Potential Role of Caffeine in the Treatment of Parkinson’s Disease

Mohsin H.K. Roshan*, Amos Tambo, Nikolai P. Pace
Department of Physiology and Biochemistry, Faculty of Medicine and Surgery, University of Malta- Msida, Malta

Article Metrics

CrossRef Citations:
Total Statistics:

Full-Text HTML Views: 9493
Abstract HTML Views: 2329
PDF Downloads: 837
ePub Downloads: 629
Total Views/Downloads: 13288
Unique Statistics:

Full-Text HTML Views: 2786
Abstract HTML Views: 1334
PDF Downloads: 602
ePub Downloads: 440
Total Views/Downloads: 5162

Creative Commons License
© Roshan et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (, which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Department of Physiology and Biochemistry, Faculty of Medicine and Surgery, University of Malta-Msida, Malta; Tel: +35699358550; E-mail:


Parkinson’s disease [PD] is the second most common neurodegenerative disorder after Alzheimer’s disease, affecting 1% of the population over the age of 55. The underlying neuropathology seen in PD is characterised by progressive loss of dopaminergic neurons in the substantia nigra pars compacta with the presence of Lewy bodies. The Lewy bodies are composed of aggregates of α-synuclein. The motor manifestations of PD include a resting tremor, bradykinesia, and muscle rigidity. Currently there is no cure for PD and motor symptoms are treated with a number of drugs including levodopa [L-dopa]. These drugs do not delay progression of the disease and often provide only temporary relief. Their use is often accompanied by severe adverse effects. Emerging evidence from both in vivo and in vitro studies suggests that caffeine may reduce parkinsonian motor symptoms by antagonising the adenosine A2A receptor, which is predominately expressed in the basal ganglia. It is hypothesised that caffeine may increase the excitatory activity in local areas by inhibiting the astrocytic inflammatory processes but evidence remains inconclusive. In addition, the co-administration of caffeine with currently available PD drugs helps to reduce drug tolerance, suggesting that caffeine may be used as an adjuvant in treating PD. In conclusion, caffeine may have a wide range of therapeutic effects which are yet to be explored, and therefore warrants further investigation in randomized clinical trials.

Keywords: Adenosine A2A receptors, Basal ganglia, Caffeine, Dopamine D2 receptor, Parkinson’s disease, α-synuclein.