PARKINSON'S DISEASE NEWS

26th September 2008 - New research

L-DOPA CO-DRUGS

Archiv der Pharmazie [2008] 341 (7) : 412-417 (Sozio P, Iannitelli A, Cerasa LS, Cacciatore I, Cornacchia C, Giorgioni G, Ricciutelli M, Nasuti C, Cantalamessa F, Di Stefano A.) Complete abstract

Since the advent of L-dopa decades ago, it has become progressively more common to simultaneously administer L-dopa in combination with other substances rather than as a single substance. Sinemet, Madopar and Stalevo all include three substances. This study reports the preliminary evaluation of new L-dopa conjugates obtained by joining L-Dopa with two different natural antioxidants, caffeic acid and carnosine. Caffeic acid is found naturally in coffee and certain foods. For more information go to Caffeic acid. Carnosine is found naturally in meat and is available as a supplement. For more information go to Carnosine.

The antioxidant efficacy of these two substances was assessed by evaluating the plasma activity of superoxide dismutase and glutathione peroxidase. Brain concentration of L-dopa and dopamine, and central nervous system effects were assessed after oral administration of each of the codrugs. The results suggest that the codrugs are devoid of significant antioxidant activity. However, it was found that they can enable sustained delivery of dopamine and can improve L-dopa and dopamine release in the brain. As L-dopa is not yet available as these two codrugs, there is the possibility of taking the additional substances with L-dopa in food or supplement form.
 

                                                                                                                                                                              19th September 2008 - News release

HUGE FUNDING FOR ENVIRONMENTAL CAUSES OF PARKINSON'S DISEASE

The National Institute of Environmental Health Sciences (NIEHS) announced today that it will award three new grants totalling more than $20 million dollars to study how environmental factors contribute to the cause, prevention and treatment of Parkinson's Disease.

The three grantees include : (1) Gary Miller of Emory University, Atlanta, who will be looking at how environmental and genetic factors interact to alter these functions in dopamine neurons. They will be attempting to develop new biomarkers in the blood that will help identify people that may be at risk for developing Parkinson's disease; (2) Marie-Françoise Chesselet of UCLA, who is aiming to show associations between high levels of exposure to specific environmental pesticides and Parkinson's' disease, and determine the mechanisms of action that may be causing this association; (3) Stuart Lipton of the Burnham Institute for Medical Research in California will explore how environmental toxicants may contribute to Parkinson's Disease by producing free radical stress that mimics or enhances the effects of known genetic mutations. For more information these projects go to the Complete article.

There are a number of known toxic causes of Parkinson's Disease. For more information go to the Toxic causes of Parkinson's Disease. However, the number of people known to be suffering from Parkinson's Diisease due to any of these toxic causes is very few. Toxicity has never been shown to be the primary cause of Parkinson's Disease.

18th September 2008 - News release

AMGEN'S GDNF GENE RESUMES USE IN PARKINSON'S DISEASE

The GDNF gene is claimed to contain the information for a protein necessary for the development and survival of nerve cells. Several years ago, Amgen's use of GDNF was being touted as a great breakthrough in Parkinson's Disease. During Amgen's clinical trials of GDNF, patients were claiming that their symptoms had been rid due to using it - even though some of those patients had been taking the placebo instead. Amidst widespread protests, Amgen ceased its use of GDNF altogether due to studies showing that it caused toxicity in animals. The patients' experiences were subsequently detailed in "Monkeys in the Middle".

Amsterdam Molecular Therapeutics (AMT) have just announced that it has obtained a license from Amgen to use their GDNF gene for the development of a gene therapy treatment for Parkinson’s disease. For more information go to AMT. In theory, GDNF could biochemically increase somebody's ability to produce their own dopamine. However, an animal study showed that this effect would reverse over time. Since the Amgen clinical trial, in two small independent open clinical trials involving 5 and 10 patients, a moderate beneficial effect was shown. However, when a large controlled clinical trial was later carried out by the same people, GDNF had no effect at all in ridding Parkinson's Disease.

16th September 2008 - New review
                                                                                                                                                                    FUNGICIDE AS A CAUSE OF PARKINSON'S DISEASE

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 [3].

Common means : Maneb is used as a fungicide. There is a greatly increased likelihood of developing symptoms by people involved in horticulture and agriculture [2].

Means of toxicity : 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. It would thereby lower dopamine levels. The effects of Maneb are potentiated when there is simultaneous exposure to the pesticide Paraquat [4-8].

Symptoms of toxicity : Plastic rigidity with cogwheel phenomenon, headache, fatigue, nervousness, memory complaints, and sleepiness, other neurologic signs, such as postural tremor, cerebellar signs, and bradykinesia [1]; damaging effects on the dopaminergic system [4-8], that it can, quite unusually, even affect prior to birth [4-8]. This suggests that somebody could be affected by fungicide because of exposure to it during their pregnancy.

References : [1] Neurology [1988] 38 (4) : 550-553 (H.B.Ferraz, P.H.Bertolucci, J.S.Pereira, J.G.Lima, L.A.Andrade), [2] Scandinavian journal of work, environment & health. [2000] 26 (4) : 359-362 (F.Tuchsen, A.A.Jensen), [3] Neurology [1998] 50 (5) : 1346-1350 (J.M.Gorell, C.C.Johnson, B.A.Rybicki, E.L.Peterson, R.J.Richardson), [4] Birth defects research. Part A, Clinical and molecular teratology [2005] 73 (3) : 136-139 (D.A.Cory-Slechta, M.Thiruchelvam, E.K.Richfield, B.K.Barlow, A.I.Brooks), [5] Developmental neuroscience [2004] 26 (1) : 11-23 (B.K.Barlow, E.K.Richfield, D.A.Cory-Slechta, M.Thiruchelvam), [6] The European journal of neuroscience [2003] 18 (3) : 589-600 (M.Thiruchelvam, A.McCormack, E.K.Richfield, R.B.Baggs, A.W.Tank, D.A.Di Monte, D.A.Cory-Slechta), [7] Neurotoxicology [2002] 23 (4-5) : 621-633 (M.Thiruchelvam, E.K.Richfield, B.M.Goodman, R.B.Baggs, D.A.Cory-Slechta), [8] The Journal of neuroscience [2000] 20 (24) : 9207-9214 (M.Thiruchelvam, E.K.Richfield, R.B.Baggs, A.W.Tank, D.A.Cory-Slechta)

9th September 2008 - New research

PAIN IN PARKINSON'S DISEASE

Archives of Neurology [2008] 65 (9) : 1191-1194 (Giovanni Defazio, Alfredo Berardelli, Giovanni Fabbrini, Davide Martino, Emiliana Fincati, Antonio Fiaschi, Giuseppe Moretto, Giovanni Abbruzzese, Roberta Marchese, Ubaldo Bonuccelli, Paolo Del Dotto, Paolo Barone, Elisa De Vivo, Alberto Albanese, Angelo Antonini, Margherita Canesi, Leonardo Lopiano, Maurizio Zibetti, Giuseppe Nappi, Emilia Martignoni, Paolo Lamberti, Michele Tinazzi) Complete abstract

The primary symptom of Parkinson's Disease is excessive muscle contraction. Muscle contraction makes muscular cramps more likely. However, Parkinson's Disease and muscular cramps are biochemically distinct. That is why there are people who have muscular cramps who do not have Parkinson's Disease, and people with Parkinson's Disease who do not have muscular cramps. A new study attempted to determine whether pain is more frequent amongst people with Parkinson Disease. The authors claim, and it has been widely reported, that pain was significantly greater in people with Parkinson's Disease than others. However, the results do not really support what has been widely reported.

The frequency of pain in Parkinson's Disease was 70%, and 63% in others. What the study shows is that pain is common in most people, regardless of whether or not they have Parkinson's Disease. Parkinson's Disease makes it more likely, but not by much. The Dystonic pain that is experienced by some in Parkinson's Disease, was claimed to make the difference between the two groups, because non-dystonic pain was almost equal in the two groups. Muscular cramps, as expected, were more common in Parkinson's Disease. What the study shows is that Parkinson's Disease, muscular cramps, and general pain should be considered as separate medical problems.

 

5th September 2008 - New product

PARKINSON'S DISEASE SUPPLEMENT

A supplement that is specifically for Parkinson's Disease has been continuously reducing and ridding symptoms in those people taking it. It consists, in optimal forms and optimal dosages, of those substances that the brain normally uses to make its own dopamine. Although it is often assumed that dopamine will make itself or has to be taken in drug form, dopamine is produced naturally using specific nutrients - most prominently, L-tyrosine, which is what L-dopa is made from. For the background biochemistry of Parkinson's Disease go to : Biochemistry of Parkinson's Disease and Causes of Parkinson's Disease. The full effects of the supplement are slow, taking a year or two or more. However, whilst reaching its full effect, the supplement does not cause any side effects, and can be taken alongside all existing forms of treating Parkinson's Disease.

The supplement is simply added on to what somebody is already taking. After lengthy use, some people have already very gradually rid their Parkinson's Disease symptoms. Others have hugely reduced their symptoms and continue to improve. This has enabled some people to also rid or greatly reduce their Parkinson's Disease drugs. A full scale clinical trial has been arranged at the Addenbrookes Hospital in Cambridge, England, but may be transferred to Ireland, as The Parkinson Association of Ireland are presently considering their involvement. The supplement is currently available as Dopavite, but will undergo a product name change and improvement in the formulation after the clinical trials, when despite still being a supplement, its status will increase to a prescribable medicine.
 

                                                                                                                                                    4th September 2008 - New research

CREATINE REDUCES DYSKINESIA

Behavioural Brain Research [2008] Aug 12; [Epub ahead of print] (Valastro B, Dekundy A, Danysz W, Quack G.) Complete abstract

Dyskinesia (involuntary movements) is a common symptom in Parkinson's Disease that is usually caused by the long term use of L-Dopa. Researchers hypothesized that oral supplements of Creatine could prevent or reduce dyskinesia in Parkinson's Disease. Creatine is a substance that the body normally produces itself in order to supply energy to muscle cells.  For more information go to Creatine.

Creatine is often used as a food supplement. In this study, rats received a creatine-supplemented diet for a month prior to L-Dopa therapy. During L-Dopa treatment, significant reductions in abnormal involuntary movements were observed in the creatine-supplemented group, without any worsening of Parkinson's Disease symptoms. Further investigation revealed significant changes in the levels of creatine both after L-DOPA alone and with the supplemented diet. The researchers stated that they had demonstrated that combining L-Dopa therapy with a diet enriched in creatine could reduce dyskinesia, and that this may represent a new way to control the motor complications associated with the use of L-Dopa.

1st September 2008 - New research

SEXUAL DYSFUNCTION IN PARKINSON'S DISEASE

European Journal of Neurology [2008] Aug 27; [Epub ahead of print] (Celikel E, Ozel-Kizil ET, Akbostanci MC, Cevik A.) Complete abstract

Sexual dysfunction in patients with Parkinson's disease has not been very well studied, as most of the research has has restrictions such as like having no control group, or has used invalid assessment tools. This study aimed to examine different sexual functions in patients with Parkinson's Disease and compare them with matched non-parkinsonian controls by using a valid questionnaire. Predicting factors of sexual dysfunction in Parkinson's Disease were also investigated. The sample consisted of an equal number of people with Parkinson's Disease and age and sex matched controls. Sexual functions were evaluated by Arizona Sexual Experiences Scale (ASEX).

There is a score of 1 to 6 for each question. Possible total scores range from 5 to 30, with the higher scores indicating more sexual dysfunction. Female patients were found to have reduced sex drive and were less satisfied with orgasm, while male patients actually had easier orgasms than did the controls. Increased age and female sex were predictive of reduced sex drive and sexual arousal. Ability to reach orgasm and satisfaction with orgasm were associated with female sex, while erection/lubrication was associated with marital status. The severity and duration of Parkinson's Disease, as well as the severity of anxiety and depression were, contrary to what is often assumed, not associated with Sexual dysfunction.