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OCTOBER 2008

24th October 2008 - New research

tremor only PARKINSON'S DISEASE

Acta Neurologica Belgica [2008] 108 (2) : 48-52 (Leventoglu A, Baysal AI.) Complete abstract

Although tremor is often considered to be a characteristic symptom of Parkinson's Disease, about 30% of people who have Parkinson's Disease don't have tremor. However, there are some people with Parkinson's Disease whose symptoms are virtually only tremor. Researchers analysed what happened to people whose first symptoms were
tremor, in order to see if they eventually developed other symptoms of Parkinson's Disease, such as rigidity and bradykinesia (slowing of movement).

Even amongst those people with only tremor there were found to be different types : those with rest tremor, mainly in the upper limbs; those with rest tremor only in a lower limb; and those with only jaw tremor. Some patients with pure Parkinsonian tremor were found to be without bradykinesia or rigidity for a long time. This means that instead of the typical (and false view) of Parkinson's Disease including tremor, rigidity and bradykinesia (slowing of movement), that there were those at one extreme with only tremor, and those at the other extreme who have no tremor at all. There is therefore clearly no characteristic set of symptoms that define Parkinson's Disease.

 

17th October 2008 - New review

implanted neurons DEVELOP PARKINSON'S DISEASE

This review details how new cells put in to the brain to rid Parkinson's Disease develop the signs of Parkinson's Disease themselves. The Neuropathological changes in Parkinson's disease usually progress slowly and spread according to a characteristic pattern. Recent papers have shed light on this progression of pathology by examining the fate of neurons grafted into the brains of patients with Parkinson's Disease.

Two of these studies demonstrate that new healthy neurons grafted in to the brains of people with Parkinson's Disease gradually develop the same pathology as the existing neurons. According to these studies, implanted neurons developed biochemical symptoms of Parkinson's Disease after transplantation : alpha-synuclein- and ubiquitin-positive Lewy bodies. It is inevitable that any new cells will eventually function at the same insufficient rate as the existing cells, because their biochemical environment would be identical.

 

15th October 2008 - New research

vitamin d deficiency in parkinson's disease

Archives of Neurology [2008] 65 (10) : 1348-1352 (Evatt ML, Delong MR, Khazai N, Rosen A, Triche S, Tangpricha V.) Complete abstract

Researchers compared the prevalence of vitamin D deficiency in patients with Parkinson's Disease with age-matched healthy controls and patients with Alzheimer disease. Significantly more patients with Parkinson's Disease (55% of them) had insufficient vitamin D, in comparison to 36% healthy controls, and 41% in people with Alzheimer's Disease. The researchers claim that this data supports a possible role of vitamin D insufficiency in Parkinson's Disease. They suggest that further studies are needed to determine the factors contributing to these differences and elucidate the potential role of vitamin D in the cause and clinical course of Parkinson's Disease. However, Vitamin D has no role at all in the formation of dopamine, the substance whose deficiency causes Parkinson's Disease. For more information go to the Biochemistry of Parkinson's Disease.

Also, in severe cases of Vitamin D deficiency, there is no known relationship with Parkinson's Disease as there would be if Vitamin D deficiency could cause it. The primary role of Vitamin D is in the formation and structure of bone. Sunlight is a known source of Vitamin D. So the link between Vitamin D and Parkinson's Disease may be due to those people with Parkinson's Disease who have mobility problems being exposed to less sunlight. Although sunlight and certain foods are sources of Vitamin D, they are usually insufficient sources. However, vitamin supplements usually supply 50%-100% of a person's needs.

 

13th October 2008 - New clinical trial

Nexalin device clinical trial

The Michael J.Fox Foundation is to carry out a clinical trial using the Nexalin Device. For more information go to The Michael J.Fox Foundation. Nexalin Therapy is a technology that uses a mild stimulation of the brain to treat a variety of mood disorders, specifically Anxiety, Depression, and Insomnia.

The waveform of Nexalin is administered by placing medical grade conductive pads produced specifically for the Nexalin device on the forehead and behind each ear, which are connected to the Nexalin device with thin cables. The patient is placed in a reclining chair for the duration of a treatment session, which typically lasts for approximately forty minutes. For more information go to Nexalin Advanced Therapy. The disorders usually treated share a similar biochemistry with Parkinson's Disease. The intended effect appears to be like a milder version of DBS (Deep Brain Stimulation) but without using surgery as DBS does. In January 2008, a number of Parkinson's Disease patients carried out their own informal study. For more information go to ParkinsonsRebels.

 

8th October 2008 - New research

THE EFFECT OF RASAGILINE ON PARKINSON'S DISEASE

Fortschritte der Neurologie Psychiatrie [2008] 76 (10) : 594-599 (Jost WH, Klasser M, Reichmann H.)
Complete abstract

Rasagiline (Azilect) is a is a MAO-B inhibitor that is sometimes used for the treatment of Parkinson's Disease on its own, or by people who are taking L-dopa, who are having end of dose fluctuations. This large study gave special attention to the effect of Rasagiline on the patients' quality of life. Different aspects of quality of life were rated by the patients using the self-rating Parkinson's Disease Questionaire (PDQ-39) and the Columbia University Rating Scale (CURS). In addition, patients documented the number of hours spend in the OFF-state. Rasagiline was found to be most used alongside L-dopa (in 82% of people taking it), and then by people taking dopamine agonists (in
66% of cases). The symptom score was reduced by 22% using Rasagiline.

The proportion of patients with OFF-periods, which is the main purpose of its use, reduced from 66% to 49%. Time spent in the OFF period was also reduced from an average of 2 hours to 45 minutes. Quality of Life improved by 15%. Rasagiline was found to give better effects than Selegiline in every respect. Besides the side effects that it causes, Rasagiline will eventually lead to an opposite effect due to a biochemical process called "feedback inhibition". This is a means the body uses to counteract anything artifical imposed on it.

 

3rd October 2008 - New review

PARAQUAT AS A CAUSE OF PARKINSON'S DISEASE

Paraquat is the trade name for N,N'-Dimethyl-4,4'-bipyridinium dichloride, a quaternary ammonium herbicide. Other members of this class include diquat, cyperquat, diethamquat, difenzoquat and morfamquat. The compound is widely used as a quick-acting, non-selective herbicide. It kills green plant tissue on contact and is redistributed within the plant but does not harm mature bark. Paraquat was first produced for commercial purposes in 1961 by ICI (now Zeneca) and is today among the most commonly used herbicides. Pesticides are known to be associated with an increased rate of Parkinson's Disease [1].

Common means : Paraquat is used as a herbicide. There is a greatly increased likelihood of developing symptoms by people involved in horticulture and agriculture [2]. Pesticides are also known to affect well water [3].

Means of toxicity : 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.

Symptoms : Paraquat is known to kill dopaminergic neurons in mice [4, 5], and is associated with the symptoms of Parkinson's Disease in humans [6]. However, it is claimed that Paraquat only potentiates the effect of Maneb - another fungicide [7, 8], and that is has no effect on humans on its own [9].
                                                                                                                                                                     References : [1] Neurology [1998] 50 (5) : 1346-1350 (J.M.Gorell, C.C.Johnson, B.A.Rybicki, E.L.Peterson, R.J.Richardson); [2] Scandinavian journal of work, environment & health. [2000] 26 (4) : 359-362 (F.Tuchsen, A.A.Jensen); [3] Pesticides in well water : http://www.pueblo.gsa.gov; [4] Antioxidants & redox signaling [2005] 7 (5-6) : 649-653 (D.Bonneh-Barkay, W.J.Langston, D.A.Di Monte); [5] Brain Research [1999] 823 (1-2) : 1-10 (A.I.Brooks, C.A.Chadwick, H.A.Gelbard, D.A.Cory-Slechta, H.J.Federoff); [6] Neurology [1997] 48 (6) : 1583-1588 (H.H.Liou, M.C.Tsai, C.J.Chen, J.S.Jeng, Y.C.Chang, S.Y.Chen, R.C.Chen); [7] Journal of Neuroscience [2000] 20 (24) : 9207-9214 (M.Thiruchelvam, E.K.Richfield, R.B.Baggs, A.W.Tank, D.A.Cory-Slechta); [8] Brain Research [2000] 873 (2) : 225-234 (M.Thiruchelvam, B.J.Brockel, E.K.Richfield, R.B.Baggs, D.A,Cory-Slechta); [9] Klinische Wochenschrift [1988] 66 (22) : 1138-1141 (T. Zilker, F.Fogt, M.Von Clarmann)

 

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