SCIENTIFIC RESEARCH

OmniMind’s unique ingredient blend supports long-term potentiation (LTP). Long Term Potentiation is an extended increase of effectiveness between the neurons and synapses in our brain. The principles of synaptic enforcement is first written about by Donald Hebb in 1949. The improvement in LTP is the founding block for learning and memory. LTP itself is first discovered by Terje Lome in 1966 and is written down in a neuroscientific research. The purified ingredients in OmniMind, enable the benefits of LTP.
Artichoke Extract contains Luteolin, which is a natural and safe inhibitor of PDE4. Reasearch has proven the effective nootropic effects of PDE4.
Forskolin activates the enzyme adenylyl cyclase. Adenylyl cyclase increases the intracellular levels of cAMP.
Another functionality in OmniMind is the unique combination of L-theanine with Caffeine. Research shows a sustained and improved mental clarity and mood is experienced by double blinded tests.
The articles hereunder will give you a better insights in the scientific background of OmniMind.
Publishment
LOCALIZATION OF PRESYNAPTIC PLASTICITY MECHANISMS ENABLES FUNCTIONAL INDEPENDENCE OF SYNAPTIC AND ECTOPIC TRANSMISSION IN THE CEREBELLUM.
Neural Plast. 2015;2015:602356. doi: 10.1155/2015/602356. Epub 2015 Jun 10.
Abstract
In the cerebellar molecular layer parallel fibre terminals release glutamate from both the active zone and from extrasynaptic “ectopic” sites. Ectopic release mediates transmission to the Bergmann glia that ensheathe the synapse, activating Ca(2+)-permeable AMPA receptors and glutamate transporters. Parallel fibre terminals exhibit several forms of presynaptic plasticity, including cAMP-dependent long-term potentiation and endocannabinoid-dependent long-term depression, but it is not known whether these presynaptic forms of long-term plasticity also influence ectopic transmission to Bergmann glia. Stimulation of parallel fibre inputs at 16 Hz evoked LTP of synaptic transmission, but LTD of ectopic transmission. Pharmacological activation of adenylyl cyclase by forskolin caused LTP at Purkinje neurons, but only transient potentiation at Bergmann glia, reinforcing the concept that ectopic sites lack the capacity to express sustained cAMP-dependent potentiation. Activation of mGluR1 caused depression of synaptic transmission via retrograde endocannabinoid signalling but had no significant effect at ectopic sites. In contrast, activation of NMDA receptors suppressed both synaptic and ectopic transmission. The results suggest that the signalling mechanisms for presynaptic LTP and retrograde depression by endocannabinoids are restricted to the active zone at parallel fibre synapses, allowing independent modulation of synaptic transmission to Purkinje neurons and ectopic transmission to Bergmann glia.
 
Publishment
A NOVEL MECHANISM FOR CYCLIC ADENOSINE MONOPHOSPHATE-MEDIATED MEMORY FORMATION: ROLE OF AMYLOID BETA.
Ann Neurol. 2014 Apr;75(4):602-7. doi: 10.1002/ana.24130. Epub 2014 Apr 14.
ABSTRACT
 
Cyclic adenosine monophosphate (cAMP) regulates long-term potentiation (LTP) and ameliorates memory in healthy and diseased brain. Increasing evidence shows that, under physiological conditions, low concentrations of amyloid β (Aβ) are necessary for LTP expression and memory formation. Here, we report that cAMP controls amyloid precursor protein (APP) translation and Aβ levels, and that the modulatory effects of cAMP on LTPoccur through the stimulation of APP synthesis and Aβ production.
© 2014 American Neurological Association.
Publishment
 
THE COMBINED EFFECTS OF L-THEANINE AND CAFFEINE ON COGNITIVE PERFORMANCE AND MOOD.
Nutr NEUROSCI. 2008 AUG;11(4):193-8. DOI: 10.1179/147683008X301513.
 
ABSTRACT
The aim of this study was to compare 50 mg caffeine, with and without 100 mg L-theanine, on cognition and mood in healthy volunteers. The effects of these treatments on word recognition, rapid visual information processing, critical flicker fusion threshold, attention switching and mood were compared to placebo in 27 participants. Performance was measured at baseline and again 60 min and 90 min after each treatment (separated by a 7-day washout). Caffeine improved subjective alertness at 60 min and accuracy on the attention-switching task at 90 min. The L-theanine and caffeine combination improved both speed and accuracy of performance of the attention-switching task at 60 min, and reduced susceptibility to distracting information in the memory task at both 60 min and 90 min. These results replicate previous evidence which suggests that L-theanine and caffeine in combination are beneficial for improving performance on cognitively demanding tasks.
Publishment
THE COMBINATION OF L-THEANINE AND CAFFEINE IMPROVES COGNITIVE PERFORMANCE AND INCREASES SUBJECTIVE ALERTNESS.
NUTR NEUROSCI. 2010 DEC;13(6):283-90. DOI: 10.1179/147683010X12611460764840.
PMID: 18681988 [PubMed – indexed for MEDLINE]
 
ABSTRACT
The non-proteinic amino acid L-theanine and caffeine, a methylxanthine derivative, are naturally occurring ingredients in tea. The present study investigated the effect of a combination of 97 mg L-theanine and 40 mg caffeine as compared to placebo treatment on cognitive performance, alertness, blood pressure, and heart rate in a sample of young adults (n = 44). Cognitive performance, self-reported mood, blood pressure, and heart rate were measured before L-theanine and caffeine administration (i.e. at baseline) and 20 min and 70 min thereafter. The combination of moderate levels of L-theanine and caffeine significantly improved accuracy during task switching and self-reported alertness (both P < 0.01) and reduced self-reported tiredness (P < 0.05). There were no significant effects on other cognitive tasks, such as visual search, choice reaction times, or mental rotation. The present results suggest that 97 mg of L-theanine in combination with 40 mg of caffeine helps to focus attention during a demanding cognitive task.
Publishment
BRAIN AND MEMORY: NEW NEURONS TO REMEMBER.
 
Biol Aujourdhui. 2015;209(3):229-48. doi: 10.1051/jbio/2015028. Epub 2016 Jan 28.
 PMID: 21040626 [PubMed – indexed for MEDLINE]
ABSTRACT
A defining characteristic of the brain is its remarkable capacity to undergo activity-dependent functional and structural remodelling via mechanisms of plasticity that form the basis of our capacity to encode and retain memories. The prevailing model of how our brain stores new information about relationships between events or new abstract constructs suggests it resides in activity-driven modifications of synaptic strength and remodelling of neural networks brought about by cellular and molecular changes within the neurons activated during learning. To date, the idea that a form of activity-dependent synaptic plasticity known as long-term potentiation, or LTP, and the associated synaptic growth play a central role in the laying down of memories has received considerable support. Beyond this mechanism of plasticity at the synapse, adult neurogenesis, i.e. the birth and growth of new neurons, is another form of neural plasticity that occurs continuously in defined brain regions such as the dentate gyrus of the hippocampus. Here, based on work in the hippocampus, we review the processes and mechanisms of the generation and selection of new neurons in the adult brain and the accumulating evidence that supports the idea that this form of neural plasticity is essential to store and lead to retrievable hippocampal-dependent memories.
 © Société de Biologie, 2016.
EPAC2 MEDIATES CAMP-DEPENDENT POTENTIATION OF NEUROTRANSMISSION IN THE HIPPOCAMPUS.
 J Neurosci. 2015 Apr 22;35(16):6544-53. doi: 10.1523/JNEUROSCI.0314-14.2015.
ABSTRACT
Presynaptic terminal cAMP elevation plays a central role in plasticity at the mossy fiber-CA3 synapse of the hippocampus. Prior studies have identified protein kinase A as a downstream effector of cAMP that contributes to mossy fiber LTP (MF-LTP), but the potential contribution of Epac2, another cAMP effector expressed in the MF synapse, has not been considered. We investigated the role of Epac2 in MF-CA3 neurotransmission using Epac2(-/-) mice. The deletion of Epac2 did not cause gross alterations in hippocampal neuroanatomy or basal synaptic transmission. Synaptic facilitation during short trains was not affected by loss of Epac2 activity; however, both long-term plasticity and forskolin-mediated potentiation of MFs were impaired, demonstrating that Epac2 contributes to cAMP-dependent potentiation of transmitter release. Examination of synaptic transmission during long sustained trains of activity suggested that the readily releasable pool of vesicles is reduced in Epac2(-/-) mice. These data suggest that cAMP elevation uses an Epac2-dependent pathway to promote transmitter release, and that Epac2 is required to maintain the readily releasable pool at MF synapses in the hippocampus.
 
Dohadwalla A.N (1985) Biological activities of forskolin. Edited by Rupp R.H; Souza N.J; Dohadwalla A.N – Proceedings of the international symposium on Forskolin: its chemical, biological and medicinal potential. Hoechst India Limited, Bombay 19-30.
Kavitha. C, Rajamani. K and Vadivel.E., Coleus forskohlii: A comprehensive review on morphology, phytochemistry and pharmacological aspects.
Journal of Medicinal Plants Research, Vol. 4(4) pp. 278-285, 18 February, 2010
http://www.biomedcentral.com/content/pdf/s12929-014-0074-2.pdf
http://link.springer.com/article/10.1007/s11055-008-9095-1