Anti- Parkinson's Disease and It's Classification.

Parkinson's Disease

1. Parkinson’s Disease Submitted To:- Ms. Neelam Painuly (Associate Professor) [email protected] Sopr, DBUU, Dehradun Submitted By:- Mr. Deepak Kumar Student, M. Pharm 1 st year (Pharmacology) [email protected] Sopr, DBUU, Dehradun 1 DBUU, Dehradun

2. Table of Content DBUU, Dehradun 2 S. No. Contents 1 INTRODUCTION 2 CLASSIFICATION 3 DOPAMINE PRECURSOR- (LD) 4 PHARMACOKINETIC 5 ADVERSE EFFECT 6 REFERENCES

3. Anti- Parkison’s Agents DBUU, Dehradun 3 INTRODUCTION:- Parkinson's disease (PD) was initially identified by Sir James Parkinson and is defined by specific motor symptoms including tremor, rigidity, bradykinesia (slow movement), and impaired postural reflexes. In idiopathic parkinsonism, there is a degeneration of dopamine-producing neurons located in the substantia nigra , leading to a deficit of dopamine within the brain.

4. Classification:- 1- Drugs Affecting the Brain Dopaminergic System: Dopamine Precursor: Levodopa Dopamine Agonists: Bromocriptine , Pergolide Dopamine Releasing Drug: Amantadine MAO-B Inhibitors: Selegiline ( Deprenyl ) Drugs Affecting the Brain Cholinergic System: Centrally Acting Anticholinergic Drug: Benztropine Antihistamines (H1-Blockers) with Anticholinergic Activity: Diphenhydramine , Promethazine . These medications exert various effects on the brain's dopaminergic and cholinergic systems, playing important roles in the management of related neurological and psychiatric conditions. DBUU, Dehradun 4

5. Dopamine Precursor: Levodopa:- Levodopa (L- Dopa ) is the primary medication utilized in the management of idiopathic Parkinson's disease. Because dopamine cannot effectively cross the blood-brain barrier (BBB), its immediate precursor, levodopa , is administered as a prodrug to facilitate entry into the brain. Levodopa is metabolized to dopamine primarily by decarboxylase enzymes. However, a significant portion of levodopa is converted to dopamine in peripheral tissues by peripheral decarboxylase enzymes before reaching the brain. This peripheral conversion can limit the amount of levodopa available to exert its therapeutic effects within the central nervous system. DBUU, Dehradun 5

6. DBUU, Dehradun 6 Pharmacokinetics:- Upon oral administration, levodopa is rapidly absorbed from the small intestine through an active transport mechanism. However, the absorption of levodopa can be influenced by the presence of amino acids in food, potentially interfering with its uptake. To optimize absorption, levodopa is typically administered 30-60 minutes prior to meals to minimize competition from dietary amino acids. The transport of levodopa into the brain can be hindered by competition with dietary amino acids, impacting its effectiveness in reaching the central nervous system. Following metabolism, levodopa primarily breaks down into homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC). These metabolites are subsequently excreted in the urine as part of the body's elimination process.

7. DBUU, Dehradun 7 Adverse Effects:- Gastrointestinal (GI) side effects such as nausea, vomiting, and decreased appetite are frequently observed early in levodopa treatment. Cardiovascular (CV) side effects primarily include postural hypotension, which often presents without symptoms. Abnormal movements, particularly tremors, may manifest as a side effect of levodopa therapy. Mental changes such as insomnia, confusion, and depression can also occur during treatment. Over time, typically after 3-5 years of therapy as the disease progresses, there may be a decrease in symptom control leading to fluctuations in response to levodopa , necessitating adjustments in treatment management.

8. DBUU, Dehradun 8 REFERENCES:- Kara Rogers is the senior editor of biomedical sciences at Encyclop e dia Britannica, where she oversees a range of content from medicine and genetics to microorganisms . https:// en.wikipedia.org /wiki/Parkinson ’ s

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