I haven't seen any comparison studies between Sulphate and Threonate. So we'll have to wait and see. The claim is that Threonate was produced to specifically heighten brain magnesium levels. If it has a better bioavailability than sulphate is for researchers to find out.
http://www.ncbi.nlm....pubmed/11035343
http://www.ncbi.nlm....pubmed/20152124
I absolutely agree and this is precisely my point. The study you have posted on MAGNESIUM THREONATE is a RODENT STUDY and does not in any regard provide the necessary scientific support to back the marketing claims being made about MAGNESIUM THREONATE. The other study you have posted is a HUMAN STUDY on MAGNESIUM SULFATE and is just one of many, many existing HUMAN studies on MAGNESIUM SULFATE.
What is most certainly required here is
more research and specifically HUMAN STUDIES on MAGNESIUM THREONATE.
You have quite rightly stated that you
"haven't seen any comparison studies between Sulphate and Threonate"; well, the reason for that is quite simple, namely that
no such studies exist yet. More research on MAGNESIUM THREONATE and studies on HUMANS not RODENTS is what is currently missing and very much needed.
Magnesium is a good brainfood and should be taken in any regime. The discussion should revolve around why magnesium improves cognitive abilities and if it's effect could be somehow improved with other supps.
You are absolutely right that MAGNESIUM is a good 'brainfood' and should be included in any regimen; it is in mine and I have supplemented with it religiously for over 20 years.
RE:
"why magnesium improves cognitive abilities and if it's effect could be somehow improved with other supps" - The primary mechansism of action via which MAGNESIUM exerts its NOOTROPIC effects is NMDA RECEPTOR ANTAGONISM. MAGNESIUM is an NMDA RECEPTOR ANTAGONIST and research has shown us that appropriate administration of supplemental NMDA RECEPTOR ANTAGONIST(S) yields NOOTROPIC effects. See here for example:
1. Nat Neurosci. 2002 Jan;5(1):48-52.NMDA receptor antagonists sustain LTP and spatial memory: active processes
mediate LTP decay.Villarreal DM, Do V, Haddad E, Derrick BE.
The Department of Biology and The Cajal Neuroscience Research Center, Division of Life Sciences, The University of Texas at San Antonio, 6900 N. Loop 1604 W., San Antonio, Texas 78249-0662, USA.
Nat Neurosci. 2002 Jan;5(1):6-8.
Although long-term potentiation (LTP) is long-lasting, it is not permanent and decays within weeks after its induction. Little is known about the processes underlying this decay.
Here we assessed the contribution of synaptic activity to LTP decay by determining the effect of the competitive NMDA receptor antagonist CPP on the decay of perforant path-dentate LTP. CPP blocked decay over a one-week period when administered daily following the induction of LTP, and blocked decay of the late, protein-synthesis-dependent phase of LTP when administered two days after LTP induction. CPP administered for a five-day period following spatial memory training enhanced subsequent memory retention. These data suggest that LTP is normally a persistent process that is actively reversed by NMDA receptor activation, and that both the early and late phases of LTP are dynamic processes
regulated by NMDA receptors. These data also support the view that LTP is involved in maintaining spatial memory.
PMID: 11740500
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Studies on MEMANTINE, another NMDA RECEPTOR ANTAGONIST, have further illustrated the precise mechanism of action via which NMDA RECEPTOR ANTAGONISTS produce their NOOTROPIC effects. See here for example:
1. Neuropharmacology. 2007 Nov;53(6):699-723. Epub 2007 Aug 10.
Memantine: a NMDA receptor antagonist that improves memory by restoration of homeostasis in the glutamatergic system --too little activation is bad, too much is even worse.Parsons CG, Stöffler A, Danysz W.
Merz Pharmaceuticals, Eckenheimer Landstrasse 100, 60318 Frankfurt am Main,
Germany.
The neurotransmitter glutamate activates several classes of metabotropic receptor and three major types of ionotropic receptor--alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate and N-methyl-D-aspartate (NMDA). The involvement of glutamate mediated neurotoxicity in the pathogenesis of Alzheimer's disease (AD) is finding increasing scientific acceptance. Central to this hypothesis is the assumption that glutamate receptors, in particular of the NMDA type, are overactivated in a tonic rather than a phasic manner. Such continuous, mild, chronic activation ultimately leads to neuronal damage/death. Additionally, impairment of synaptic plasticity (learning) may result not only from neuronal damage per se but may also be a direct consequence of this continuous, non-contingent NMDA receptor activation. Complete NMDA receptor blockade has also been shown to impair neuronal plasticity, thus, both hypo- and hyperactivity of the glutamatergic system leads to dysfunction. Memantine received marketing authorization from the EMEA (European Medicines Agency) for the treatment of moderate to severe AD in Europe and was subsequently also approved by the FDA (Food and Drug Administration) for use in the same indication in the USA. Memantine is a moderate affinity, uncompetitive NMDA receptor antagonist with strong voltage-dependency and fast kinetics. This review summarizes existing hypotheses on the mechanism of action (MOA) of memantine in an attempt to understand how the accepted interaction with NMDA receptors could allow memantine to provide both
neuroprotection and reverse deficits in learning/memory by the same MOA.
PMID: 17904591
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MEMANTINE also yields other highly useful beneficial effects, such as REVERSING STIMULANT TOLERANCE, however it is not without potential SIDE EFFECTS, which should be reviewed by anyone considering trying it.
Consequently, coming back to you question regards whether MAGNESIUM's NOOTROPIC effect
"could be somehow improved with other supps" one possibilty might be to combine supplemental MAGNESIUM with an appropriately low dose of MEMANTINE (N.B. when taking MEMANTINE it is recommended to commence with a very low dose and then very gradually ramp up the dosage so as to avoid manifestation of SIDE EFFECTS).
Alternatively, further to maximising the NOOTROPIC effect exerted via NDMA RECEPTOR ANTAGONISM specifically, one could stack MAGNESIUM with other NOOTROPICS whose mechanisms of action are entirely different, thereby yielding a stack that produces a greater potency of NOOTROPIC effect via multiple mechanisms of action
Edited by ScienceGuy, 15 December 2012 - 10:44 AM.