Parkinsonís disease is a progressive neurological condition
classified as a neurodegenerative disorder associated with a
loss of dopamine production in the brain. Clinically, signs of
Parkinsonís disease (PD) typically include rigidity, resting
tremor, postural changes such as stooping and akinesia, defined
as the absence or loss of voluntary motion.1
Parkinsonís disease arises from the loss of sufficient dopamine
production in the portion of the brain called the substantia
nigra. To understand Parkinsonís disease, it is necessary to
have a brief understanding of where the dopamine-producing cells
are located. The basal ganglia is a round mass in the center of
the brain that includes the substantia nigra that contains
dopaminergic (dopamine-producing) cells.2
The basal ganglia is located at the base of the cerebral
cortex that helps control coordination and movement. Dopamine is
a neurotransmitter responsible for controlling voluntary
movement and coordination. The death of these dopaminergic cells
is responsible for this loss of coordination and voluntary
In the majority of individuals with Parkinsonís disease the
cause remains unclear, although it is strongly associated with
environmental toxins, such as long term exposure to industrial
solvents, Rotenone, MPTP, and welding, in addition to excess
oxidative damage and genetic causes.3
Studies conducted on Parkinsonís patients from 2001 through
2008 have concluded that PD may be caused by genetic
susceptibility to neurotoxins. A 2008 study in the Faroe Islands
concluded that ďthe high frequency of PD in the Faroes is most
likely the result of interactions between multiple genetic and
environmental factors, still to be identified.Ē4,5
However, the most powerful evidence that Parkinsonís disease
is caused by environmental exposures and not hereditary factors
comes from the studies showing that the degree of hydrocarbon
solvent exposure during a personís lifetime is a major risk
factor for Parkinsonís. This began when groups of patients with
Parkinsonís disease revealed a chronic history of hydrocarbon
Researchers then examined 990 Parkinsonís patients. Exposure
to hydrocarbon solvents directly correlated to disease severity
and inversely correlated to latency period. Nine blue collar
occupations accounted for 91.1 percent of exposures. The
conclusion of the study was that ďOccupations involving the use
of hydrocarbon solvents are a risk factor for earlier onset of
symptoms of PD and more severe disease throughout its course.
Hydrocarbon solvents may be involved in the etiopathogenesis of
PD, which does not have a major genetic component.Ē≠
Functions of the Substantia Nigra
- Controls Voluntary Movement
- Produces the Neurotransmitter Dopamine
- Regulates Mood
Hydrocarbon solvents cause damage to cells by a process
called lipid peroxidation, which is cell membrane damage caused
by free radicals attacking the fatty acid layers in the
membranes. Numerous other environmental neurotoxins have been
shown to work through free radical damage. Antioxidants and
nutritional supplements have been shown to block these
free-radical-mediated pathways very effectively and therefore
play an important part in protecting against neurotoxin-mediated
free radical damage.6-10 I would suggest performing an organic
acid test with environmental pollutants to identify xylene,
toluene, benzene and other contaminants in the body.
Below, I will outline an approach to optimal neurological
health. This approach includes using CoQ10-H2ô, choosing a
supplement that contains a synergistic blend of natural
substances designed to promote cognitive health, and adding a
formula specifically designed to promote neurite and dendrite
Improving Neurological Health
Coenzyme Q10 has been widely studied for its role in
neurological health due to its ability to help restore impaired
mitochondrial function. The 100 to 300 mitochondria in every
cell produce the vast majority of free radicals as a byproduct
of oxygen reduction. The brain is a high-fat content organ like
the liver and has low antioxidant capacity. CoQ10 therefore
becomes important because it provides protection from lipid
peroxidation. Coenzyme Q10 is part of the mitochondrial
respiratory chain and it also donates an electron to the
mitochondrial inner membrane to terminate free radical
reactions. CoQ10 helps to restore mitochondrial function, which
declines with age along with CoQ10 serum levels in humans.
The first significant clinical trial of Coenzyme Q10 in early
stage Parkinsonís patients was conducted in 2002. Subjects were
given 300, 600 or 1,200 mg per day of CoQ10 with 300 mg of
vitamin E. The CoQ10 and vitamin E were consumed for 16 months
or to a point where levodopa standard therapy was required. The
Unified Parkinson Disease Rating Scale (UPDRS) was used to
record functional decline between visits. A significant positive
association was observed between the CoQ10 dosage level and the
mean change in the UPDRS score. The conclusion of the study was
that coenzyme Q10 was well tolerated at all doses and was
effective ďin reducing the functional disability in patients in
the early stages of Parkinson disease.Ē11
The first generation of supplemental coenzyme Q10 (CoQ10-Ox),
which is the form used in the above study, although still
absorbed by the human body to produce some benefits, isnít
nearly as effective at increasing blood levels as its newer,
more biochemically active, second generation form, CoQ10-H2ô.
Many of the clinical studies that have shown positive
neurological effects used rather large doses of CoQ10. For
example, a 16-month randomized, placebo-controlled pilot trial
in 80 subjects with mild Parkinsonís disease found significant
benefits for oral CoQ10 at 1,200 mg per day. At this dose,
coenzyme Q10 appeared to slow functional deterioration.12
However, 1,200 mg per day is a substantial and expensive dose of
this antioxidant. Achieving similar benefits with a much lower
amount of CoQ10-H2ô would obviously be ideal.
High homocysteine levels are common in Parkinsonís patients.
The use of levodopa treatment in Parkinsonís patients further
depletes vitamin B12 and folic acid, two vitamins known to
reduce homocysteine levels. Increased homocysteine levels
accelerate dopaminergic cell death (dopamine-producing cells) in
Parkinsonís patients through neurotoxic effects.13,14
Choline and DMAE (Dimethylamino≠ethanol)
Choline and dimethylaminoethanol (DMAE) are the dietary
precursors of the brain neurotransmitter acetylcholine.
Acetylcholine plays a vital role in the cortical cholinergic
system. Abnormalities of the cortical cholinergic system
contribute significantly to the type of dementia found in
Parkinsonís disease and Alzheimerís disease. The enzymes that
manufacture acetylcholine from dietary choline or DMAE are
extremely low in Parkinsonís brains upon postmortem examination
of patients who had a history of the disease. Levels of choline
acetyltransferase (CAT), the enzyme that makes acetylcholine,
are severely depleted in Parkinson brains, creating a
Studies with animals show that choline is rapidly taken up by
the tissues and the cholinergic neurons in the brain where it
enhances both the release and the biosynthesis of acetylcholine.
Other studies have shown that choline supplementation protects
the brain from choline depleting chemicals. Studies
investigating the release of choline from the brain showed that
more choline was released in tissues from choline supplemented
rats than from controls. Supplemental choline is clearly a
protective mechanism against acetylcholine depletion in brain
cells whether the cause is from chemical or disease
Pyroglutamic acid (L-Pyroglutamic acid)
Pyroglutamic acid is a natural amino acid that has shown
brain cell protection in a variety of studies. It is present in
large amounts in the human brain, blood and cerebrospinal fluid.
Pyroglutamic acid has a number of cognitive-enhancing effects.
Pyroglutamic acid stimulates memory and the ability to focus.
The primary function of pyroglutamic acid as a protector of
brain cells (neurons) is to remove excess glutamate from the
brain. It does so by regulation of sodium-dependent glutamate
transport. In one key study, it stimulated sodium-dependent
transport of glutamate by 46 percent. Other studies reviewing
amino acid transport in the brain show pyroglutamic acid is a
key transporter of all amino acids in and out of the brain and
maintains total amino acid balance in that organ.18-19
Ginkgo biloba is a well-known herbal memory enhancer and
supplement known to improve brain circulation. Numerous human
trials with ginkgo have demonstrated that it improves cognitive
The latest 2008 trial with ginkgo lasting 42 months involved
118 patients 85 years and older who showed no evidence of any
cognitive decline. Using the standard Clinical Dementia Rating
test (CDR), researchers demonstrated that ginkgo biloba extract
reduced the progression of clinical dementia and protected
against memory decline.20
Reviews have focused on the biochemical mechanisms by which
ginkgo reduces or blocks neuronal (brain cell) death. Nuclear
transcription factor (NFkappaB) is believed to be most
responsible for brain cell death by causing brain cells to
induce apoptosis, or cellular suicide. Ginkgo biloba blocks this
pathway through its antioxidant properties.21
Vinpocetine is a compound isolated from the Vinca family of
plants and has been proven to be a potent neuroprotective agent
in humans and animals. Vinpocetine increases blood circulation
and metabolism in the brain. Animal studies show that
vinpocetine reduces the loss of neurons caused by decreased
In three human trials with older persons, vinpocetine
produced more improvement than placebo on global cognitive tests
of memory, attention and concentration. The adults in the study
had either poor brain circulation or dementia-related diseases,
including Parkinsonís or Alzheimerís disease.22
Vinpocetine is a supplement of choice in Europe as a
neuroprotective agent. Diseases of brain circulation are major
contributors to all dementia-related diseases, including
Parkinsonís and Alzheimerís. In humans, vinpocetine works by
increasing cerebral glucose uptake and supports glucose
metabolism in regions of the brain where patients have had a
stroke. Two week long supplementation with vinpocetine also
increased cerebral blood flow in the thalamus, basal ganglia and
visual cortex of the brain in both normal volunteers and in
In animal models of Parkinsonís, huperzine A prevents the
loss and degeneration of dopamine-producing neurons in the
substantia nigra caused by two powerful neurotoxins, both of
which have been detected in Parkinsonís brains. The substantia
nigra is the exact area of the brain in humans where
dopamine-producing cells are lost resulting in Parkinsonís.25
In a trial of 104 patients with presenile and senile simple
memory disorders, memory improved in 2 weeks in subjects using
huperzine A.26 In the same study, an additional 56 patients had
multi-infarct dementia, a more serious form of dementia. All
patients in this subgroup responded well to 4 weeks of huperzine
A at a slightly higher dose.26
Neuron Growth Factors
In previous articles in this newsletter, it was shown that
when acetyl carnitine and acetyl carnitine arginate are combined
together they dramatically stimulate nerve growth factor levels
in the brain. In a study of mouse brain neurons, the presence of
nerve growth factor protected the brain cells against glutamate
toxicity and 59 percent of the brain cells survived the massive
influx of glutamate as opposed to no survival in the brain cell
Combining acetyl carnitine and acetyl carnitine arginate with
uridine, ginkgo biloba and gotu kola can have an even more
pronounced effect on neurological health.
One of the best approaches to ensuring optimal neurological
health is to use a supplement that contains Vitamins B12, DMAE (Dimethylaminoethanol),
choline, pyroglutamic acid, ginkgo biloba, vinpocetine and
huperzine A. This approach can be made even more effective when
combined with acetyl carnitine, acetyl carnitine arginate and
other compounds that synergistically produce nerve growth factor
and other brain growth factors necessary for regrowth of brain
communication pathways and for protection of brain cells.
Finally, adding CoQ10-H2ô can provide additional neurological
Get Neuron Growth Factors
source of nutrients and supplements.
did we qualify them ?
1. Stedmanís Medical Dictionary, 29th edition,
Williams & Wilkens, Publishers.
2. Parkinsonís Disease: An Overview,
University of Minnesota Department of Neurology, 2007, U. of
3. Pazzoli, G., Canesi, M., Antonini, A.,
Righini, A. Hydrocarbon exposure and Parkinsonís disease.
Neurology. 2000 Sep 12; 55(50:667-73.
4. Payami, H., Lee, N., Zareparsi, S.
Parkinsonís disease, CYP2D6 polymorphism, and age. Neurology.
2001 May 22; 56 (10): 1363-70.
5. Halling, J., Petersen, MS., Grandjean, P.
Genetic predisposition to Parkinsonís disease: CYPD26 and HFE in
the Faroe Islands. Pharmacogenet Genomics. 2008 Mar; 18 (3):
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7. Lee, SR., Im, KJ., Suh, SI., Jung, JG.
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