A deficiency of dopamine is associated with Parkinson's disease.?

A deficiency of dopamine is associated with Parkinson's disease.
Discuss or research your knowledge regarding Parkinson鈥檚 disease.

here is a good link to look at... http://tcw2.ppsw.rug.nl/~vdbosch/pd.html

Parkinson's disease (PD) is believed to be caused by a deficiency of dopamine. Dopamine is a neurotransmitter, a chemical messenger between nerve cells in the mammalian brain. In this paper I explore how dopamine is exactly related to PD, and how insights about that relation are used to understand and treat PD.

After a general introduction, I first go into the basics of the working of nerve cells and signal transmission between them. Then I go into the basal ganglia, the neural circuitry that partly controls voluntary movement, and how a defect in it causes Parkinsonian symptoms. I close this paper with a short survey of treatments that aim to restore neural communication in the brains of PD patients back to normal







People with Parkinson's Disease (PD) suffer an increasing motor behaviour impairment, usually at an older age. The primary symptoms include: muscular rigidity, resting tremor, difficulty with movement initiation (bradykinesia), slowness of voluntary movement, difficulty with balance, and difficulty with walking. This disease was named after the English MD. James Parkinson, who in 1817 was the first person to describe these symptoms as 'the shaking palsy'.

dopamine deficiency
More than a century later, one believes that the cause of the disease is a dopamine deficiency in the basal ganglia of the brain. Dopamine is a neurotransmitter, a chemical messenger in the nervous system. In PD the neural cells which produce dopamine deteriorate. When these neurons start to disappear, the normal rate of dopamine production decreases. It was discovered that when dopamine supply is abnormally low, Parkinson's symptoms start to appear. Next to PD's primary symptoms mentioned above, a patient may also start to suffer from secondary symptoms which include: depression, senility, postural deformity, and difficulty in speaking.

Dopamine is synthesised in the presynaptic terminal by several metabolic pathways (see Figure 2). First tyrosine in the cell is converted to L-DOPA with the help of the enzyme tyrosine hydroxilase (TH). L-DOPA on its turn is converted into dopamine by the enzyme aromatic amino acid decarboxylase (AADC). The synthesised dopamine molecules in the presynaptic terminal are then taken up by synaptic vesicles. After the dopamine is released from the vesicles into the synaptic cleft, the remaining molecules are taken back into the synaptic terminal by transporters in the membrane. There they are transported back into vesicles or broken down to DOPAC by the enzyme monoamine amine oxidase type B (MOA-B)