PARKINSON'S DISEASE NEWS
30th December 2007 - New research
PARK 7 (dj-1) - a genetic CAUSE of parkinson's disease
Neuroscience Letters  Dec 4; [Epub ahead of print] (Maita C, Tsuji S, Yabe I, Hamada S, Ogata A, Maita H, Iguchi-Ariga SM, Sasaki H, Ariga H.) Complete abstract
DJ-1 is a gene, that when mutated is believed to be a genetic cause of Parkinson's Disease known as PARK7. For more information go to PARK 7. The function of DJ-1 is in protein formation and oxidative stress. Its loss of function is thought to be related to age of onset, mode of progression and clinical severity of both inherited and sporadic genetic forms of Parkinson's Disease. However, in this study, results showed that DJ-1 was secreted into the serum of both healthy controls and people with Parkinson's Disease. There was no significant difference between the levels of secreted DJ-1 in the two groups. There was also found to be no relationship between the amount of DJ-1 secreted, and the age of onset and clinical severity of Parkinson's Disease, and there was no relationship with the amount of oxidative stress either.
The lack of difference in the results brings in to question whether DJ-1 is actually a genetic cause of Parkinson's Disease. It was already known that genetic causes of Parkinson's Disease at most normally only incline somebody to Parkinson's Disease rather than make Parkinson's Disease inevitable.
29th December 2007 - News report
Most older adults have brain disease
Both Parkinson's Disease and Alzheimer's Disease become progressively more common with age. Results of a brain autopsy study indicate that most older adults at the end of their life have significant brain pathology (disease), regardless of the presence or absence of outward signs of dementia.
Only 1 in 7 older people were free of brain disease. Most older persons with dementia had more than one type of pathology in their brain causing the impairment. "This most commonly was Alzheimer's disease pathology and cerebral infarcts (strokes), followed by Alzheimer's disease and Lewy body disease, a disease related to Parkinson's disease", the author said. "Older persons can often handle one pathology in their brain, but the burden of more than one pathology may tip them over the threshold of clinical dementia." For more information go to the Complete article.
27th December 2007 - New research
trichloroethylene - new TOXIC CAUSE of parkinson's disease
Annals of Neurology  Dec 21; [Epub
ahead of print] (Gash DM, Rutland K, Hudson NL, Sullivan PG, Bing G, Cass
WA, Pandya JD, Liu M, Choi DY, Hunter RL, Gerhardt GA, Smith CD, Slevin
JT, Prince TS)
Industrial coworkers with Parkinson's disease and Parkinsonism were examined who had been subjected to chronic exposure to trichloroethylene. 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. Coworkers more distant from the trichloroethylene source, receiving chronic respiratory exposure, displayed many features of Parkinsonism, including significant motor slowing. Neurotoxic actions of trichloroethylene were also demonstrated in accompanying animal studies. Trichloroethylene joins other toxins as a risk factor for Parkinsonism.
26th December 2007 - New research
the effect of tea on parkinson's disease
American journal of Epidemiology  Dec 20; [Epub ahead of print] (Tan LC, Koh WP, Yuan JM, Wang R, Au WL, Tan JH, Tan EK, Yu MC.) Complete abstract
A very large study assessed dietary and lifestyle factors in relation to Parkinson's disease. Just as was confirmed by previous studies, current versus never smokers exhibited a reduced risk of Parkinson's disease, and caffeine intake was inversely related to Parkinson's disease risk.
Contrary to what is often claimed, green tea drinking was completely
unrelated to Parkinson's disease risk. However, black tea, a
caffeine-containing beverage, lowered the risk of Parkinson's disease.
Yet it was not affected by the total caffeine intake as might have been
assumed. This led the researchers to suggest that ingredients of black tea
other than caffeine appear to be responsible for the beverage's inverse
association with Parkinson's disease. However, they did not know what
these ingredients were.
24th December 2007 - News report
ADENOSINE SUBSTITUTES FOR DBS SURGERY
DBS is a method of reducing symptoms that uses electrodes implanted into the brain. For more information go to Deep Brain Stimulation. It has long been debated exactly how the procedure works. Adenosine, a brain chemical most widely known as the cause of drowsiness, has now been found to be central to the effect of DBS.
Adenosine in the brain is largely a byproduct of the chemical ATP, the source of energy for all our cells. DBS causes the release of ATP, which is then broken down into adenosine. The extra adenosine then reduces abnormal signaling among the brain's neurons. However, even without DBS surgery, adenosine reduced abnormal brain signaling. The researchers have consequently suggested that it may be possible to enhance the effect of DBS by using substances that enhance adenosine, or to using adenosine in a way that does not even involve DBS surgical procedure at all. For more information go to the Complete article.
22nd December 2007 - News report
NEW BLOOD TEST FOR PARKINSON'S DISEASE
A simple blood test that can diagnose Parkinson's disease could be available from next year, according to Diagenic. The test could lead to earlier diagnosis. The research, which was funded by the Michael J Fox Foundation, suggests that genetic alterations caused by the condition can be detected by chemical changes in the blood. Diagenic claim that being able to base a diagnosis on the analysis of gene expression signatures in sample material taken at a distance from the site of the disease, such as peripheral blood, has clear advantages for both patients and clinicians. For more information go to Diagenic.
As part of this work
they also discovered 500 genes that are affected by Parkinson's Disease
which trigger chemical changes that can also be identified in blood
samples. DiaGenic's preliminary findings will be tested using blood
samples already collected from 300 patients. They expect to be able to
apply for a licence so that doctors could use the test by the end of next
For more information go to the
21st December 2007 - New research
Can Olfactory Testing Differentiate Parkinsonian Disorders ?
The Neurologist  13 (6) : 382-385
(McKinnon JH, Demaerschalk BM, Caviness JN, Wellik KE, Adler CH,
Each study examined different test methods : the University of Pennsylvania Smell Identification Test, and "Sniffin' Sticks". The University of Pennsylvania Smell Identification Test is moderately sensitive (77%) and specific (85%) for differentiation of Parkinson's Disease from other Parkinsonian syndromes, but is less specific (62%) for distinguishing Parkinson's Disease from multiple system atrophy. Olfactory testing can differentiate between Parkinson's Disease and other Parkinsonian disorders, but the diagnostic accuracy was not certain enough to justify its routine clinical use.
20th December 2007 - News report
KINESIA - A NEW MEANS OF ASSESSING PARKINSON'S DISEASE
Cleveland Medical Devices has been awarded $1.5 million to fund further development and clinical validation of Kinesia, a quantitative motor assessment system for evaluating Parkinson's disease symptom severity. Kinesia is a compact lightweight system worn on a patient's wrist and hand. For more information go to Kinesia.
The device monitors three-dimensional motion and electrical muscle activity (EMG) to objectively quantify the severity of Parkinson's disease symptoms, such as tremor, bradykinesia (slowed movements) and dyskinesias (wild, involuntary movements). Patients follow on screen video instruction while data is wirelessly transmitted to a computer to enhance user safety and comfort. A previous clinical study showed good correlation between Kinesia and the UPDRS. The UPDRS, a subjective assessment scale, is the current standard in rating Parkinson's symptom severity. For more information go to the Complete article.
19th December 2007 - News report
NEW METHOD OF DIFFERENTIATING BETWEEN PARKINSON'S DISEASE AND ESSENTIAL TREMOR
Tremor disorders are diagnosed by subjective clinical evaluation, which is associated with an error rate among general neurologists of 25% to 35%. Consequently, hundreds of thousands of people are being treated for Parkinson's Disease that don't actually have it, or that have mild Parkinson's Disease and a quite separate medical disorder that causes their tremor. Alseres Pharmaceuticals has started phase III clinical trials of Altropane, which is a new diagnostic molecular imaging agent being developed to aid in the differentiation of Parkinsonian Syndromes from non-Parkinsonian tremor.
Altropane is a molecular imaging agent that binds to the dopamine transporter (DAT) protein found on the surface of dopaminergic neurons, making it visible during "SPECT" imaging. Since most forms of Parkinsonian Syndromes result in decreased activity of dopaminergic neurons, it is expected that these patients have fewer DATs than do patients without Parkinsonian Syndromes. For more information go to the Complete article.
Analysis : The theory behind the use of Altropane appears to be scientifically sound. So if successful, Altropane could be of considerable benefit to the millions who have been, or will be, misdiagnosed with Parkinson's Disease. They make no mention of the f-Dopa PET scan, an existing method of physically determining Parkinson's Disease, that is little used because it is so expensive. For Altropane to be of widespread practical use it would have to be cheap enough to make it a standard procedure.
18th December 2007 - New research
THE CAUSE OF FATIGUE IN PARKINSON'S DISEASE
Revista de Neurologia  45 (12) :
725-728 (Katsarou Z, Bostantjopoulou S, Hatzizisi O, Giza E, Soler-Cardona
A, Kyriazis G.)
However, immunological factors have also been implicated. The purpose of this study was to assess fatigue in people with Parkinson's Disease in relation to depression and various immunological factors. People with Parkinson's Disease were found to suffer more from fatigue than other people. When depression was taken account of, immunological factors were found not to be the reason for the fatigue. It was depression rather than immunological factors that was most related to the cause of fatigue.
Analysis : The primary fault in Parkinson's Disease is the formation of dopamine. For more information go to Biochemistry of Parkinson's Disease. Besides affecting the muscles, dopamine stimulates the emotions. This is why the lack of dopamine that occurs in Parkinson's Disease can also cause depression. In other cell types dopamine goes on to produce noradrenaline and adrenaline. Noradrenaline and adrenaline both act as stimulants. So as somebody produces less dopamine, they will usually produce less noradrenaline and adrenaline as well, because they are both made from dopamine. So fatigue in Parkinson's Disease is not due to depression. Muscular symptoms, depression and fatigue experienced in Parkinson's Disease are all ultimately due to the same biochemical fault.
17th December 2007 - News report
FAST TRACK FOR PARKINSON'S DISEASE GENE THERAPY
The U.S. Food and Drug Administration has granted Fast Track Designation for Neurologix's experimental gene transfer procedure for the treatment of advanced Parkinson's Disease. The Neurologix procedure delivers a gene (glutamic acid decarboxylase, or GAD) to the subthalamic nucleus of the brain, where it makes an inhibitory neurotransmitter called GABA that helps to quiet the abnormal brain activity that is correlated with motor deficits characterizing Parkinson's disease.
Results of a Phase 1 clinical study showed that the procedure was well tolerated and resulted in improved motor function and brain metabolism for patients with advanced Parkinson's disease over the course of the one-year study. Neurologix is currently preparing to initiate a Phase 2 study by early 2008, subject to final FDA consent to the study protocol. For more information go to the Complete article.
Analysis : The approach does not address the primary fault in Parkinson's Disease, which is a lack of dopamine rather than a lack of GABA. If somebody did want to increase their GABA levels somebody could do it far more readily by taking the well established precursors and coenzyme precursors of GABA formation, which are glutamic acid and pyridoxine. Both of these nutrients are readily available and free of side effects.
15th December 2007 - New book
Living Well with Parkinson's Disease
Gretchen Garie, Michael J. Church, Winifred Conkling
"Living Well with
Parkinson's Disease : What your doctor doesn't tell you...that you need to
know" is a guide to Parkinson's Disease from two people who cofounded a
national support and advocacy organization. A couple who both have
Parkinson's Disease and live daily with the effects of the disease,
discuss diagnosis, treatment options, and the emotional consequences of
this difficult illness. They deal with how Parkinson's Disease affects
relationships; and the role of diet, supplements, and rest and relaxation;
strategies for navigating professional life and the maze of the
health-care system; as well as handling everyday challenges such as
buttoning a shirt or rolling over in bed, and more.
Click here for more details
14th December 2007 - News report
CAN GREEN TEA PROTECT AGAINST PARKINSON'S DISEASE ?
Researchers have suggested that the consumption of green tea, widely touted to have beneficial effects on health, can also protect brain cells. The authors investigated the effects of green tea polyphenols, a group of naturally occurring chemical substances found in plants that have antioxidant properties in an animal model of Parkinson's Disease.
The authors discovered that green tea
polyphenols protect dopamine neurons and that the effect increases with
the amount consumed. They claim that this protective effect is mediated by
inhibition of the ROS-NO pathway, a pathway that may contribute to cell
death in Parkinson's Disease. They hope that eventually "green tea
polyphenols may be developed into a safe and easily administrable drug for
Parkinson's disease.", and that "if green tea consumption can be shown to
have meaningful neuroprotective actions in patients, this would be an
extremely important advance."
For more information go to the
13th December 2007 - New research
DRUG INDUCED PARKINSONISM
Movement Disorders  Dec 7; [Epub ahead
of print] (Esper CD, Factor SA.)
Of those cases of Drug Induced Parkinsonism, 46% were found to be caused by Atypical antipsychotics, and 29% were caused by metoclopramide (which is sold as Reglan and various other names) - a drug used to treat nausea and vomiting, or to facilitate gastric emptying. Other drugs accounted for about 25% of cases of Drug Induced Parkinsonism. These people were kept on Parkinson's Disease drugs and also the drug that induced their symptoms. This is despite the fact that Drug Induced Parkinsonism is reversible when the drug that causes it is ceased.
12th December 2007 - New research
LIFE EXPECTANCY IN PARKINSON'S DISEASE
Journal of Neurology, Neurosurgery and Psychiatry  78 (12) : 1304-1309 (Ishihara LS, Cheesbrough A, Brayne C, Schrag A.) Complete abstract
Studies in different countries in Europe were used to assess life expectancy for people with Parkinson's Disease in comparison to normal life expectancy.
The life expectancy was : 38 years instead of the expected 49 years for those whose onset was 25-39 years old, 21 years instead of the expected 31 years for those whose onset was 40-64 years old, and 5 years instead of the expected 9 years for those whose onset was after they were 64 years old. The anticipated age of death was 71 instead of 82 for those whose onset was 25-39 years old, and was 88 instead of 91 for those whose onset was after they were 64 years old. In summary, life expectancy was found to be much shorter in Parkinson's Disease, regardless of the age of onset. An earlier age of onset lessened the life expectancy even further.
Analysis : As can be seen from the figures, Parkinson's Disease is not a fatal illness, because even in those with early onset there was a life expectancy of decades. Parkinson's Disease can reduce the ability to cope with certain medical disorders and thereby make fatality more likely. This is why some people are reported as having died of the complications of Parkinson's Disease. However, it is not indicated in the research whether this is the reason for the much lower life expectancy in Parkinson's Disease. There may be common factors that increase the likelihood of Parkinson's Disease and that quite independently lower life expectancy.
11th December 2007 - News report
24 HOUR VERSION OF REQUIP
The F.D.A. (the U.S. medical authority) has approved the sale of Requip XL 24-hour™, a once-daily prolonged release reformulation of the Parkinson's Disease drug Requip. For more information go to the Complete article. Requip® is a dopamine agonist, a class of drug increasingly recommended as first-line therapy.
The new once-daily
has been developed utilizing SkyePharma's Geomatrix™ prolonged release
technology. It aims at providing additional therapeutic benefits compared
with the current three times a day version of Requip, by evening out the
effect of the Requip, and simplifying the treatment regime for patients,
thus improving patient convenience and compliance. For more information go
9th December 2007 - New research
ANTI-Parkinson DRUG Mucuna pruriens shows antioxidant and chelating activity
Phytotherapy Research  Dec 7; [Epub ahead of print] (Dhanasekaran M, Tharakan B, Manyam BV.) Complete abstract
Mucuna Pruriens is the oldest treatment for Parkinson's Disease. In ancient India, as far back as 5000 B.C., they described the symptoms of Parkinson's Disease, which they treated using the seeds of Mucuna Pruriens. Mucuna Pruriens has been used continuously since then, and is presently being used progressively more as a replacement for L-dopa, due to the seeds of Mucuna Pruriens being a natural source of high quantities of L-dopa. For more information go to Mucuna Pruriens.
Researchers have shown that Mucuna Pruriens also possesses anti-oxidant qualities, which help to protect against cell damage, and also metal chelating activity, which helps to protect against excessive quantities of metals. It is suggested by the authors that the effect of Mucuna Pruriens may also be related to its antioxidant activity independent of the symptomatic effect.
Analysis : When comparing Mucuna Pruriens and modern forms of L-dopa such as Sinemet, Mucuna Pruriens has other advantages. Mucuna Pruriens is milder and so greatly lessens the problem of excessive dosage that often occurs with Sinemet. Mucuna Pruriens is far more adjustable in its dosages in comparison to Sinemet, which has only two possible dosages. Besides L-dopa, Sinemet contains a substance that prevents the breakdown of L-dopa before it reaches the cells. It is claimed that Mucuna Pruriens has the equivalent, but it is not certain if this is true.
8th December 2007 - New research
Complex I deficiency in Parkinson's disease
Brain Research  Nov 1; [Epub ahead of
print] (Parker WD Jr, Parks JK, Swerdlow RH.)
A study of Complex I activity in Parkinson's Disease brain has identified loss of activity in the substantia nigra (the part of the brain primarily affected in Parkinson's Disease). There were found to be increasingly significant losses of complex I activity in Parkinson's Disease as increasingly pure mitochondria were studied. There was little difference in the next steps in the energy producing process (Complexes II, III, and IV) when compared with people that did not have Parkinson's Disease.
Analysis : Complex I (NADH:ubiquinone oxidoreductase) needs Coenzyme Q10 in order to function properly. This may be why Coenzyme Q10 appears to have a beneficial effect in some people - because it is correcting the deficiency of Complex I that often occurs in Parkinson's Disease. However, it is not clear how this could positively affect Parkinson's Disease, because increasing energy production has no direct effect on increasing dopamine formation.
7th December 2007 - New research
PARKINSON'S DISEASE RELATIVES AT HIGHER RISK OF ESSENTIAL TREMOR
Movement Disorders  22 (11) : 1607-1614 (Rocca WA, Bower JH, Ahlskog
JE, Elbaz A, Grossardt BR, McDonnell SK, Schaid DJ, Maraganore DM.)
6th December 2007 - News report
PARKINSON'S DISEASE RELATIVES AT HIGHER RISK OF ANXIETY AND DEPRESSION
Because many patients with Parkinson's disease develop anxiety and depression after and even before the onset of the disease, researchers explored whether this tendency was present to a greater extent in family members of people with Parkinson's Disease.
Immediate relatives (brother, sister, mother, father, son or daughter) of people who have Parkinson's disease were found to at increased risk for developing depression and anxiety disorders. The risk is particularly increased in families of patients who develop Parkinson's disease before age 75. The authors emphasizes that the familial susceptibility factors may be genetic, environmental or a combination of the two, and that further research is needed to determine their exact nature. For more information go to the Complete article.
5th December 2007 - History
THE ROMANS TREATMENT OF TREMOR
The Roman, Aulus Cornelius Celsus (c25BC-c50AD), although apparently not a physician himself, compiled an encyclopedia entitled De artibus (25AD-35AD) that included De medicina octo libri (The Eight Books of Medicine). He advised against administering those who suffered tremor of the sinews with emetics or drugs that promoted urination, and also against baths and dry sweating. Relief from worry, rubbing of the limbs and their exercise by ball games and walking were indicated. The patient could eat whatever he wanted, but sexual activity should be restricted. If he should succumb, he should afterwards be rubbed in bed with olive oil, by boys, not men. Fine tremor was distinguished from a coarser shaking, which was independent of voluntary motion. So it resembled resting tremor. It could be alleviated by the application of heat and by bloodletting.
4th December 2007 : News report
development of a new class of drugs
It is suggested that selective activation of mGluR4 is one way to do this and could correct the circuitry that modulates motor excitability. Published research suggests that mGluR4 activators could work via two distinct mechanisms to alleviate symptoms of Parkinson's disease. For more information go to the Complete article.
Analysis : The primary biochemical fault in Parkinson's
Disease is insufficent formation of dopamine. Even in theory, this
approach can not increase dopamine formation, and so could not rid
Parkinson's Disease. However, having exhausted all drug approaches based
on dopamine, many pharmaceutical companies are now trying very different
non-dopamine approaches. Consequently, they would eventually mean merely
adding another drug to those already being taken.
3rd December 2007 : New book
Making the Connection Between Brain and Behavior : COPING WITH PARKINSON'S DISEASE
While patients and families are aware of the physical challenges that accompany Parkinson’s disease, few are prepared for the common behavioral issues that impact their quality of life, including depression, anxiety, dementia, paranoid delusions, and sleep disorders. "Making the Connection Between Brain and Behavior : Coping with Parkinson's Disease", the only one of its kind, focuses entirely on an area that most doctors overlook. Written in layman’s terms, it helps readers understand and cope with a wide variety of Parkinson’s-related behavioral issues and offers guidance on communicating with the healthcare team. Click here for more details
2nd December 2007 : New research
115 year old without any sign of dementia
Neurobiology of Aging  Nov 26; [Epub ahead of print] (Price JL.) Complete abstract
Up to 30 % of people with Parkinson's have dementia and it is claimed that almost all patients with Parkinson's disease develop dementia over time. Rightly or wrongly, Dementia is almost seen as an inevitable part of Parkinson's Disease and growing old. The Dutch woman, Hendrikje van Andel-Schipper (1890-2005) was the oldest person in the world until her death. For more information go to Hendrijke van Andel-Schipper.
She donated her body to science. So after her death an autopsy was carried out. There was no sign at all of dementia or Alzheimer's disease. Several similar non-demented cases aged 85-105 years have been reported previously, who had neurofibrillary tangles in the medial temporal lobe, but no deposition of amyloid plaques. Critical questions raised by the present study include what factors allowed her to be completely free of dementia despite being 115 years old. Hendrikje van Andel-Schipper had stated that the secret of her health was a serving of herring every day and drinking orange juice. She also drank Advocaat (an egg liqueur).
Analysis : Dementia is primarily due to a lack of acetylcholine, a substance produced in the brain. Acetylcholine is made in the brain from choline - a vitamin like substance. The richest sources of choline are eggs and oily fish (such as herrings and sardines). So her choline intake was inadvertently high, due to her daily herring consumption, enabling her to produce more acetylcholine. She also consumed daily orange juice - a rich source of vitamin C. Vitamin C is needed for Catalase, the primary enzyme required to prevent damage to the nerve cells. So rather than assuming that dementia is inevitable as people age, she is evidence that dementia can be prevented biochemically by consuming substances that the brain uses naturally in order to avoid it.
1st December 2007 : New research
anger in parkinson's disease
Movement Disorders  Nov 28; [Epub ahead of
print] (Macias Y, Benito-Leon J, Louis ED, Cano-Vindel A.)
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