coffee's caffeine effects on parkinson's disease

[sciencerocks18]

Hi,

I just have another quick question.
What unit is used to measure the number of adenosine a2a receptor antagonists that are present in the caffeine found in a standard cup of coffee? Do you think that I should also include some statistical data based on this to support my idea?

I would like to thank you once again for your time and cooperation!!!

From
Hareshan

[PharmaMan]

For your project, you will need to have an introduction with background information on the biology of the disease as well as current treatment options. This is where you will lead into your central hypothesis by talking about how caffeine can serve as a treatment based on prior work showing that it can have therapeutic effects.

For the results section, you will be presenting work done by others that shows how/why caffeine is a suitable treatment option. It is within this section that you will present the signaling diagram that illustrates how caffeine affects the proteins downstream of the A2A receptor. You won't really have a methods section since the experiments aren't your own, but you can describe in your own words some of the major experimental methods used in the papers (any in vivo experiments, cell culture work, etc.).

Lastly, you will provide a discussion/future directions section. Here, you essentially provide a critical analysis of why/how caffeine is effective based upon the experimenter's results. In addition, you can talk about additional experiments to perform, or even something else that could be done to increase the therapeutic efficacy of caffeine.

Pre-synaptic versus post-synaptic is referring to the orientation of the cells relative to the synapse. If A2A receptors influence the release of dopamine, then the A2A receptors are located on the pre-synaptic cell, and dopamine is also released from the same pre-synaptic cell to affect the cell across the synapse (i.e. the post-synaptic cell).

For the antagonists, caffeine is the component within coffee that is serving as the receptor antagonist. The concentration of caffeine will vary depending upon a lot of factors, but you can measure it in molar (micromolar, or millimolar as a unit, for example). I don't think you need to include any statistics for this, but I would try to see what levels of caffeine could be reached in the bloodstream and compare that to levels that are known to saturate levels of the A2A receptor in the human brain (if that is known).

Let us know if you have further questions. Best of luck!

-Pharma

[sciencerocks18]

Hi,

Thanks for your suggestions. I also think that this would make an excellent layout for the order/sequence of my presentation orally. However, what components should I paste on the tri-panel board. E.g. (abstract, hypothesis, conclusion etc.)
Since my project is only a study, am I still allowed to include the procedure that the other scientists have used to test whether caffeine can have therapeutic effects and its results too?
In terms of visual representations, I have the signalling pathway diagram. In addition I also created a mind map which includes all of the different neuropathalogic symptoms of Parkinson's disease such as bradykinesia, DA neuronal loss, etc. These symptoms branch out into factors that influence or cause fluctuations in these sympatoms such as caffeine (adenosine a2a receptor antagonists) and the effects of L-Dopa too. I was also able to find a diagram talking about how the synapse occurs and how this process is interrupted with adenosine receptors. I also have graphs from the experimental procedure carried out by the scientists showing the fluctuations in dopaminergic neurons in their study. Do you think that I have enough visual representations to support my presentation? Can you please suggest potential visual diagrams/images that will further enhance my project?
What does the discussion part mean? Is it similar to a conclusion?

From,
Hareshan

[sciencerocks18]

Hi,

I am also planning on submitting a research report to submit to the
judges or at least let them glance at during my presentation. Some of my peers
are doing the same. I already have all my research done and I have grouped
information with the same content together too.

Do you think that a research report is necessary to submit to the judges?
If it is, what are the different components that I must incorporate to make it
appealing to the judges?

From
Hareshan

[sciencerocks18]

Hi,

Adding on to that, the science fair is coming up soon!!!
Can you please post questions that the judges can potentially ask me after my presentation?
I will like to thank you very much for your support and time!!!

From
Hareshan

[PharmaMan]

I think that you can paste the same sections on a tri-panel board for your project. When we design posters for presentations, we will follow the same format. The first section will be the project abstract (which includes a hypothesis), followed by materials/methods, the results, and a discussion/conclusion. I think you can also put the experimental procedures there, but be sure to cite the original authors of the study. This will add further detail illustrating how the results were obtained.

You certainly have enough images/diagrams for your project. My only recommendation would be to put the signaling diagram last; you can put the other images as introductory information, because ultimately you will narrow it down to how caffeine is a suitable treatment option which targets the adenosine receptor. And yes, a discussion is more or less a conclusion. However, a discussion is critical because it also suggests further experiments that can be done in addition to what the results of the current study (your project) mean. It is more like a critical analysis of the results and what any future directions are.

For your last question, I'm not sure if a report would add anything to your project, unless you plan to include additional information/studies into it. Typically, judges will assess your poster and will ask you questions on the spot about the research. I do not feel they would read any other material in depth that you may hand out. However, I'm not sure about your school's setup for your fair. I'm simply going off of personal experience with poster presentations/judging.

Some judging questions I could pose to you could be the following:

-What plasma concentrations of caffeine would be necessary to have a therapeutic effect?
-How does caffeine inhibit the action of the adenosine receptor? (competitive versus non-competitive inhibition, etc.)
-Following caffeine administration, how are the levels of dopamine ultimately regulated by the receptor? (Going back to the signaling diagram)
-What other treatments could be coupled to caffeine treatment to have maximum benefit to the patient?

Best,
Pharma

[sciencerocks18]

Hello Dr. Pharma,

I have a small doubt.
For the first question which asks "what plasma concentrations of caffeine would be necessary to have a therapeutic effect?"; do you want me to support my response with the concentration of caffeine that will be dissolved in the rodent's blood based on that vivo study or do you want me to make an estimated guess to determine the plasma concentration that will be mixed in the human blood stream?

Thanks,
Hareshan

[PharmaMan]

I'm sorry, I should have specified further. I meant within the human bloodstream; so, what concentrations may have a therapeutic effect and how could this treatment be administered?

[sciencerocks18]

Hello Dr. Pharma,

I have the answers to the sample questions you sent me to prepare me for the science fair.

1. What plasma concentrations of caffeine would be necessary to have a therapeutic effect and how can this treatment be administered into the human bloodstream?
Note: plasma concentration is the amount of a compound present in the portion of the blood.

Approximately, humans consume 300-400 mg of caffeine a day. However, the half life of caffeine in humans is approximately five hours. So it takes about 5 hours for the our bodies to get rid of half of the caffeine concentration after consuming a cup of coffee. Caffeine is absorbed and passes quickly into the brain. It does not collect in the bloodstream or get stored in the body. It leaves the body in the urine many hours after it has been consumed. We cannot expect any therapeutic results immediately, my research only supports that chronic consumption of coffee (caffeine treatment) can have therapeutic effects. Often doctors use Mini-Osmotic Pumps to infuse similar drugs/compounds into the human body. However, a daily supplement of coffee with the presence of caffeine of about 300-400 mg is sufficient to have a therapeutic effect on PD in the long term.

2. How does caffeine inhibit the action of the adenosine receptor? (competitive versus noncompetitive inhibition, etc.)

Caffeine inhibits the action of the adenosine receptor by the activation of adenosine a2a receptor antagonists that are present in caffeine. It up regulates the two major enzymes in the signaling pathway known as adenylyl cyclase (AC) and the cAMP production in cells so that there will be enhanced synaptic responses between dopaminergic neurons.

3.Following caffeine administration, how are the levels of dopamine ultimately regulated by the receptor? (Going back to the signaling diagram)

Through the administration of caffeine, the levels of dopamine are ultimately regulated by the adenosine a2a receptors antagonists that are present in this compound. Adenosine A2A receptors signal or activate phosphorylate (PDE) to a greater degree which degrades the cyclic AMP into AMP (adenosine monophosphate) and effect the neuron communication poorly. The process of degrading cAMP can impact various intracellular activity (responses). cAMP plays a fundamental role in the cellular response to many hormones and neurotransmitters. The level of intracellular cAMP is regulated by the balance between the activity of two types of enzyme: adenylyl cyclase (AC) which activations cAMP and the cyclic nucleotide phosphodiesterase (PDE). So inhibiting these a2a receptors using caffeine can enhance the intracellular signalling by the inhibition event of PDE and the reinforcement of AC resulting in elevated cAMP levels and stopping PD.

4. What other treatments could be coupled to caffeine treatment to have maximum benefit to the patient?

I think that caffeine treatment coupled with Levodopa (L-Dopa) and Carbidopa treatment can provide maximum benefit to the patient because the combination of these two drugs are capable of protecting the existing DA neurons and reducing the severity of the symptoms. So the addition of caffeine will increase the effectiveness of the neuroprotection process and thus we can prevent the progression or beginning of PD at a much greater degree.

Do you think that I must be also prepared to answer general questions such as "what inspired you to do this project", " who might want to know this information", " what was the hardest part/easiest part", " What will you do next", and etc?

I kindly request you to provide some feedback as to the quality of my answers and how I can modify my responses accordingly to address the question in a highly effective manner.

From,
Hareshan

[sciencerocks18]

Hi,

Can you please help me find the correct answer for question 1 because I wasn't able to find any studies that indicated the plasma concentration of caffeine that should be present in the human bloodstream to have therapeutic effects.
I just tried answering how this treatment is administered and the half life of caffeine.
Can you please think of more questions regarding my project so that I will be more prepared?

From.
Hareshan

[PharmaMan]

Hello,

Here is some feedback from your responses:

1) You sufficiently answered this question; the end of your response where you indicate therapeutic doses of caffeine for PD treatment looks good to me.

2) For this question, caffeine is the antagonist that inhibits the receptor. However, there are differing mechanisms of action for receptor inhibition. For example, caffeine could compete with the natural ligand for the receptor (competitive inhibition) or it could bind at an allosteric site (non-competitive inhibition). Were you able to find this information?

3) So in this mechanism, caffeine inhibits the receptor, leading to decreased PDE activity and increased cAMP. Then, cAMP plays a role in the upregulation of dopamine. This answer looks good, but what about the other components of your previous schematic (ERK1/2, etc.)?

4) The answer to this question looks great.

You can definitely include answers to the other questions you posed. I think overall you have a good handle on how to address these questions, and you have definitely done a lot of research. I don't feel there is much else I could ask in relation to your project. Do you have any further questions?

Best,
Pharma

[sciencerocks18]

Hi,

For question #2, I understand that caffeine is the antagonist that inhibits the receptor. However, I wasn't able to find any information regarding the differing mechanisms of action for receptor inhibition as you stated.
Can you please explain the competitive vs. non-competitive inhibition?

The York Region Science and Technology Fair is on the upcoming Saturday April 2nd, 2016.
I have less than a week!!!
So, can you please help me with this asap?

Thanks for supporting me throughout this project!

From
Hareshan

[sciencerocks18]

Hi Dr. Pharma,

The science fair went well yesterday. I won a bronze medal at the fair.
I was also on ctv news when I was presenting my project.
Here is the cite that you can use to check it out.
http://toronto.ctvnews.ca/video?playlistId=1.2843034

Thank you very much for helping me through the the entire project
from helping me create a signaling pathway diagram to helping me
plan the layout of this presentation. It was a great experience working
with you.

I hope that you can help me with other health Science projects
in the future as well.

Thanks,
Hareshan

[PharmaMan]

Hi Hareshan,

I'm so sorry for the late reply. I'm very glad to hear that the fair went very well. A congratulations is in order for you on your medal! I'm happy to be of assistance to you for this project. Feel free to come back to the forums anytime for help on any future projects.

Best,
Pharma

[sciencerocks18]

Hello scientist Pharma,

Happy New Year!!! This is Hareshan from last year. Thanks for helping me with my science fair project last year and I couldn't have been successful last year without your guidance.
This year, I am going to participate in the York Region Science Fair again and my goal is to win gold so that I can go to the Canada Wide Science fair. Last Year I won bronze.
I am interested in doing research into diabetes because currently there is no cure.
I was doing some research to see whether I could do anything with regards to genetic modifications or stem cell treatment to treat diabetes but that had already been done as well.
I was doing some more research on diabetes and I came across diabetic retinopathy which is one of the chronic effects caused by diabetes due to hyperglycemia. As you may know, this condition is associated with damage to the tiny blood vessels in the retina which ultimately leads to hemorrhage (bleed), distorting vision. In its most advanced stage, new abnormal blood vessels proliferate (increase in number) on the surface of the retina, which can lead to scarring and cell loss in the retina. I was wondering whether I can develop some form of lens that can convert ultraviolet radiation to kill some of the proliferative leaking blood vessels which can be equivalent to laser eye surgery, one or the current methods of treating this condition.
Is there any research that has been done on this?
If not, can you help me with my research for this science fair project?
Once again, I would like to convey my heartfelt thanks for being my mentor and guiding me through this project

Regards,
Hareshan