Udaan(1997)Jai Mata Di Bol!

http://en.wikipedia.org/wiki/Psychosis
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Industry Pharmaceuticals
Founded 1996 (from merger)
Comtan- $420 M (2007)- Parkinson's disease
Sandimmune and Neoral- $944 M (2007)- Organ transplantation
The Taliban seized Kabul on September 27, 1996, and established the Islamic Emirate of Afghanistan.
http://en.wikipedia.org/wiki/Taliban
http://bjp.rcpsych.org/cgi/content/full/181/4/271
Dopamine and antipsychotic drug action revisited
H. M. JONES, MRCPsych and L. S. PILOWSKY, MRCPsych

Institute of Psychiatry, London, UK


A reasonable goal for effective, less-toxic treatment of schizophrenia is the regionally sensitive stabilisation of dopamine function, and not the blunderbuss dopaminergic paralysis induced by classical antipsychotic drugs. This selective targeting could come about by exploiting behaviour intrinsic to compounds with low D2 affinity, by designing compounds selective for dopamine receptor subtypes found at greater densities in limbic or cortical regions (for example D3 receptors), or by modulating dopamine release through action at alternative systems (novel candidates include serotonin, sigma and glutamate receptor sites). Such ideas are certainly relevant to current therapeutics and future drug development. Novel agents with specific action at presynaptic D3 autoreceptors controlling central dopamine release may offer more physiological modulation of dopamine than conventional antagonists (Reavill et al, 2000; Strange, 2001). It is apparent that as the neurochemical pathology of schizophrenia is not fully understood, and as many patients are only partially responsive or are insensitive to dopaminergic antagonism, many non-dopaminergic sites (especially those mediated by glutamate and serotonin) remain potent targets for future drug discovery. The availability of high- and low-affinity D2/D3 receptor antagonist antipsychotic drugs offers clinicians much choice, and the above data provide a rational evidence base for prescribing, tailored as far as possible to individual patient responses.
DOPAMINERGIC PATHWAYS AND RECEPTOR PHYSIOLOGY

Dopamine is one of the principal modulatory neurotransmitters in the brain. Dopamine systems arise from two primary midbrain clusters, the ventral tegmental area (A10) and the substantia nigra (A9), which have discrete projections to mesolimbic, mesocortical and striatal regions of the brain. A separate tuberoinfundibular pathway runs from hypothalamic neurons to the pituitary gland. The dopamine receptor family separates into two major subtypes: D1-like (D1 and D5) and D2-like (D2, D3, D4). Variants of the dopamine receptors exist with different DNA and amino acid sequences. Receptor cloning has identified two isoforms of the D2 receptor (D2short and D2long), which are differentially localised in the brain. The neurochemical anatomy of dopamine differs in cortical and striatal regions, and it now appears that dopamine concentration, receptor regulation and D2-like receptor subtype density vary greatly between striatal and extrastriatal regions (Lidow et al, 1998; Strange, 2001). Antipsychotic drugs are thought to achieve their main effects (both beneficial and unwanted) by acting on D2 receptors.

DOPAMINE RECEPTORS AND ANTIPSYCHOTIC DRUG ACTION

The D2 receptor blockade hypothesis
Without exception, effective antipsychotic drugs have at least some degree of antagonism of the dopamine D2 receptors.

MAKING A WOMAN OLD BEFORE HER TIME AND ALL SYMPTOMS OF PARKINSON'S DISEASE OCCURS.

http://en.wikipedia.org/wiki/Parkinson's_disease

Parkinson's disease (also known as Parkinson disease or PD) is a degenerative disorder of the central nervous system that often impairs the sufferer's motor skills, speech, and other functions.

Parkinson's disease belongs to a group of conditions called movement disorders. It is characterized by muscle rigidity, tremor, a slowing of physical movement (bradykinesia) and, in extreme cases, a loss of physical movement (akinesia). The primary symptoms are the results of decreased stimulation of the motor cortex by the basal ganglia, normally caused by the insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the brain. Secondary symptoms may include high level cognitive dysfunction and subtle language problems. PD is both chronic and progressive.

Treatment
Levodopa
Stalevo for treatment of Parkinson's disease

The most widely used form of treatment is L-dopa in various forms. L-dopa is transformed into dopamine in the dopaminergic neurons by L-aromatic amino acid decarboxylase (often known by its former name dopa-decarboxylase). However, only 1-5% of L-DOPA enters the dopaminergic neurons. The remaining L-DOPA is often metabolised to dopamine elsewhere, causing a wide variety of side effects. Due to feedback inhibition, L-dopa results in a reduction in the endogenous formation of L-dopa, and so eventually becomes counterproductive.

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