Research Highlights

doi:10.1038/nindia.2015.73 Published online 1 June 2015

Nanotherapy for Parkinson’s disease

Researchers have synthesized dopamine-loaded polymer nanoparticles that can replenish depleted dopamine levels in patients with Parkinson’s disease1. This method of delivering dopamine is a promising therapeutic option for treating the disease.

Currently used drugs for treating Parkinson’s disease trigger dyskinesia, a condition that makes it difficult to perform voluntary movements.

The researchers trapped dopamine in the biodegradable polymer poly (lactic-co-glycolic acid) and analysed the nanoparticles’ ability to deliver and release dopamine in cultured cells used to study neurodegenerative disorders and across the blood–brain barrier in rats with Parkinson’s disease.

Previous studies had shown that uncoated dopamine readily forms reactive oxygen species in cellular environments. The researchers found that the dopamine-loaded nanoparticles permeated the cultured cells but did not produce harmful reactive oxygen species in them. In contrast, bulk dopamine produced reactive oxygen species that damaged the cells.

The scientists explored the therapeutic potential of dopamine-loaded nanoparticles by intravenously injecting rats with Parkinson’s disease with the dopamine-loaded nanoparticles. A week later, the rats did not exhibit neurobehavioural abnormalities. Furthermore, the dopamine released by the nanoparticles did not harm normal brain cells or other vital organs.

“Currently, we are modifying the dopamine-loaded nanoparticles so that they can be delivered orally, which is preferable to intravenous injection,” says lead researcher Kailash Chand Gupta.

The authors of this work are from: CSIR-Indian Institute of Toxicology Research and CSIR-Central Drug Research Institute, Lucknow, CSIR-Institute of Genomics & Integrative Biology and Academy of Scientific and Innovative Research, Delhi, India.


References

1. Pahuja, R.et al. Trans-blood brain barrier delivery of dopamine-loaded nanoparticles reverses functional deficits in Parkinsonian rats. ACS Nano 9, 4850–4871 (2015)