"Pharmacological blockade (by caffeine or specific A(2A) antagonists) or genetic depletion of the A(2A) receptor attenuated dopaminergic neurotoxicity and neurodegeneration in animal models of Parkinson's disease."
Kalda et al, 2001 J Neurol Sci. 2006
Novel neuroprotection by caffeine and adenosine A(2A) receptor antagonists in animal models of Parkinson's disease.
see also Chen et al, 2001 J Neurosci
Neuroprotection by caffeine and A(2A) adenosine receptor inactivation in a model of Parkinson's disease.
Caffeine is to improve micro-circulation in brain by raising heart rate moderately, provided that the patient is not moving at all and caused sphincters limit blood supply to brain cells. But I don't know how much Parkinson's can affect the heart rate increase. There is one other thing. If the patient is not able to do deep breathing, the healing effect will also be discounted. Therefore, one must train Parkinson's patients to do deep breathing (or put on oxygen masks) before using stimulants, cycling, or taichi type of exercise to increase heart rates.
Caffeine is known to have an A2A receptor blocker action. It was seen to have a neuroprotective effect in animal models of Parkinson’s disease. In fact, istradiphylline, another Adenosine receptor blocker, has been approved in Japan (MArch 2013) for adjunctive treatment of PD and is marketed under the brand name of Nouriast 20 mg tablets. The most commonly cited mechanisms of action for Adenosine A2A receptor blockers are as follows.
1.Neuroprotection afforded by blockade of A2A receptor blockade in striatopallidal neurons mediated via the modulation of glutamate levels.
2. Inhibition of microglial activation and preventing the microglial mediated neuronal inflammation and cell death.
3. Some studies have shown a improvement in motor as well as non motor symptoms.
In fact, the neuroprotective role of adenosine receptor blockers is being investigated not only in PD, but also in a wide array of CNS disorders that show underlying neuron cell death. As yet, the clinical trials with caffeine have been done on a small sample size and for a short duration of about 6 weeks. In addition, the optimum dose that offers neuroprotection also needs to be confirmed.The dose of caffeine used in the RCT was 200-300mg. A promising treatment strategy, but going by the history of 'neuroprotective drugs' studied earlier, a guarded enthusiasm is warranted.
Kindly refer to publication by Ruis DS. Prediger (2010) for further details.
Epidemiological data is clear, moderate consumption coffee and tea appears protective against PD. However, I think a more cautious approach is needed before jumping to the conclusion that the effect is caused by A2A alone. See.Ann Neurol. 2001 Jul;50(1):56-63. "Results of case-control studies and of a prospective investigation in men suggest that consumption of coffee could protect against the risk of Parkinson's disease, but the active constituent is not clear. " If it is A2A alone why is the effect more pronounced in men than women. If it is A2A alone why doesn't >4 cups a day offer less protection.
My thought on micro-circulation came from my observation of taichi healing. When I looked further into yoga, lucid dream, red wine, green tea, cannabis, hyperbaric oxygen chamber, and even ECT, I found that they all share 3 common factors – the induction of moderate heart rate elevation (for a certain time period), more oxygen, and not moving (or moving very slowly to cheat your brain that you are not moving). I called this taichi healing hypothesis “Pao’s Law of Exercise”..........and I don’t take decaf coffee.
One more thing - "healing" here is a process referring to sending oxygenated blood to organ cells and let them produce new cells with normal DNA's. So, it takes time.
Caffeine and uric acid are both xanthines. The powerful antioxidant and antiexcitotoxin uric acid seems to be an important endogenous neuroprotectant in PD, as well as other diseases . Urate is even in clinical trials for PD, MS, and acute ischemic stroke.
Dimethyuric acid and tetramethyuric acid are important metabolites of caffeine and have similar antioxidant and reducing properties to uric acid. So it is possible that these also play a role in protection against PD.
Most people still don't understand how we can send more blood to brain cells and other organs. Therefore, I have written a shorter article to explain how we elevate our heart rates to do this feat. But, we must do it before meals and must not have any physical movements. Taking stimulant in moderation is one of the ways.
Article A Brief Introduction to "Taichi Healing & Pao's Law of Exerc...
another possibility is that the epidemiologic associations may be due largely to individuals with a lower number of dopaminergic cells in the pigmented brainstem nuclei (SN, LC) in midlife (decades before PD manifestions) being both very sensitive to the unpleasant affects of caffeine, and more likely to develop PD when these neurons finally reach 80+ % depletion levels... such persons may not like how coffee makes them feel... so they choose to avoid coffee. A similar process may be working for smoking. We find that individuals who neither smoked nor drank coffee in midlife had a 6-9 fold increase in the development of late life; those who came to autopsy without having developed clinical PD had lower neuron counts in their substantia nigra, and often had "incidental" Lewy bodies
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