DIABETES TREATMENT FOR PARKINSON'S DISEASE \

9th May 2014 - New research

Journal of Parkinson's Disease [2014] Mar 24 [Epub ahead of print] (I.Aviles-Olmos,
J.Dickson, Z.Kefalopoulou, A.Djamshidian, J.Kahan, P.E.Fmedsci, P.Whitton, R.Wyse, T.

Isaacs, A.Lees, P.Limousin, T.Foltynie)


Exenatide, which is a treatment for diabetes, has been tested as a disease modifying treatment
for Parkinson's Disease. Exenatide is an injected glucagon-like peptide-1 agonist medication
marketed as Byett and Bydureon and is used in the treatment of insulin resistance in patients
with Type 2 diabetes. It differs in pharmacological action and chemical structure from
insulin. For more information go to : http://www.rxlist.com/byetta-drug.htm 

The authors do not suggest how this diabetes drug can have effect in Parkinson's Disease.
Using the MDS-UPDRS, which is a means of assessing the
extent of Parkinson's Disease symptoms, people with
Parkinson's Disease were assessed who had previously taken
Exenatide. People with Parkinson's Disease had an advantage
of 5.6 points (with a range of 2.2 to 9.0) on the assessment.
They also had a better score when assessed concerning
dementia. Unusually, the effect of Exenatide on Parkinson's
Disease had continued beyond its use.
In a previous study, when people with moderate Parkinson's Disease received subcutaneous
injections of Exenatide for a year there were marginal improvements in Parkinson's Disease
motor and cognitive measures. Exenatide treated patients had a mean improvement after one
year on the UPDRS of 2.7 compared with a mean decline of 2.2 points in controls. Exenatide
was well tolerated but weight loss was common.

Complete abstract : http://www.ncbi.nlm.nih.gov/pubmed/23728174

http://www.viartis.net/parkinsons.disease/news/140509.pdf

mail@viartis

10 Early Warning Signs of Parkinson's Disease

I was ask to show this again.

Sometimes it is hard to tell that you might have Parkinson's disease. Parkinson's disease is when your brain stops making an important chemical called dopamine. This chemical helps your body to move, and helps your mood. If you do have Parkinson's, you can feel better by taking a pill that helps your body to replace that chemical. Parkinson's disease will get worse slowly over time, and your doctor can help you stay healthy longer. Some of the problems listed here could be signs of Parkinson's disease.

No single one of these signs means that you should worry about Parkinson's disease. If you have more than one symptom, you should make an appointment to talk to your doctor. 

Early diagnosis of Parkinson's disease gives you the best chance of a longer, healthier life.

What you can do if you do have Parkinson's disease:

• Work with your doctor to create a plan to stay healthy. This plan might include:
  • A referral to a neurologist, a doctor who specializes in the brain
  • Care from an occupational therapist, physical therapist or speech therapist
  • Meeting with a medical social worker to talk about how Parkinson's will affect your life
• Start a regular exercise program to delay further symptoms.
• Talk with family and friends who can provide you with the support you need.

Tremor or Shaking

Have you noticed a slight shaking or tremor in your finger, thumb, hand, chin or lip? Does your leg shake when you sit down or relax? Twitching or shaking of limbs is a common early sign of Parkinson’s disease.
What is normal? Shaking can be normal after lots of exercise, if you have been injured, or could be caused by a medicine you take.

Small Handwriting

Has your handwriting suddenly gotten much smaller than in it was in the past? You may notice the way you write words on a page has changed, such as letter sizes are smaller and the words are crowded together. A sudden change in handwriting is often a sign of Parkinson’s disease.
What is normal? Sometimes writing can change as you get older, if you have stiff hands or fingers or poor vision, but this happens over time and not suddenly.

Loss of Smell

Have you noticed you no longer smell certain foods very well? If  you seem to have more trouble smelling foods like bananas, dill pickles or licorice, you should ask your doctor about Parkinson’s disease.
What is normal? Your sense of smell can be changed by a cold, flu or a stuffy nose, but it should come back after you are better.

Trouble Sleeping

Do you thrash around in bed or kick and punch while you are deeply asleep? You might notice that you started falling out of bed while asleep. Sometimes, your spouse will notice, or will want to move to another bed. Sudden movements during sleep may be a sign of Parkinson’s disease.
What is normal? It is normal for everyone to have a night when they ‘toss and turn’ instead of sleeping.

Trouble Moving or Walking

Do you feel stiff in your body, arms or legs? Sometimes stiffness goes away as you move. If it does not, it can be a sign of Parkinson’s disease. You might notice that your arms don’t swing when you walk, or maybe other people have said you look stiff. An early sign might be stiffness or pain in your shoulder or hips. People sometimes say their feet seem ‘stuck to the floor.’
What is normal? If you have injured your arm or shoulder, you may not be able to use it as well until it is healed or another illness like arthritis might cause the same symptom.

Constipation

Do you have trouble moving your bowels without straining every day? Straining to move your bowels can be an early sign of Parkinson’s disease and you should talk to your doctor.
What is normal? If you do not have enough water or fiber in your body, it can cause problems in the bathroom. Also some medicine will cause constipation too. If there is no other reason such as diet or medicine that would cause you to have trouble moving your bowels, you should speak with your doctor.

A Soft or Low Voice

Have other people told you that your voice is very soft when you speak in a normal tone, or that you sound hoarse? If there has been a change in your voice you should see your doctor about whether it could be Parkinson’s disease. Sometimes you might think other people are losing their hearing, when really you are speaking more softly.
What is normal? A chest cold or other virus can cause your voice to sound different but you should go back to sounding the same when you get over your cough or cold.

Masked Face

Have you been told that you have a serious, depressed or mad look on your face more often, even when you are not in a bad mood? This serious looking face is called masking. Also, if you or other people notice that you have a blank stare or do not blink your eyes very often, you should ask your doctor about Parkinson’s disease.
What is normal? Some medicines can cause you to have the same type of serious or staring look, but you would go back to the way you were after you stopped the medication.

Dizziness or Fainting

Do you notice that you often feel dizzy when you stand up out of a chair? Feeling dizzy or fainting can be signs of low blood pressure and can be linked to Parkinson’s disease.
What is normal? Everyone has had a time when they stood up and felt dizzy, but if it happens on a regular basis you should see your doctor.

Stooping or Hunching Over

Are you not standing up as straight as you used to? If you or your family or friends notice that you seem to be stooping, leaning or slouching when you stand, it could be a sign of Parkinson’s disease.
What is normal? If you have pain from an injury or if you are sick, it might cause you to stand crookedly. Also, a problem with your bones can make you hunch over.

New concept may explain vision problems in Parkinson's disease

(Medical Xpress)—Are patients with Parkinson's disease "blind to blindsight?" That's not a trick question, but the focus of an inquiry by neuroscientists from Rush University Medical Center as well as the Centre Hospitalier and University of Luxembourg.

The "blind to blindness" concept is described in the June issue of the journal Brain by Dr. Nico J. Diederich, from Centre Hospitalier and University of Luxembourg, who is a visiting scholar at Rush University. He was joined by the Rush researchers Glenn Stebbins, PhD, and Dr. Christopher G. Goetz, and neuropsychologist Christine Schiltz, PhD, from the University of Luxembourg.

The scientists developed the concept of "blind to blindsight" to integrate data on visual impairments that contribute to the disability and diminished quality of life in patients with Parkinson's disease.

Blindsight is observed in people who are blind as a result of a lesion in the visual cortexof their brain. Although these individuals are blind, they maintain the ability to sense accurately a light source or a rapid movement without being aware of it. Strangely, blindsighted patients even can respond appropriately to emotional facial expressions, especially those expressing fear or danger. It is believed that these visual stimuli can be turned directly into actions (e.g., movement of the eyes) by passing through lower areas of the brain. Thus, these retained visual functions operate as unconscious responses to visual stimulation even when there is extensive damage to the visual cortex. .

Conversely, patients with Parkinson's disease, who do not have a problem with their general vision, are unable to do these tasks: they display slowness and reduced accuracy of pursuit eye movements. They often have difficulties grasping a moving object, and show decreased sensitivity to low contrast and impaired ability to read "right away" other people's facial expressions.

Taken together, these Parkinson's disease symptoms represent major impairments in blindsight – hence, "blind to blindsight." Based on this new concept, the researchers could now propose a new concept how to comprehensively understand within one visual system—blindsight—numerous visual signs and symptoms of patients with Parkinson's disease. Impairment of the evolutionary old networks in the brain operating within the blindsight visual system form the basis of the visual problems in Parkinson's disease.

Smartphone App Could Be Used To Diagnose Parkinson’s Disease

Thursday May 01, 2014

Nastassia Baroni

NewsFeeds - Programs are being developed for smartphones that could be used to detect whether or not a person has Parkinson’s disease. A new initiative hopes to use the technology to circumvent the lengthy diagnosis process and help detect the disease and track symptoms.

Sky News reports, the Parkinson’s Voice Initiative was launched by British born mathematician and visiting professor at MIT, Max Little, and is funded by the Wellcome Trust and Michael J Fox Foundation.

The initiative aims to find a cheaper, more accessible method to diagnosis by categorising people’s voice patterns. Soon it will launch a new trial wherein up to 1,500 people will download software on to their smartphone that will track their body movement, voice and other data over six months.

“We have a hypothesis formed from earlier research that you can detect whether someone has Parkinson’s disease on the basis of their body movements, recorded using a smartphone,” Mr Little told Sky News.

His last study involved 17,000 people, both Parkinson’s sufferers and non-sufferers who called special numbers to record their voice tracks. Now, Little is analysing the recordings and once finished he hopes to create a system that analyses the voices automatically.

“The ultimate vision for Pakinson’s is you have smartphone software that you download, it would track your movement for a week, and then it would give you a probability that you might develop Parkinson’s,” he explained. “If we get sufficient data – it’s all down to participants – this is only a few years away.”

A new follow-on study has been announced and the Initiative is looking for participants. Visit www.parkinsonsvoice.org to register your interest.

Baroni, Nastassia (30 April 2014). NewsFeeds. Smartphone App Could Be Used To Diagnose Parkinson’s Disease. http://newsfeeds.com.au/technology/smartphone-app-could-be-used-to-diagnose-parkinsons-disease/

Retinal Measurements Associated with Parkinson’s Disease Duration

Thursday May 01, 2014

Sarah Pritchard

News Medical - The inner retinal layers in the eyes of patients with Parkinson’s disease (PD) are thinner than those of healthy people’s eyes, except for the inner nuclear layer, which is thicker, show the results of a prospective study involving the latest optical coherence tomography (OCT) methods.

Inner retinal layers were also more greatly affected in PD patients with a disease duration of 10 years or more versus those who were diagnosed more recently, report the researchers in the American Journal of Ophthalmology.

“OCT technology allows for precise measurements of retinal layer thickness, and these measurements may reflect the number of human retinal cells with dopaminergic activity”, explain Elena Garcia-Martin (Miguel Servet University Hospital, Zaragoza, Spain) and colleagues.

They examined the retinal layers in the eyes of 129 patients with PD and 129 age- and gender-matched healthy controls. The PD patients had a mean 8.4-year disease duration and were aged a mean 68.8 years. Controls were 69.0 years old on average.

Using OCT with an automated system that separates the retina into 10 layers, the team observed significant reductions in the thickness of the retinal nerve fibre layer (RNFL) in PD patients compared with controls, at 6.06 versus 6.26 µm, in the ganglion cell layer, at 6.30 versus 6.49 µm, and the inner and outer plexiform layers, at 6.64 and 7.17 µm, respectively, versus 6.77 and 7.31 µm.

By contrast, the inner nuclear layer was significantly thicker in PD patients versus controls, at 7.39 versus 7.14 µm.

RNFL, ganglion cell layer and inner plexiform measurements were all significantly thinner in PD patients with at least 10 years’ disease duration compared with those who were diagnosed more recently, at 5.89 versus 6.06 µm, 5.96 versus 6.40 µm and 6.11 versus 6.47 µm.

“This could be attributable to primary neurodegeneration of the retinal ganglion cells and their axons in [PD] patients or to retrograde trans-synaptic degeneration of the retinal ganglion cell layer and its axons owing to [PD] lesions of the posterior visual pathways”, note Garcia-Martin et al.

They add that ganglion cell layer thickness was borderline significantly inversely associated with PD duration, and in regression analysis, only ganglion cell layer thickness predicted PD axonal damage.

The team suggests that future research using OCT is needed to determine the extent to which each retinal layer could predict PD in its early stages.

Pritchard, Sarah. (1 May 2014). News Medical. Retinal measurements associated with Parkinson’s disease duration. http://www.news-medical.net/news/20140501/Retinal-measurements-associated-with-Parkinsone28099s-disease-duration.aspx

Penn Neurologists Report on Promise of Statins, Estrogen and Telemedicine in Parkinson's

Monday April 28, 2014

Phys.org - A trio of studies from the Perelman School of Medicine at the University of Pennsylvania demonstrate new approaches to understanding, treating and potentially staving off Parkinson's disease (PD). Studies show that factors such as estrogen exposure and statin use have an impact on the onset of Parkinson's disease. And a new look at telemedicine demonstrates feasibility in providing care for Parkinson's patients using remote video visits to expand access and center care around the needs of Parkinson's patients. These studies and more will be presented at the American Academy of Neurology's 66th Annual Meeting at Philadelphia's Pennsylvania Convention Center from April 26 to May 3, 2014.

"Researchers at Penn Medicine are looking at Parkinson's disease from all angles - ways to improve treatment methods for those currently battling the disease, understanding the root causes of disease, and identifying potential interventions to delay the onset of disease," said Matthew Stern, MD, professor of Neurology in the Perelman School of Medicine at the University of Pennsylvania and director of Penn's Parkinson's Disease and Movement Disorders Center. "We are persistent and eager to find better targets and treatments to help patients with Parkinson's disease, which affects up to 1 million Americans and 10 million people globally." Dr. Stern is the current president of the International Parkinson and Movement Disorder Society.

Statins May Delay Onset of Parkinson's Disease

Research presented by Yosef Berlyand, undergraduate in the laboratory of Alice Chen-Plotkin, MD, MSc assistant professor of Neurology, suggests that statins may be beneficial in Parkinson's disease. In collaboration with Roy Alcalay, MD and colleagues at Columbia University School of Medicine, members of Dr. Chen-Plotkin's research group demonstrated that blood levels of the protein Apolipoprotein A1 (ApoA1) are lower in people with Parkinson's disease than those without disease. PD patients taking statin medications, which can elevate levels of ApoA1, had an older age of disease onset, which appears to be driven by PD patients taking statins. Previous work led by Dr. Chen-Plotkin has suggested that ApoA1 levels may be a new biomarker for PD risk. The team is in the midst of a follow-up study on plasma ApoA1 and statins, evaluating participants in the Michael J. Fox Foundation's Parkinson's Progression Marker Initiative (PPMI) cohort, to confirm whether ApoA1 modifying drugs such as statins may be a promising neuroprotective therapy for Parkinson's disease.

— Yosef Berlyand will present [P2.055] Statin Use, Apolipoprotein A1, and Parkinson's Disease on Tuesday, April 29, 2014 at 7:30 a.m., during P2: Poster Session II: Movement Disorders: Co-morbidities and Novel Care Models from 7:30 a.m. to 11 a.m. in Hall E.

— Christine Swanson, MD, postdoctoral fellow in Neurology [S17.004] Apolipoprotein A1 Levels Are Associated with ApoA1 Promoter Variation and Influence Parkinson's Disease Risk on Tuesday, April 29, 2014 at 4:00 p.m., during S17: Scientific Session: Parkinson's Disease: Genetics and Epidemiology in Room 108 AB.

Estrogen Investigated for Protection from Parkinson's

In another study, an analysis by Kara Smith, MD, a Movement Disorders fellow in Neurology at Penn's Perelman School of Medicine, and colleagues, investigated the role estrogen plays in decreasing lifetime risk of PD, in light of the fact that men have a relative risk of 1.5 of having Parkinson's disease compared to females. In a systemic review of studies using animal models of PD, the team found consistent evidence that 17-estradiol, in particular, may play a key role in binding to the estrogen receptor and protecting cells from Parkinson's pathology. The team says further research needs to look at 17-estradiol in more accurate animal models of PD, before results can be translated to clinical trials in people with Parkinson's.

— Dr. Smith will present [P3.068] Neuroprotection by Sex Steroid Hormones in Parkinson's Disease on Tuesday, April 29, 2014 during P3: Poster Session III: Movement Disorders: Clinical Features of Parkinson's Disease from 3:00 p.m. to 6:30 p.m. in Hall E.

Telemedicine Improves Access to Specialty Parkinson's Care

An additional Penn study being presented at the AAN meeting examined use of telemedicine visits to increase access to specialty care for Parkinson's patients, in an effort to help remove barriers to specialty care experienced by many patients who live far from care or have disabilities that make it difficult to travel. A Penn Medicine team led by Jayne Wilkinson, MD, and Meredith Spindler, MD, conducted a randomized controlled trial using video telemedicine in the patient's home or at a facility near the patient (in this case, VA Community Based Outpatient Clinics (CBOCs), connecting them to a neurologist specializing in movement disorders and Parkinson's disease, based at the Parkinson's Disease Research, Education, and Clinical Center (PADRECC) at the Philadelphia VA Medical Center. Early results demonstrate that the process of using telemedicine for Parkinson's specialty care is feasible, provided similar quality of life, care and communication, and significantly decreased travel. This is the largest study to evaluate telemedicine in this Parkinson's patient population.

— Drs. Wilkinson and Spindler will present [P2.048] Telehealth in the Parkinson's Disease Subspecialty Clinic: The Key to the Patient-Centered Medical Home on Tuesday, April 29, 2014 during P2: Poster Session II: Movement Disorders: Co-morbidities and Novel Care Models from 7:30 a.m. to 11 a.m. in Hall E. The study was supported by the Veterans Affairs Medical Center's VISN 4 Center for Evaluation of Patient-Aligned Care Teams (CEPACT).

Provided by University of Pennsylvania School of Medicine

Science News Wire. (28 April 2014). Phys.org. Penn Neurologists Report on Promise of Statins, Estrogen and Telemedicine in Parkinson's. http://phys.org/wire-news/160135712/penn-neurologists-report-on-promise-of-statins-estrogen-and-tele.html

Marine Sponge Research May Help Scientists Understand Parkinson's Disease

Monday April 28, 2014

Elise Worthington & Elaine Ford

ABC News Australia - Researchers are using a new technique to find a compound in a type of marine sponge that may help in the fight against Parkinson's disease.

Scientists at Queensland's Griffith University tested more than 200 sea sponges and identified a compound that caused changes in cells extracted from Parkinson's disease patients.

It is the start of a program using the new method to test more than 200,000 natural compounds.

Researcher Professor Ronald Quinn says the results are promising, but there are more than 200,000 samples left to test.

"We've developed a technique using spectroscopy to look for something that's novel, so that part of it gives us a compound that has not been found previously by anyone else, so it's unique," he said.

"Then what we've done we've looked at that compound on cells that we've obtained from patients who have Parkinson's disease.

"When we looked at those 220 using this MMR fingerprinting, that allowed us to see which of those 220 had an unique component and that really allowed us to hone, and isolate and identify this compound that's new."

He says the technique could be used to treat a variety of conditions, but is a way off yet.

[In this study] if we get one [compound] out of 200 - and we have 200,000 - that's quite a lot of potential that we can find that may help in trying to understand Parkinson's disease in this particular program," Professor Quinn said.

"It's a tool or a probe to try to understand the biology behind the disease - what may cause Parkinson's disease.

"Hopefully with this sort of technique, we can use tools similar to this to reverse the phenotype and bring the Parkinson's disease patient back to normal.

"This is very early - this is a molecule that allows us to understand the system.

"Any therapeutic use or drug use is well down the track."

Needle in a haystack research

Professor Quinn says the marine sponges are complex organisms that contain a lot of compounds.

"We're trying to find within that haystack if you like - the needle - the single compound that's quite unique and different and can be useful to be developed towards understanding the disease, and then later on to try to treat the disease," he said.

Professor Quinn says marine sponges have very little protection in nature and their way of surviving predators is the chemicals it uses to achieve that.

"Because it's producing chemicals for protection and other functions, then those compounds may be useful in a therapeutic sense on a human target," he said.

"It is a chemical factory producing lots of compounds to respond to its environment and some of them might be useful to develop into a therapeutic.

"In this case, one of those compounds shows a very unique action on cells from people with Parkinson's disease."

He says the program has a strong focus on Parkinson's disease because of its research base.

"It's mainly fuelled by the fact that we have isolated cells and we're able to culture them up and we have a terminology what we call 'neurobank'," he said.

"We have quite a number of patients that have donated some tissue and we've grown up the cells, so we have this array of cells so we can investigate the disease.

"We can then compare them against people who don't have the disease and try and see what's the difference.

Professor Quinn says doctors currently treat the symptoms of Parkinson's disease, but scientists still do not understand what causes it.

"What we're hoping here by using this compound and others that we find, hoping that it gives us some ideas of how the disease occurs and then we can treat the cause of the disease rather than treat the symptoms of the disease," he said.

Worthington, Elise & Elaine Ford. (28 April 2014). ABC News Australia. Marine Sponge Research May Help Scientists Understand Parkinson's Disease. http://www.abc.net.au/news/2014-04-28/marine-sponge-research-may-help-fight-parkinsons-disease/5415622

TOXIC CAUSES OF IDIOPATHIC PARKINSON'S DISEASE

PARAQUAT

Paraquat is a quaternary ammonium herbicide. Other members of this class include

 diquat, cyperquat, diethamqua, difenzoquat and morfamquat. Pesticides are known

 to be associated with an increased rate of Parkinson’s Disease.

 Paraquat structurally resembles MPTP and its metabolite MPP+. MPTP and

 MPP+ are neurotoxic chemicals, that induce Parkinson’s Disease in exposed humans.

Paraquat might therefore might, as do MPTP and MPP+ inhibit tyrosine hydroxylation,

which is essential for the formation of dopamine.

ROTENONE Rotenone is an insecticide that has the potential to cause Parkinson's disease. Insecticides are also known to affect well water. Rotenone is commonly used in powdered  form to treat parasitic mites on chickens and other fowl, and of certain tropical legumes. Rotenone inhibits of dopamine. So rotenone could cause   Parkinson's disease by lowering dopamine levels. When given intravenously to mice, rotenone has been demonstrated to cause a model of Parkinson's disease. Rotenone toxicity is tyrosine hydroxylation, which is essential for the formation also caused by complex I inhibition, depletion of cellular and oxidative damage. These processes cause loss of midbrain  dopaminergic neurons, leading to depletion of dopamine in the brain. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ MANEB Maneb is a fungicide that contains manganese. The major active element of Maneb is manganese ethylene-bis-dithiocarbamate. Pesticides are known to be associated with an increased rate of Parkinson's disease, so there is a greatly increased the  likelihood of developing toxic symptoms by people involved in horticulture and agriculture. As Maneb contains manganese it is possible that it causes Parkinson's Disease symptoms via the same means as manganese, which is by inhibiting tyrosine hydroxylation, which is essential for the formation of dopamine. The effects of Maneb are potentiated when there is also exposure to the pesticide Paraquat. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ MANGANESE Manganese can cause manganism, an irreversible neurological disorder similar to Parkinson's disease. Occupational exposures occur mainly in welding, mining as miners are surrounded by manganese dust and airborne manganese particles, alloy production, processing, ferro-manganese operations  especially in which manganese ore or manganese compounds are turned into steel, and work with agrochemicals. The towns and communities surrounding the areas of manganese heavy industry could also become affected by toxic exposure to manganese. It is also hypothesized that long-term exposure to the naturally-occurring manganese in shower water also puts people at risk. Manganese inhibits tyrosine hydroxylation, which is essential for the formation of dopamine. So manganese may cause Parkinson's disease by lowering dopamine levels. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ MPTP MPTP (1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine) is a chemical that may be  produced accidentally during illicit manufacture of the recreational drug MPPP,  which is a synthetic heroin substitute. The neurotoxicity of MPTP wasdiscovered in 1976  after a chemistry graduate student synthesized MPPP incorrectly and injected the result.  It was contaminated with MPTP, and within three days he began exhibiting symptoms  of acute Parkinson's disease. It was also developed but unused as a herbicide and  was distributed on the streets as a synthetic opioid-like drug.  MPTP inhibits tyrosine hydroxylation, which is essential for the formation of dopamine.  So MPTP causes acute Parkinson's disease by lowering dopamine levels. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ TOLUENE Toluene is a solvent that has been shown to cause Parkinson's Disease, or that has been  associated with people with Parkinson's disease. Toluene is used as an octane booster  in fuel, as a solvent in paints, paint thinners, chemical reactions, rubber, printing,  adhesives, lacquers, leather tanning, disinfectants, and to produce phenol and TNT (a component of explosives). It is also used as a raw material for toluene  di-isocyanate, which is used in the manufacture of polyurethane foams.  The precise means of toxicity of toluene is not known. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ N-HEXANE N-hexane, a constituent of solvents has been shown to cause parkinsonism. Most of the  n-hexane used in industry is mixed with similar chemicals called solvents. The major  use for solvents containing n-hexane is to extract vegetable oils from crops such as soybeans.  These solvents are also used as cleaning agents in the printing, textile, furniture, and shoe   making industries, and also by chemists. Certain glues used in the roofing, and shoe  and leather industries also contain n-hexane. Several consumer products contain n-hexane,  such as gasoline, spot removers, quick-drying glues, and also rubber cement.  The means of  toxicity of n-hexane is still unknown. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ CARBON DISULFIDE Carbon disulfide, usually in solvents or pesticides, can cause Parkinson's disease that is  associated with other neurological symptoms. The toxic effects can persist for years  after exposure to the carbon disulfide has ceased. Potential sources include pesticides  used as fumigants, disulfiram (a drug used in the treatment of chronic alcoholism), i ndustrial solvents, solvents used in the production of viscose rayon and cellophane film.  Means of toxicity is not established. However, carbon disulphide interferes with  pyridoxal 5-phosphate. Pyridoxal 5-phosphate is essential for the formation of  dopamine from L-dopa. So carbon disulphide may cause Parkinson's disease symptoms  by reducing the formation of L-dopa. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ CARBON MONOXIDE Carbon monoxide toxicity is frequent due to the formation of carbon monoxide  by very common means such as gas cookers and exhaust fumes. However, it normally  requires severe exposure (e.g. the person going into a coma as a result of the  carbon monoxide poisoning) before symptoms of Parkinson's disease develop.  Carbon monoxide causes hemoglobin (which transports oxygen) to turn in to  carboxyhemoglobin (which does not transport oxygen). Oxygen is required  for the formation of L-dopa. So carbon monoxide may cause Parkinson's  disease symptoms by interfering with the availability of oxygen to the brain.  However, the means by which it can cause parkinsonism has still not been proven. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ MERCURY Mercury toxicity is a known cause of symptoms that mimic Parkinson's disease, especially  tremor. One of the chief targets of the toxin is the enzyme pyruvate dehydrogenase (PDH).  The enzyme is irreversibly inhibited by severalmercury compounds, the lipoic acid  component of the multienzyme complex binds mercury compounds tightly and  thus inhibits PDH. However, the cause of the symptoms of Parkinson's disease  is likely to be due to the fact that mercury potently causes the release of dopamine,  thereby lowering dopamine levels. Mercury is found in a wide variety of sources:  dietary fish intake, ethnic over-the-counter medications, occupational exposures to mercury  vapour, possession of dental amalgam fillings, gold production, skin ointment, some soaps. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ CYANIDE Cyanide, usually from the consumption of potassium cyanide or sodium cyanide can  result in Parkinsonism. Cyanide is also produced by certain bacteria, fungi, and algae,  and are found in a number of foods and plants, such as unprocessed cassava, cherry pits,  apricot pits, bitter almonds. Hydrogen cyanide is contained in vehicle exhaust  and in tobacco smoke, as does burning plastic. Cyanides are also found in gold processing.  Cyanide interrupts the electron transport chain in the inner membrane of the   mitochondrion. Cyanide also occupies the place of oxygen in hemoglobin  (which transports oxygen). Oxygen is required for the formation of L-dopa. So carbon   monoxide may cause Parkinson's disease symptoms by interfering with the availability  of oxygen to the brain. However, the precise toxic means by which it causes  Parkinson's disease has still not been proven. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ COPPER Copper accumulates in Wilson's disease, which is associated with Parkinson's disease. Although copper may cause symptoms by other means, there do not appear to be published studies in which copper has otherwise caused Parkinson's disease. This may be because copper is not normally formed in to a vapour or dust that can readily be inhaled or consumed. Copper can be found in high quantities in copper mines, copper cooking pots, copper plumbing, very excessive consumption of copper nutritional supplements. Excess copper can cause the formation of a copper-dopamine complex,  which leads to the oxidation of dopamine to amino chrome. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ LEAD Prolonged exposure to lead can double the likelihood of developing Parkinson’s Disease. Common means of lead poisoning are lead contaminated soil, and ingestion of lead  dust or chips from deteriorating lead-based paints. Lead has also been found in drinking  water, from plumbing fixtures that are either made of lead or have trace amounts of  lead in them. Lead can be found incosmetics in some countries, and in toys such as  many from China. Due to the similarity of their structures, lead can inadvertently replace  iron in enzymatic reactions, but it does not properly function as a cofactor. This might  cause a reduction in L-dopa because iron is an essential cofactor for L-dopa formation.  Lead can also interfere with oxygen transport by reducing hemoglobin biosynthesis. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ TRICHLOROETHYLENE People subjected to chronic industrial exposure of the solvent Trichloroethylene have been  found to have Parkinson’s Disease. Trichloroethylene is a solvent, that is used  extensively in industry and the military and is a common environmental contaminant.  It has been used to extract vegetable oils, in coffee decaffeination, and in the preparation  of flavouring extracts from hops and spices. The precise means of toxicity is unknown. Workers with workstations adjacent to the source of trichloroethylene and who were subjected to chronic inhalation and dermal exposure from handling trichloroethylene-soaked metal parts all had Parkinson's disease. Lesser chronic  respiratory exposure to trichloroethylene led to many features of Parkinsonism,  including significant motor slowing. Under the trade name Tilene, trichloroethylene was used as an anesthetic and as an  inhaled obstetrical analgesic in millions of patients.  Tilene has been found to cause shaking and stiffness.