7 replies to this topic

[JornT]

First post on immmins!

I'm very interested in DAA's effect on the brain (good or bad for cognition/nootropic effects, safe or dangerous for long term use?

However, neuroscience is far from my expertise.



Evidence for the involvement of D-aspartic acid in learning and memory of rat.

D-Aspartic acid (D-Asp) is an endogenous amino acid present in neuroendocrine systems. Here, we report evidence that D-Asp in the rat is involved in learning and memory processes. Oral administration of sodium D-aspartate (40 mM) for 12-16 days improved the rats' cognitive capability to find a hidden platform in the Morris water maze system. Two sessions per day for three consecutive days were performed in two groups of 12 rats. One group was treated with Na-D-aspartate and the other with control. A significant increase in the cognitive effect was observed in the treated group compared to controls (two-way ANOVA with repeated measurements: F ((2, 105)) = 57.29; P value < 0.001). Five further sessions of repeated training, involving a change in platform location, also displayed a significant treatment effect [F ((2, 84)) = 27.62; P value < 0.001]. In the hippocampus of treated rats, D-Asp increased by about 2.7-fold compared to controls (82.5 +/- 10.0 vs. the 30.6 +/- 5.4 ng/g tissue; P < 0.0001). Moreover, 20 randomly selected rats possessing relatively high endogenous concentrations of D-Asp in the hippocampus were much faster in reaching the hidden platform, an event suggesting that their enhanced cognitive capability was functionally related to the high levels of D-Asp. The correlation coefficient calculated in the 20 rats was R = -0.916 with a df of 18; P < 0.001. In conclusion, this study provides corroborating evidence that D-aspartic acid plays an important role in the modulation of learning and memory. PMID: 19890700



What is the HED for the dose used in the above study? An attempt from me:

molweight DA: 133.1027 (http://www.drugbank.ca/drugs/DB02655)

mol x mol weight = weight (in grams?)

40 x 10^-3 x 133.1027 = 5,324 (g?)

bodyweight adult rat = ~ 500 mg(http://research.uiow...animal/?get=rat)

Rat KM = 6
Human KM = 37

5324/0,5 x 6/37 = 1726 mg

Something like that?

[Ark]

I don't remember where i read, but as far as the brain goes its not its friend.

[kilgoretrout]

I read that a combination of potassium and magnesium aspartate has alot of very beneficial effects.

Just google "potassium magnesium aspartate" and a huge number of articles and research will result, far too extensive to summarize here, just check it out yourself.

Once I came across a very nice summary, if I notice that page again I'll post it. Probably the mineral bound forms are better than pure aspartic acid though I would bet. And if I recall it was said the combo was best. GNC and alot of places carry it. I think I recall that about 1g each (a total of 4 caps normally each containing 250mg of both salts), and thats its best absorbed with food. That was the recommendation I settled on. Help reduce lactic acid in muscles and other biochemical stress markers, good for cardio system, nervous system, other things.

[rwac]

You're both confusing D-Aspartic Acid with the L form, because that's what's found in most supplements.

[JornT]

The D-form can be bad for the brain, because of NMDA excitoxicity. Therefore I'm trying to figure out at which dose it is beneficial or dangerous for the brain.

A pharmacist told me on the same question as I posted in the OP:

HED is based on the principle that receptors depend surface(square) while concentration depends on volume(cube) and is thus best applied on pharmacodynamical drugs. On supplements it does not necessarily apply. As an example of that the RDA of many nutrients for humans and rats is painfully close (in mg/kg). DAA is a precursor. On NMDA HED would basically apply. Whether it applies on DAA or not would depend on the % of conversion of rats/humans. If we suppose it is a simple enzymatic Ki dependent conversion then it would be concentration dependent.



@kilgoretrout: The D-form is also beneficial for fitness goals. It has shown to increase testosterone and GH in humans.

[Galantamine]

Directly agonizing the receptor comes with many downsides - which is why the racetams where developed --> to potentiate the receptor, not activate it.

We already have drugs like D-asp: d-cycloserine, which is used for mycobacterial infectious. It comes with it serious CNS toxicity. If you look it up on pubmed, you'll see its also commonly used for memory extinction, and other prototypical 'nootropic' modalities, in mice.

Similar to phenobarbital (vs. benzo's), the dose-response curve will never plateau, but simply extend endlessly into excitotoxic territory - and so much be kept within a narrow range.

Combinding DAA with a racetam may be practical if one is attempting to avoid excitotoxicity.

In the anterior pituitary, DAA may facilitate Ca2+-mediated LH/FSH granular release by agonizing the Glut receptor, but unlikely to actually increase LH/FSH transcription, which is usually mediated by the GnRH receptor and protein kinase C. If this is true, then prolonged DAA supplementation would result in LH/FSH depletion and temporary hypogonadism.

[NR2(x)]

Correlation does not prove Causation, The fact that people who achieve well on a creteria, have a greater level of asparte does not prove that increased asparte will improve performance. I would venture that people who have better cognition are more tolerant to asparte, and therefore utilize to a greater degree to cause excitation. This theroy is based on knowledge of extrasynatpic NMDAs receptors verses synaptic NMDAs. Bad stuff in my opinion with strong neurotoxic potential that the FDA is fully aware of, implimented to cause harm?
If you want to enhance excitation this must be done through the bodies natural pathways, natural stranded proteins, you cannot short circuit it. If you have to use glutamine but try to avoid amino acids generally. I would never take supplemental DAA(no diet coke) but in really foods its ok

[JornT]

Big thanks Neuron!