Amal Alachkar, University of California Irvine – Why Parkinson’s Drug Improves, then Diminishes Quality of Life

Treating Parkinson’s disease is never an easy prospect.

Amal Alachkar, associate professor of teaching pharmaceutical sciences at the University of California, Irvine, breaks down the issues with one method of treatment.

Dr. Amal Alachkar is a Syrian-American neuroscientist and pharmacologist whose research focuses on dissecting the genetic, molecular, and chemical mechanisms underlying cognitive and emotional functions. She is particularly interested in understanding how the dysregulations of particular brain circuits lead to neurological and psychiatric disorders such as Parkinson’s disease, schizophrenia, autism, and depression. Her research aims to identify novel therapeutic strategies and molecular targets for the treatment of the neurological and psychiatric disorders.

Why Parkinson’s Drug Improves, then Diminishes Quality of Life

My research team is working to answer questions surrounding Levodopa’s – or L-dopa – efficacy and development of dyskinesia, which is critical for Parkinson’s patients, caregivers, and providers everywhere.

Because L-dopa is considered the gold standard drug for Parkinson’s, researchers have been studying the tens of thousands of patients who have developed dyskinesia where involuntary, erratic muscle movements of the patient’s face, arms, legs and torso are common.

My researchers and I focused on figuring out why this very popular drug loses its efficacy and causes patients to develop side effects that ultimately ruin their quality of life.

L-dopa is designed to replace the lost dopamine caused by the degeneration of nerve cells in the brain. This drug, along with an enzyme inhibitor is administered to patients to increase the amount of dose that reaches the brain and prevents side effects such as heart problems.

Our research consisted of studying L-dopa and the protein siderocalin. Through studying their interactions, we noticed it caused a cellular iron overload. This overload leads to an imbalance between free radicals and antioxidants. The imbalance leads to neuroinflammation in the brain which triggers dyskinesia; thus diminishing quality of life.

For patients, this means long term use of the drug will lead to more health issues down the road. As researchers, this information is not only vital to share with patients but helps us learn more about the side effects this popular drug may have.

Based on these findings, my team and I are exploring other non-dopamine drug options as potential therapeutics for Parkinson’s. We hope that in the future, we’ll be able to find a safer and more effective way for Parkinson’s patients to live a great quality of life.