the United States.

Dr. Imam joined the U.S. Food and Drug Administration (FDA) after the research was conducted. Co-authors are from the Health Science Center’s Barshop Institute for Longevity and Aging Studies; the South Texas Veterans Health Care system; and the Hertie Institute for Clinical Brain Research in Tübingen, Germany.

The mechanism

After analyzing cells and post-mortem brain tissue from animals and humans, researchers noted that oxidative stress – a known culprit in neuron death – activated a protein called tyrosine kinase c-Abl in the nigra-striatum area of the brain. Neurons in this part of the brain are particularly vulnerable to Parkinson’s injury.

Activation of this protein led to changes in another protein called parkin, which is known to be mutated in hereditary Parkinson’s. the altered parkin lacked the capacity to break down other proteins, leading to harmful clumps of unprocessed protein in the neuron. the scientists believe this accumulation leads to progressive neuron death, resulting in Parkinson’s symptoms that worsen over time.

Implications

“When we blocked tyrosine kinase c-Abl activation, parkin function was preserved and neurons were spared,” Dr. Imam said. “We believe these studies provide sound rationale for moving forward with a preclinical trial of tyrosine kinase c-Abl inhibitors, with the goal of developing a potent therapeutic drug for slowing the progression of Parkinson’s.”

If preclinical trials in animal models of Parkinson’s disease yield positive results, the next step would be clinical trials in human patients, Dr. Imam said.

Tyrosine kinase c-Abl inhibitors are approved by the FDA for treating myeloid leukemia and gastrointestinal tumors. This could speed approval of the drug for Parkinson’s and its translation from bench research to clinical practice.

“The race is on to understand the mechanism of the 95 percent of Parkinson’s cases with no known cause, and our finding certainly is a building block,” Dr. Imam said. “We have found a specific signaling mechanism that is only turned on by oxidative stress and is selective only to Parkinson’s-affected neurons of the nigra-striatum, which is the area that sends signals for balance to the cerebellum.”

Acknowledgements

Co-authors from the UT Health Science Center San Antonio are Senlin Li, M.D., senior author; Qing Zhou, Ph.D.; Anthony J. Valente, Ph.D.; Mona C. Bains, Ph.D.; Robert a. Clark, M.D.; and James L. Roberts, Ph.D., whose primary appointment is now at Trinity University in San Antonio. Co-authors represent the School of Medicine and the Graduate School of Biomedical Sciences as well as the Barshop Institute.

The National Institutes of Health, Michael J. Fox Foundation, American Parkinson’s Disease Association, Parkinson’s Disease Foundation, San Antonio Area Foundation and Health Science Center Presidential Research Enhancement Fund supported the research.

On the Net:

• HSC News
• The Journal of Neuroscience

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Last updated at 2:02 PM on 3rd January 2011

A major study into the progression of Parkinson’s disease, which will include British patients, is being launched by actor Michael J Fox.

The research is the first of its kind and will involve 400 people from five sites in Europe and 14 hospitals in the US.

Patients in the earliest stages of Parkinson’s – before they have started any treatment – will be enrolled in the study to find key biomarkers for the disease.

Michael J. Fox with his wife Tracy Pollan. Fox, who was diagnosed with young-onset Parkinson’s aged 30, said the research was important because ‘better treatments aren’t going to fall from the sky’

Fox, who was diagnosed with young-onset Parkinson’s aged 30, said the research was important because “better treatments aren’t going to fall from the sky” and “real challenges stand in the way of the results we need”.

Currently, there is no definitive way of measuring how Parkinson’s progresses.

Fox and with former boxer Muhammad Ali who was diagnosed with the condition in 1984.

This means it is difficult for doctors to work out whether a drug is slowing down or halting the disease’s advances.

Reliable and robust biomarkers to monitor the progression of Parkinson’s would improve patient care, lead to new drugs and enhance understanding of the condition.

Some 120,000 Britons have Parkinson’s, which is caused by a loss of brain cells that produce a chemical messenger called dopamine.

Symptoms include a tremor or fine shake while the person is at rest, rigidity of muscles, slowness of movement and an unsteady balance.

In the new study, samples taken from patients will help identify what is happening in the body, and will include data on motor skills, samples of blood, urine and spinal fluid, and brain scans.

This data will be then used either alone or in combination to track progression of the disease.

The research starts in early 2011 and is being co-ordinated and part-funded by the Micheal J Fox Foundation for Parkinson’s Research.

The Foundation has spent almost ?30 million so far on studies looking for Parkinson’s biomarkers.

Debi Brooks, co-founder of the Michael J Fox Foundation, said patients will be followed for between three and five years, and compared with healthy volunteers.

“The great thing is we don’t have to wait until the end of the five years to start using the data,” she said, adding it would be made available to researchers through a publicly-accessible website, with patient details anonymised.

A scene from back to the Future 2 where Fox co-starred as Marty McFly with Christopher Lloyd. the success of the film trilogy helped Fox become a household name

So far, several pharmaceutical giants, including Roche, Pfizer, Merck, GE Healthcare and Genentech, have put millions of dollars into the research.

The Foundation wishes to recruit another three to five partners and hopes, in total, to receive 20 million US dollars (?12,896,100) from pharmaceutical companies as well as contributing 20 million itself.

As well as the US sites, there will be research centres at Imperial College London, one in Italy, two in Germany and one in Austria.

Ms Brooks said: “We are really excited to see this field-wide commitment to really going after these markers of disease progression.

“It’s a key tool for our ability to develop and test new treatments for Parkinson’s.

“Without it, there’s a risk that developing and testing treatments will remain too challenging.

“The patients really are the ones who hold the scientific secrets about Parkinson’s disease and it’s a remarkable contribution they are making to this study.”

Patients will not be on any medicines at the start of the study, although they may start taking them during the course of the research.

Ms Brooks said there is often a long time lag between developing potential treatments and getting regulatory approval.

Finding the key biomarkers for Parkinson’s would “compress” these time frames, she added.

David Brooks, professor of neurology at Imperial College, London, will lead the study at the UK site.

He said: “To develop life-transforming treatments for the millions of people living with Parkinson’s disease worldwide, we need consistent and reliable biomarkers – measurable indicators of disease risk, onset and progression.

“This study will leverage our group’s expertise in developing imaging-based biomarkers, and allow us to take our Parkinson’s biomarker programme to the next level through open collaboration with the Michael J Fox Foundation and top-flight investigative teams across Europe and the United States.”

Author: Juliet Cohen

Parkinson’s is found all over the world. Exact global figures are not always available, though it is estimated that four million people worldwide have the condition. Parkinson’s disease belongs to a group of conditions called movement disorders. Parkinson’s disease afflicts 1 to 1 1/2 million people in the United States. the disorder occurs in all races but is somewhat more prevalent among Caucasians. People with the disease may have trouble walking, talking or doing simple tasks. Dysfunctional antioxidative mechanisms are associated with older age as well, suggesting that the acceleration of age-related changes in dopamine production may be a factor. Parkinson’s disease patients have at least one relative with parkinsonian symptoms, suggesting that a genetic factor may be involved. There is no cure for Parkinson’s at present, drugs are used to try to control symptoms of Parkinson’s. the most widely used form of treatment is L-dopa in various forms. L-dopa is transformed into dopamine in the dopaminergic neurons by L-aromatic amino acid decarboxylase (often known by its former name dopa-decarboxylase). the most widely practiced treatment for the speech disorders associated with Parkinson’s disease is Lee Silverman Voice Treatment (LSVT). LSVT focuses on increasing vocal loudness. Regular physical exercise and/or therapy can be beneficial to the patient for maintaining and improving mobility, flexibility, balance and a range of motion. Nutrients have been used in clinical studies and are widely used by people with Parkinson’s disease in order to partially treat PD or slow down its deterioration.

Causes of Parkinsons Disease

Common Causes and Risk factors of Parkinsons Disease

Environmental toxins.

Carbon monoxide poisoning.

Signs and Symptoms of Parkinsons Disease

Common Sign and Symptoms of Parkinsons Disease

Depression and other emotional changes.

Difficulty in swallowing.

Chewing, and speaking.

Trembling of hands, arms, legs, jaw and face.

Treatment of Parkinsons Disease

Common Treatment of Parkinsons Disease

Successful treatment of Parkinson’s disease involves much more than just the use of drugs. Levodopa and carbidopa combined (Sinemet) is the mainstay of Parkinson’s therapy.

Tolcapone inhibits the COMT enzyme, thereby prolonging the effects of L-dopa, and so has been used to complement L-dopa.

The most widely practiced treatment for the speech disorders associated with Parkinson’s disease is Lee Silverman Voice Treatment (LSVT).

Nutrients have been used in clinical studies and are widely used by people with Parkinson’s disease in order to partially treat PD or slow down its deterioration.

Catechol O-methyl transferase (COMT) inhibitors act by inhibiting catabolism of dopamine, thereby extending L-dopa’s peripheral half-life.

Surgical treatment for PD is generally considered for patients who respond to medications.

Azilect was approved for use as an initial single drug therapy in early Parkinson’s disease. Azilect (rasagiline), a new molecular entity, for the treatment of Parkinson’s disease.

Physical therapy can help strengthen and tone underused muscles, and give rigid muscles a better range of motion.

Article Source: articlesbase.com/diseases-and-conditions-articles/parkinsons-disease-causes-symptoms-information-with-treatment-241827.html

About the Author

Juliet Cohen writes articles on diseases and conditions and skin disorders. she also writes articles on herbal home remedies.

Posted on: Friday, 3 December 2010, 07:12 CST

(Ivanhoe Newswire) – Children with autism are much more likely to have deficits in their ability to produce cellular energy than typically developing children.

The researchers found that cumulative damage and oxidative stress in mitochondria, the energy producer of the cell, could influence the onset and severity of autism, suggesting a strong link between autism and mitochondrial defects.

The authors believe that lack of ability to fuel the brain neurons might lead to some of the cognitive deficits associated with autism, since the brain consumes the second most energy in the body. Mitochondria are the primary source of energy production in the cells. They carry their own set of genetic instructions, mtDNA, that carry out aerobic respiration.

Dysfunction in mitochondria already is associated with a number of other neurological conditions, including Parkinson’s disease, Alzheimer’s disease, schizophrenia and bipolar disorder.

"Children with mitochondrial diseases may present exercise intolerance, seizures and cognitive decline, among other conditions. some will manifest disease symptoms and some will appear as sporadic cases," Cecilia Giulivi, the study’s lead author and professor in the Department of Molecular Biosciences in the School of Veterinary Medicine at UC Davis, was quoted as saying. "Many of these characteristics are shared by children with autism."

The researchers stress that these new findings, which may help physicians provide early diagnoses, do not identify the cause or the effects of autism, which affects as many as 1 in every 110 children in the United States, according to the U.S. Centers for Disease Control and Prevention.

"it is remarkable that evidence of mitochondrial dysfunction and changes in mitochondrial DNA were detected in the blood of these young children with autism," Geraldine Dawson, chief science officer of Autism Speaks, which provided funding for the study was quoted as saying. "One of the challenges has been that it has been difficult to diagnose mitochondrial dysfunction because it usually requires a muscle biopsy. if we could screen for these metabolic problems with a blood test, it would be a big step forward."

For the study, Giulivi and her colleagues recruited 10 autistic children aged 2 to 5, and 10 typically developing children of the same ages and backgrounds. the children were randomly selected from Northern California subjects who previously had participated in the 1,600-participant Childhood Autism Risk from Genetics and the Environment (CHARGE) Study and who also consented to return for a subsequent study known as CHARGE-BACK, conducted by the UC Davis Center for Children’s Environmental Health and Disease Prevention.

The researchers got blood samples from each child and analyzed the metabolic pathways of mitochondria in immune cells called lymphocytes, which use aerobic respiration via mitochondria.

The researchers found that mitochondria from children with autism consumed far less oxygen than mitochondria from the group of control children, a sign of lowered mitochondrial activity. "a 66 percent decrease is significant," Giulivi said. "When these levels are lower, you have less capability to produce ATP (adenosine triphosphate) to pay for cellular work. Even if this decrease is considered moderate, deficits in mitochondrial energy output do not have to be dismissed, for they could be exacerbated or evidenced during the prenatal period but appear subclinical in the adult years."

Reduced mitochondrial enzyme function proved widespread among the autistic children. eighty percent had lowered activity in NADH oxidase than did controls, while 60 percent, 40 percent and 30 percent had low activity in succinate oxidase, ATPase and cytochrome c oxidase, respectively. the researchers went on to isolate the origins of these defects by assessing the activity of each of the five enzyme complexes involved in mitochondrial respiration. Complex I was the site of the most common deficiency, found in 60 percent of autistic subjects, and occurred five out of six times in combination with Complex V. Other children had problems in Complexes III and IV.

Levels of pyruvate, the raw material mitochondria transform into cellular energy, were also elevated in the blood plasma of autistic children. this suggests the mitochondria of children with autism are unable to process pyruvate fast enough to keep up with the demand for energy, pointing to a novel deficiency at the level of an enzyme named pyruvate dehydrogenase.

Mitochondria also are the main intracellular source of oxygen free radicals. Free radicals are very reactive and can harm cellular structures, including DNA. Cells are able to repair typical levels of such oxidative damage. Giulivi and her colleagues found that hydrogen peroxide levels in autistic children were twice as high as in normal children. As a result, the cells of children with autism were exposed to higher oxidative stress.

"the various dysfunctions we measured are probably even more extreme in brain cells, which rely exclusively on mitochondria for energy," Isaac Pessah, director of the Center for Children’s Environmental Health and Disease Prevention, a UC Davis MIND Institute researcher and professor of molecular biosciences at the UC Davis School of Veterinary Medicine was quoted as saying.

Giulivi cautions that these findings do not amount to establishing a cause for autism.

"this important exploratory research addresses in a rigorous way an emerging hypothesis about potential mitochondrial dysfunction and autism," Cindy Lawler, program director at the National Institute of Environmental Health Sciences (NIEHS), which provided funding for the study was quoted as saying. "Additional research in this area could ultimately lead to prevention or intervention efforts for this serious developmental disorder."

SOURCE: JAMA, published online December 2, 2010

Source: Ivanhoe Newswire

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Calcium activity in the brain plays an important role in the onset of Parkinson’s disease, according to a study in mice. The finding helps explain why common calcium-blocking drugs, such as those used to control blood pressure, appear to protect against the disease.

Damage to dopamine-releasing cells in a brain area called the substantia nigra (SN) is known to be involved in the onset of Parkinson’s disease. “Pacemaking” cells in this area release pulses of dopamine, a hormone crucial for movement and balance. so damage to these cells leads to the symptoms of Parkinson’s – such as tremors and stiffness.

A key question is why cells of the SN are so much more susceptible to damage than those in surrounding areas. Now it seems that calcium, which enters these cells to regulate their activity, is the culprit.

Jaime Guzman from Northwestern University in Chicago and colleagues compared the effect of calcium activity in two brain areas in mice – the pacemaking SN and a neighbouring area where there was no pacemaking activity.

Oxidative stress

They found that the calcium influx in the SN caused much higher levels of oxidative stress – pressure on cells to counteract the effects of molecules such as free radicals, that can damage proteins and DNA. Oxidative stress is thought to be the source of the cell damage that leads to Parkinson’s disease.

“Although calcium channels normally participate in pacemaking, they aren’t essential as other ion channels can pick up the slack,” says James Surmeier, who was part of the team. Treating mice that had Parkinson’s disease with calcium-channel-blocking drugs might therefore prevent cell damage without hindering essential pacemaking activity.

To investigate this possibility, the team used mice lacking a gene called DJ-1. The absence of this gene causes early onset Parkinson’s disease, and mice who lacked the gene showed much higher levels of damage to the dopamine-releasing cells of the SN than normal mice. When treated with drugs that block calcium channels, however, the degree of cell damage dropped to levels seen in other types of brain cells that are relatively resistant to oxidative stress.

The right drug

The findings explain why previous research conducted by Christoph Meier at University Hospital Basel in Switzerland showed that calcium-blocking hypertension drugs reduced the risk of Parkinson’s disease, while other types of drug used to treat high blood pressure did not.

“A lot seems to point towards a potential benefit of calcium-channel blockers in Parkinson’s disease,” says Meier, “but it’s too early to tell whether they help prevent the disease or could improve the situation of patients who already have a diagnosis.”

Surmeier is more confident. “We think that anyone at risk of developing Parkinson’s disease should benefit by the use of calcium blockers such as isradipine,” he says, as it appears that the dopamine-producing cells in the SN begin to disappear well before the onset of symptoms.

Isradipine is already in a phase II clinical trial for people with early stage Parkinson’s disease, and Surmeier is now planning to investigate more selective and potent drugs.

Journal reference:

Nature, DOI: 10.1038/nature09536

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