Comment · Tue, November 13, 2012 · Ceretropic
I am creating a nootropics mind map. Does anyone want to give me constructive criticism or contribute?
Original post in this thread
Rage_Boner · 104 points
Here is a screenshot. http://i.imgur.com/EfFy2.png
It's obviously far from finished, but here is what I've got after about an hour of working on it last night. I'm using this format because this is how I learn most effectively. I apologize if this is not "official" enough with citations, etc. It's a work in progress. If anyone wants to contribute, I've selected Xmind as the format, and I could host it in a shared dropbox folder, unless you have better ideas.
EDIT 1: Thanks for the positive. Let's make this a collaborative effort. Instead of hosting and getting multiple random versions, I think it would be best if we all share a folder. That way we can track version changes and roll back if needed, e.g. someone deletes everything then saves. Please PM me your email address (the one linked to your dropbox) and I will invite you to my dropbox folder...unless someone can suggest a better way to host this for collaboration.
UPDATE: I've added a little more data to the TLDR noot map. I am going to host it here for download.. New Screenshot http://i.imgur.com/CGdfg.png Here is where you can download the Xmind file. https://www.dropbox.com/s/bkd1o0kvzmmpg5u/Cognitive%20Enhanc…
What they were answering
judasblue · 1 points
Yeah, there is a good bit of guesswork in all this anyway. Educated guesswork, but as you say, no one is doing really good research on these stack effects, much less when you add more interesting drugs to the mix. And given some of your other apparent personal interests from a previous look at your posting history, I can see why you would want to stay on the conservative side of this one. Since I am pretty much straight-edge with the exception of my rather vested interested in non-mood-altering cognitive enhancers I tend to go with the higher dosages. For a while stupidly high as an experiment, but have since settled down to about standard dosages (which many people seem to think is an attack dose, but whatever).
Although, just to play devil's advocate, the stuff in these papers is pretty severe brain trauma, which isn't really in the ballpark with recreational or therapeutic MDMA or amphetamine use (alcohol and bartbituates, as you know, is another story entirely). It's the like the excitotoxicity discussion that keeps going around lately. The difference between slightly elevating or increasing the effectiveness of various neurotransmitters and ischemic cascade where the studies people keep citing are is kind of a leap.
But yeah, staying on the safe side makes complete sense.
u/MisterYouAreSoDumb · Ceretropic
I agree. Yes, piracetam is a positive allosteric modulator of NMDA receptors. Yes, it increases the influx of calcium through one's ion channels into their neurons. However, I cannot find any evidence that the channels remain open past the voltage point of safe operation. Since excessive NMDA receptor activation may also be a common mechanism causing neuronal cell death in stroke, traumatic brain injury, and various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and Huntington's, and piracetam has been shown to protect against said traumas, I feel as though it's pretty safe to assume that it does have a mechanism for preventing excessive NMDA receptor activation. I just cannot find any studies proving the mechanism with which it does it. Here is a study that shows vinpocetine has this effect.
A neuron's normal resting electrical potential is -90 millivolts. Magnesium is a voltage-dependent NMDA receptor antagonist. It will prevent the ion channel from opening even if glutamate binds to the NMDA receptor. However, if the surface membrane's electrical charge drops to -65 millivolts or less, the magnesium block is overcome, and the ion channel is opened. This allows calcium and sodium to influx into the neuron. Piracetam, being a positive allosteric modulator of NMDA receptors, has been proven to increase the excitability of the NMDA receptors. I also have a feeling that it has a way of closing the ion channel once a certain level of calcium is reached inside of the neuron. This would allow it to potentiate the activity of glutamate, without the added danger of excitotoxicity.
This study proves that piracetam protects against aptosis. I want to know how it does it! Does it close the ion channel before the calcium enters the neuron? Does it increase the efficiency of the membrane pumps that send the calcium and sodium back out of the neuron?