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Dopamine biosynthesis

The primary fault in Parkinson's Disease is that, whatever the cause, there is insufficient dopamine.Dopamine is formed in the dopaminergic neurons by the following pathway :

L-tyrosine >>> L-dopa >>> Dopamine

The first step is biosynthesised by the enzyme Tyrosine 3-Monooxygenase [1.14.16.2] (which is morecommonly called by its former name tyrosine hydroxylase). The following is the complete reaction :

L-tyrosine + THFA + O2 + Fe2+ >>> L-dopa + DHFA + H2O + Fe2+

So for L-dopa formation, L-tyrosine, THFA (tetrahydrofolic acid), and ferrous iron are essential. The activityof this enzyme is often as low as 25% in Parkinson's Disease, and in severe cases can be as low as 10%.This indicates that one or more of the elements required for the formation of L-dopa are in insufficientquantities.

The second step in the biosynthesis of dopamine is biosynthesised by the enzyme Aromatic L-amino aciddecarboxylase [4.1.1.28] (which is more commonly called by its former name dopa decarboxylase). Thefollowing is the complete reaction :

L-dopa + pyridoxal phosphate >>> dopamine + pyridoxal phosphate + CO2

So for dopamine biosynthesis from L-dopa, pyridoxal phosphate is essential. The activity of the enzymerises and falls according to how much pyridoxal phosphate there is. The level of this enzyme in Parkinson'sDisease can also be around 25% or even far less.

Coenzymes involved in Dopamine biosynthesis

Besides two enzymes being required for the formation of dopamine from L-tyrosine (L-tyrosine >>> L-dopa>>> Dopamine), three coenzymes are also required. Enzymes are substances that will enable a specific

chemical reaction to take place in the body. Coenzymes are substances that assist enzymes. Someenzymes (including those involved in dopamine biosynthesis) will not function without coenzymes.

The three coenzymes involved in the formation of dopamine are : THFA (for L-tyrosine to L-dopa), Pyridoxalphosphate (for L-dopa to dopamine), and NADH (for the formation of THFA and Pyridoxal phosphate). Theyare made from vitamins via the following means :

Folic acid >>> Dihydrofolic acid >>> Tetrahydrofolic acid

Pyridoxine >>> Pyridoxal >>> Pyridoxal 5-Phosphate (this requires zinc as a cofactor)

Nicotinamide >>> NMN >>> NAD >>> NADH (or NADP) >>> NADPH

PART 3 : CELL DAMAGE

The first step in the formation of dopamine (L-tyrosine > L-dopa > dopamine) is the formation of L-dopa fromL-tyrosine.

L-dopa is normally formed in the dopaminergic neurons by the following pathway :

L-tyrosine + THFA + O2 + Fe2+ >>> L-dopa + DHFA + H2O + Fe2+

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There are two problems with this reaction not working. Primarily, if somebody does not form L-dopa, they willalso lack the dopamine required to prevent Parkinson's Disease from occurring. No L-dopa formation endsup in somebody developing Parkinson's Disease.

However, there is also a cellular symptom of a failure to form L-dopa from L-tyrosine. This is the cell damagethat occurs in Parkinson's Disease.

The primary natural means via which cell damage can occur in Parkinson's Disease is due to the reactionfrom L-tyrosine to L-dopa not taking place. The following is what should happen :

L-tyrosine + THFA + O2 + Fe2+ >>> L-dopa + DHFA + H2O + Fe2+

However, if for example, the THFA in the above reaction is lacking, the following can happen instead :

L-tyrosine + Fe2+ + O2 >>> L-tyrosine + Fe3+ + O-2 (superoxide anion)

As can be seen there is no L-dopa formed in the faulty reaction, and the superoxide anion is formed instead.The superoxide anion is one of the most highly destructive elements in cells. OXIDATIVE DAMAGE.So you get a double problem : symptoms of Parkinson's Disease and cell damage.

The formation of L-dopa can also fail to take place if L-tyrosine is deficient.

So the simplest means of preventing cell damage from taking place is to ensure that you have thosesubstances required for the formation of L-dopa, which are L-tyrosine, THFA (which is made from thevitamin folic acid using nicotinamide), and ferrous iron.

However, many people have instead tried to solve the problem of cell damage by other means, largelybecause they did not known the primary cause of the cell damage.

Vitamin C and Vitamin E have been used to try to help to prevent cell damage in Parkinson's Disease. Thisis because they are claimed to assist in two enzyme reactions in the brain that get rid of the superoxideanion once it has been formed :

Superoxide Dismutase [1.15.1.1] : 2O-2 + 2H+ >>> H2O2 + O2

Catalase [1.11.16] : H2O2 >>> H2O + 1/2 O2

G proteins

In order to relieve Parkinson's Disease, dopamine (or dopamine agonists) must stimulate dopaminereceptors, which must in turn stimulate the G proteins :

L-tyrosine > L-dopa > dopamine > dopamine receptors (D2, D3, D4) > G proteins

G proteins consist of three parts : alpha - beta - gamma, that are lined to each other. There are three typesof beta unit (1, 2, 4), and seven types of gamma unit (2, 3, 4, 5, 7, 10, 11). However, they do not mattermuch to Parkinson's Disease. What matters to Parkinson's Disease are the alpha subunits, because it isactually these that ultimately relieve (or aggravate) Parkinson's Disease. There are five types :

G proteins that aggravate Parkinson's Disease : Gs 1 alpha G proteins that relieve Parkinson's Disease : Gi1 alpha, Gi 2 alpha, Gi 3 alpha G proteins that have little effect on Parkinson's Disease : Go alpha

The sole purpose of dopamine (or dopamine agonists) stimulating dopamine receptors is to cause the alphasubunits (the active part of G proteins) to break away from the rest of the G protein. Without this occurringalmost everybody would have Parkinson's Disease. Once the alpha part of G proteins is released, via cyclic

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AMP, it takes the final action in the series of event that leads to the ridding of Parkinson's Disease, which isto inhibit the cells it has effect on.

Alpha-synuclein is a normalprotein found in the brain. It is predominantly apresynapticneuronal protein ofunknown function, but can also be found inglial cells.

Recent evidence suggests that alpha-synuclein functions as a molecular chaperone in the formation ofSNARE complexes.

Normally an unstructured soluble protein, alpha-synuclein can aggregate to form insoluble fibrils inpathological conditions characterized byLewy bodies, such as Parkinson's disease,dementia with Lewybodies, and multiple system atrophy. Alpha-synuclein is the primary structural component of Lewy bodyfibrils. In addition, an alpha-synuclein fragment, known as the non-Abeta component (NAC) is found inamyloid plaques inAlzheimer's disease.

In rare cases of familial forms ofParkinson's disease there is a mutation in thegenecoding for alphasynuclein. Threepoint mutationshave been identified thus far: A53T, A30P and E46K. In addition,triplication of the gene appears to be the cause of Parkinson's disease in another lineage.

Antibodies against alpha-synuclein have replaced antibodies againstubiquitin as the gold standard forimmunostaining of Lewy bodies.

Lewy bodies are abnormal aggregates ofproteinthat develop insidenerve cells.

They are identified under themicroscopewhen histologyis performed on the brain. They appear asspherical masses that displace other cell components. There are two morphological types: classical (brainstem) Lewy bodies and cortical Lewy bodies. A classical Lewy body is aneosinophiliccytoplasmic inclusionthat consists of a dense core surrounded by a halo of 10-nm wide radiating fibrils, the primary structuralcomponent of which isalpha-synuclein. In contrast, a cortical Lewy body is less well-defined and lacks thehalo. Nonetheless, it is still made up of alpha-synuclein fibrils.

A Lewy body is composed of the proteinalpha-synuclein associated with other proteins such asubiquitin,neurofilament protein, andalpha B crystallin. It is believed that Lewy bodies represent an aggresomalresponse in the cell.

Dyskinesia is a medical condition meaning the person afflicted makes bador abnormal movements.Dyskinesia is sometimes caused by long-term use ofanti-psychoticdrugs or otherdopamine antagonistslike the antiemeticmetoclopramide. The effect of these drugs can be tardive, meaning the dyskinesiacontinues or appears even after the drugs are no longer taken (seeTardive dyskinesia).

Akinesia is the inability to initiate movement, due to problems with selecting and activatingmotor programsin thebrain. It is a common consequence ofParkinson's diseasecausingdopamine loss in the directpathway of movement.

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Dopamine is synthesized in the body (mainly by nervous tissue and adrenal glands) first by the dehydrationof the amino acid tyrosineto DOPA by tyrosine hydroxylase and then by thedecarboxylationofDOPAbyaromatic-L-amino-acid decarboxylase. Inneurons, dopamine is packaged after synthesis into vesicles,which are then released in response to the presynaptic action potential. The inactivation mechanism ofneurotransmission are 1) uptake via a specific transporter; 2) enzymatic breakdown; and 3) diffusion. Uptake

back to the presynaptic neuron via the dopamine transporteris the major role in the inactivation of dopamineneurotransmission. The recycled dopamine will face either breakdown by an enzyme or be re-packaged intovesicles and reused.

Treatments for PD

[edit]

Levodopa

The most widely used form of treatment is L-dopa in various forms, although due to feedback inhibition, L-

dopa treatment causes a reduction in the endogenous formation of L-dopa. Levodopa was discoveredas a Parkinson's treatment byArvid Carlsson. L-DOPA is a dopamine precursor that is transfomed intodopamine by dopa-decarboxylase, present in the pre-synaptic terminals of dopaminergic neurons present inthe basal ganglia. However, only 1-5% of L-DOPA makes it's way to this target site. The remaining 95% ofthe remaining L-DOPA is converted to dopamine in the periphery by enzymes and is rapidly absorbed intothe bloodstream where it causes side effects including nausea and dizzyiness. Also Oxidativedisadvantages. Levodopa treatment may further accelerate the death of neurons in the parscompacta of the substantia nigra through heightened oxidative stress.

Therapy for Parkinson disease typically requires an evolving regimen of multiple medications. Medicating tocontrol the side effects of other medications contributes to polypharmacy. To treat the side effects caused bythe L-DOPA in the plasma, a drug needed to be developed to successfully inhibit the dopa decarboxylaseoutside of the central nervous system. Such drugs need to be large molecules that are hydrophillic. Thedrug, carbidopa, does this and reduces the effective dose of L-DOPA by 75%. Together, L-DOPA is

marketed with carbidopa in one pill as Sinemet.

Unpredictable absorption and transport of levodopa across the blood-brain barrier.

To complement Sinemet, Talcopone (Tasmar), was developed. Talcopone inhibits the COMT enzyme,thereby prolonging the effects of L-Dopa. This too has side effects. Tolcapone has been linked to possibileof liver failure and has been pulled from the market in Canada. It is still available in the United States.

A similar drug, entacapone was released in 2000 and has similar efficacy but has not been shown to causesignificant alterations of liver function.

Foods rich in proteins can reduce the uptake of levodopa, because some amino acids compete withlevodopa for cellular receptor sites. This can usually be dealt with by offsetting medication and meal times:consuming the majority of required proteins towards the evening allows patients to use dopaminemedication more effectively during the morning and mid-day when mobility is more critical.

[edit]

Dopamine Agonists

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Other treatments, such as the Dopamine-agonists, bromocriptine(Parlodel), pergolide (Permax),pramipexole (Mirapex) andropinirole (Requip) exist and are moderately effective. These have their own sideeffects including those listed above in addition to somnolence, hallucinations and /or insomnia. There arealso some reports of people suddenly falling asleep while on these agonists. Dopamine agonists initiallystimulate the dopamine receptors but then make them progressively less sensitive, thereby increasing thesymptoms.

AADC/VMAT gene therapy enhances the effect of L-DOPA treatment, higher and sustained levels ofdopamine delivery.

[edit]

MAO-B Inhibitor

Selegiline (Eldepryl) reduces the symptoms by inhibiting monoamine oxidase-B (MAO-B), which inhibits thebreakdown of dopamine secreted by the dopaminergic neurons in the basal ganglia. By-products ofselegiline include amphetamine and methamphetamine - each can have side effects that kill Dopaminergicneurons, thus worsen the clinical case. Use of L-DOPA in conjunction with Selegiline has increased mortality

rates that have not been effectively explained.

[edit]

SSRI's and SSNRI's

Dopamine deficiency is central, but deficits of serotonin, norepinephrine, and acetylcholine are also typical.The depression and anxiety states that predominate when serotonin and norepinephrine are deficient areoften treated with selective serotonine reuptake inhibitors (SSRIs) like Paxil, Zoloft, or Celexa; there isemerging evidence that the SSNRI (selective serotonin and norepinephrine reuptake inhibitor) Effexor maybe particularly effective in Parkinson's disease because it augments two deficient neurotransmitters.

Amphetimine-like drugs (Ritalin, Concerta) are being prescribed with increasing frequency to treat theAttention Deficit Disorder (ADD)-like attention problems that are almost universal in Parkinson's disease.

[edit]

Surgical Interventions

Surgical interventions are an active area of current research, anddeep brain stimulationis presently themost popular and effective such treatment. In the future, implantation of cells genetically engineered toproduce dopamine or stem cells that transform into dopamine-producing cells may become available. Eventhese, however, will not constitute cures because they do not address the widespread loss of activity inseveral different types of cells in the brain and even for the dopamine-producing cells, do not re-establish allof the original connections with neighboring brain cells.

Transplantation of embryonic dopamine neurons for severe Parkinsons disease. Those with less severedisease, improved significantly.

Nutrients

Nutrients have been used in clinical studies and are widely used by people with Parkinson's Disease inorder to partially treat Parkinson's Disease or slow down its deterioration. The L-dopa precursor L-tyrosinewas shown to relieve an average of 70% of symptoms.[14]Ferrous iron, the essential cofactor for L-dopabiosynthesis was shown to relieve between 10% and 60% of symptoms in 110 out of 110 patients.[15][16] Alsoused alongside existing treatments is a Parkinson's Disease supplementthat contains both of these

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substances and all the other nutrients required for dopamine formation. More limited efficacy has beenobtained with the use of THFA, NADH, and pyridoxine - coenzymes and coenzyme precursors involved indopamine biosynthesis. Vitamin C and Vitamin E in large doses are commonly used by patients in order tolessen the cell damage that occurs in Parkinson's Disease. This is because the enzymes SuperoxideDismutase and Catalase require these vitamins in order to nullify the superoxide anion, a toxin commonlyproduced in damaged cells. Coenzyme Q10 has more recently been used for similar reasons.

[edit]

Physical exercise

Regular physical exercise and/or therapy are beneficial to the patient and essential for maintaining andimproving mobility, flexibility, balance and a range of motion, and for a better resistance against many of thesecondary symptoms and side effects. There is increasing evidence that exercise is both neuroprotectiveagainst the development of Parkinson's disease, and also ameliorative of both severity of symptoms, andalso possibly of progression. "Alternative" exercise modalities such as yoga, tai chi, and dance may alsohold promise as rehabilitation therapies, due to their integration of movement, thought, feeling, and sensoryexperience. Exercise has also been shown to effectively improve mild-moderate/ depression.

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