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Keeping the Neurons Awake

Authored by Jimin Kim

Art by Daisy Meng


The alarm goes off, and we wake up every morning to drink a cup of a darkly colored, bitter drink, commonly known as coffee. Coffee has caffeine, which acts as a central nervous system stimulant that wards off drowsiness and restores alertness [1]. However, the overdose of caffeine results in adverse health effects, such as vomiting, rapid breathing, and shock, many of which people go through the consequences after the countless number of cups they had throughout the day[2]. Therefore, more people are attempting to avoid caffeine by choosing alternatives to decaf coffee and lower caffeine content drinks. But could we use this chemical as a health treatment and prevention?


Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder, “characterized by dopaminergic neurodegeneration, motor impairment and non-motor symptoms” [3]. Investigations have shown that there may be a potential in caffeine acting as a psychoactive substance to exert neuroprotective and cognitive benefits in Parkinson’s disease. This inverse relationship between coffee consumption and the risk of developing Parkinson’s disease initially supported that caffeine may play a role in preventing PD. Animal studies stating that “caffeine confers neuroprotection against dopaminergic neurodegeneration in neurotoxin PD models using mitochondrial toxins (MPTP, 6-OHDA and rotenone)” further supported this claim [4]. Thus, neurodegeneration can be protected by using toxins that are structurally similar to caffeine. Moreover, caffeine targets its antagonist receptor, the adenosine A2A receptor, to enhance locomotor activity, preventing PD from developing. The receptors,located in the striatum, specifically in neurons that coexpress D2 dopamine receptors, play a critical role in the indirect motor pathway [5]. This suggests that coffee consumption can be encouraged to show the protective effects of caffeine by protecting motor capabilities. Thus, by using pharmacological blockade or genetic deletion of the receptor, we can preserve dopaminergic neurodegeneration [4]. 


We are already exploring pharmaceutical developments in the industry for possible treatment options for PD. For instance, “one open label trial of theophylline, a methylxanthine A2A receptor antagonist,” has been given to patients with Parkinson’s disease, and significant improvement in motor function has been observed [6]. This already shows substantial clinical relevance for new PD treatments. 


In addition to caffeine being used to prevent PD, ongoing research has shown that combining common tension-type headache treatments, like ibuprofen and aspirin, with caffeine demonstrated efficacy as an analgesic agent [7]. Compared to using ibuprofen alone, the combination with caffeine showed an enhanced efficacy where peak pain relief was achieved. However, the study showed that caffeine has low effectiveness in treatment. Thus, caffeine can possibly enhance treatment options for various diseases. Another example is the treatment of apnea of prematurity in infants. We are capable of saving premature infants with caffeine by reducing the duration of respiratory support, improving survival rates, and lowering the incidence of cerebral palsy and cognitive delay [8]. Some research says that Methylxanthines raise central sensitivity to carbon dioxide, which plays a role in reducing the duration of respiratory support. Yet, these studies are ongoing, and there is little evidence to support the long-term effects of caffeine on brain development. 


This has shown that there is a possibility that caffeine can be appropriately used for medical advancement. Even though it is commonly known that caffeine has adverse effects, there are unlimited possibilities that caffeine could ring to the healthcare treatment world. Not only does it influence our cardiovascular and neurological health, but it can significantly impact our mood if we continue to rely on numerous cups of coffee and energy drinks to keep us awake during the day. 












References

  1. Nehlig, A., Daval, J. L., & Debry, G. (1992). Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain research. Brain research reviews, 17(2), 139–170. https://doi.org/10.1016/0165-0173(92)90012-b

  2. Murray, A., & Traylor, J. (2023, June 26). Caffeine Toxicity. Nih.gov; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK532910/

  3. ‌Ren, X., & Chen, J. (2020). Caffeine and Parkinson’s Disease: Multiple Benefits and Emerging Mechanisms. Frontiers in Neuroscience, 14. https://doi.org/10.3389/fnins.2020.602697

  4. Chen, J. F., Xu, K., Petzer, J. P., Staal, R., Xu, Y. H., Beilstein, M., ... & Schwarzschild, M. A. (2001). Neuroprotection by caffeine and A (2A) adenosine receptor inactivation in a model of Parkinson's disease. The Journal of neuroscience: the official journal of the Society for Neuroscience, 21(10), RC143-RC143.

  5. Muñoz, D. G., & Fujioka, S. (2018). Caffeine and Parkinson disease. Neurology, 90(5), 205–206. https://doi.org/10.1212/wnl.0000000000004898

  6. G. Webster Ross, & Petrovitch, H. (2001). Current Evidence for Neuroprotective Effects of Nicotine and Caffeine Against Parkinson's Disease. Drugs & Aging, 18(11), 797–806. https://doi.org/10.2165/00002512-200118110-00001

  7. Diamond, S., & Freitag, F. G. (2001). The use of ibuprofen plus caffeine to treat tension-type headache. Current Pain and Headache Reports, 5(5), 472–478. https://doi.org/10.1007/s11916-001-0060-8

  8. Atik, A., Harding, R., Robert De Matteo, Delphi Kondos-Devcic, Jeanie L.Y. Cheong, Doyle, L. W., & Tolcos, M. (2017). Caffeine for apnea of prematurity: Effects on the developing brain. NeuroToxicology, 58, 94–102. https://doi.org/10.1016/j.neuro.2016.11.012

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