NeuroStim

NEUROSTIM

GET NEUROLOGICALLY OPTIMIZED

A breakthrough in neuro-cognitive support

Neurostim is a scientifically formulated neurological tissue, bioenergetic and cognition compound that provides a synergistic blend of powerful nootropics, nutraceuticals, anti-oxidants, anti-inflammatory modulators and ketones that provide the brain with protection against negative bioenergetics and tissue degradation.

Alpha GPC helps maximize acetylcholine levels while other ingredients assist in elevating dopamine and GABA levels, crucial compo­nents to remaining calm, focused, and mentally driven. Vinpocetine assists in delivering oxygen and nutrients to the brain via increased blood flow, and the combination of neuro-specific antioxidants, including HPL’s proprietary Poly-BHB, helps to clear away mental fog and reduce free radical burden. Phosphatidylser­ine (PS), is a well-known cognitive enhancer that is widely used to improve both focus and memory.

Neurostim’s synergistic combination of proven nootropics and cognition enhancement technology enhances mental drive, focus, memory, and mental acuity.


NeuroStim provides superior neurological support…

 Powerful Blend of Nootropics for Improved Cognitive Function

Neurostim cognition panel

Complete Anti-Oxidant Profile for Reduction in Cellular Emissions

Neurostim antioxidant panel

Ketone Bodies for Superior Neurological Energy and Protection Against Hypoxic Induced Trauma and Metabolic  Energy Dysregulation

Neurostim Ketone Bodies panel

Complex Nutraceuticals to Enhance Neurological Co-Processor Efficiency

Neurostim Neurological Efficiency panel

NEUROSTIM

BACKED BY RESEARCH, PROVEN BY SCIENCE…

Neurostim for Energy
  • Ketone bodies represent an important alternative energy substrate for cerebral metabolism, sparing amino acid utilization for gluconeogenesis. A Cause of Permanent Ketosis: GLUT-1 Deficiency. Alexis Chenouard ,Sandrine Vuillaumier-Barrot, Nathalie Seta, Alice Kuster 09/2014

 

  • Ketone bodies supply energy to non-hepatic tissues, mainly brain and skeletal muscles. MacDonald MJ, Dobrzyn A, Ntambi J, Stoker SW. The role of rapid lipogenesis in insulin secretion: Insulin secretagogues acutely alter lipid composition of INS-1 832/13 cells. Arch Biochem Biophys 2008;470:153–162. [PubMed: 18082128]

 

  • Consistent with the observed improvements in mitochondrial respiration, β –hydroxybutyrate increased ATP production substantially in isolated brain mitochondria and brain homogenates and acetoacetate increased phosphocreatine levels in cardiac myocytes (Suzuki et al. 2001; Squires et al. 2002 Tieu et al. 2003). These findings provide further support for the hypothesis that ketone bodies improve mitochondrial function and explain how ketone bodies increase myocardial hydraulic work and sperm motility described in previous work (Veech et al. 2001; Veech 2004). These findings also suggest that ketone bodies and calorie restriction enhance mitochondrial function through similar mechanisms. The Neuroprotective Properties of Calorie Restriction, the Ketogenic Diet, and Ketone Bodies.. Maalouf, et al. Brain Res Rev. 2009 March ; 59(2): 293–315. doi:10.1016/j.brainresrev.2008.09.002

 

  • Compared with fatty acid oxidation, ketone bodies are more energetically efficient, yielding more energy available for ATP synthesis per molecule of oxygen invested. Furthermore, the oxidation of ketone bodies may attenuate ROS production associated with the oxidation of fatty acids suggesting that myocardial ketone body oxidation could protect against injury and adverse ventricular remodeling responses, which promote the development of cardiomyopathy and heart failure.

 

  • Ketone bodies may be more energetically favorable substrates than fatty acids, in part through the maintenance of a favorable NAD/NADH ratio as well as their ability to maintain ubiquinone in the oxidized state, which increases redox span in the electron transport chain and thus diminishes superoxide production and increases energy available for ATP synthesis. In our study, Acetoacetate diminished the rate of superoxide production in mitochondria isolated from hearts of both SCOT-Heart-KO and control mice, which suggests that Acetoacetate-mediated suppression of mitochondrial superoxide emission is likely due to a non-oxidative role of Acetoacetate, whose mechanisms could include ROS scavenging by Acetoacetate, or diminished mitochondrial inner membrane potential through non-oxidative mechanisms.

 

  • Ketone bodies are also utilized by glial cells and are the primary substrates for glial synthesis of glutamine, where it is buffered in a large glial glutamine pool, and not highly contributing to neuronal glutamate and thus GABA.

 

  • Ketone bodies have been shown to increase cerebral blood flow and perfusion. Also, ketone bodies have been shown to increase ATP synthesis and enhance the efficiency of ATP production. Effects of exogenous ketone supplementation on blood ketone, glucose, triglyceride, and lipoprotein levels in Sprague–Dawley rats. Shannon L. Kesl, et al. Kesl et al. Nutrition & Metabolism (2016) 13:9 DOI 10.1186/s12986-016-0069-y

 

  • Ketone bodies provide a metabolic fuel for extrahepatic tissues. Energy Metabolism in the Liver. Liangyou Rui. Compr Physiol. 2014 January ; 4(1): 177–197. doi:10.1002/cphy.c130024.

 

  • Metabolism of ketone bodies provides a high energy yield- roughly 23-26 ATP/one BHB molecule. Moreover, BHB is the most efficient fuel per molecule of oxygen consumed when compared to glucose, pyruvate, or free fatty acids, due to its ability to widen the redox potential gap between the respiratory complex-I (NADH/NAD) and CoQ/CoQH2. Grabacka MM, Wilk A, Antonczyk A, Banks P, Walczyk-Tytko E, Dean M, Pierzchalska M and Reiss K (2016) Fenofibrate Induces Ketone Body Production in Melanoma and Glioblastoma Cells. Front. Endocrinol. 7:5. doi: 10.3389/fendo.2016.00005

 

  • Ketone oxidation increases the redox span between complex-I and complex-III by keeping mitochondrial ubiquinone oxidized. Ketone Body β-hydroxybutyrate Blocks the NLRP3 Inflammasome-Mediated Inflammatory Disease. Yun-Hee Youm, et al. Nat Med. 2015 March; 21 (3): 263-269. DOI:10.1038/nm.3804

 

  • Briefly, when BHB is converted to acetoacetate it generates NADH (the reduced form of nicotinamide adenine dinucleotide [NAD]), thereby reducing the mitochondrial NAD/NADH couple and increasing the oxidation of the co-enzyme Q couple. In addition, KB metabolism increases the mitochondrial pool of acetyl- CoA and succinate. The net effect of these changes is increased metabolic efficiency. Ketone Bodies as a Therapeutic for Alzheimer’s Disease. Samuel T. Henderson. Accera, Inc., Broomfield, Colorado 80021. Neurotherapeutics: The Journal of the American Society for Experimental NeuroTherapeutics

 

  • KBs, especially BHB, can enter the TCA cycle directly in the absence of Pyruvate Dehydrogenase enzyme complex. Astroglia and neurons responded to hypoxia by enhancing KB production, and KBs produced by astroglia or neurons or both might be used as a neuronal energy substrate. The activation of astroglial ketogenesis through activated AMPK might reduce ischemic cell damage. Roles and Regulation of Ketogenesis in Cultured Astroglia and Neurons Under Hypoxia and Hypoglycemia Shinichi Takahashi, et al.  ASN Neuro July-September 2014: 1–14. DOI: 10.1177/1759091414550997

 

  • Even in the presence of glucose, the heart muscle preferentially utilizes fatty acids, ketone bodies, or lactate for an oxidative generation of ATP. The Role of Glucose Metabolism and Glucose-Associated Signalling in Cancer. Rainer Wittig and Johannes F. Coy. Perspectives in Medicinal Chemistry 2007:1 64–82

Neurostim for Neuroprotection
  • Ketone bodies protect neurons against multiple types of neuronal injury and the underlying mechanisms are similar to those of calorie restriction and of the ketogenic diet. Simultaneous quantification of salivary 3‑hydroxybutyrate, 3‑hydroxyisobutyrate, 3‑hydroxy‑3‑methylbutyrate, and 2‑hydroxybutyrate as possible markers of amino acid and fatty acid catabolic pathways by LC–ESI–MS/MS. Miyazaki et al. SpringerPlus (2015) 4:494 DOI 10.1186/s40064-015-1304-0

 

  • Rise in β -hydroxybutyrate concentration is associated with a more significant reduction in the vulnerability of hippocampal neurons to kainate injections.

 

  • In animal models of Parkinson’s disease, chronic subcutaneous infusion of β –hydroxybutyrate in mice conferred partial protection against dopaminergic cell loss and motor deficits induced by MPTP (Tieu et al. 2003). β -hydroxybutyrate also protected cultured mesencephalic dopaminergic neurons from the toxic effects of MPTP and rotenone, another inhibitor of mitochondrial complex I (Kashiwaya et al. 2000; Imamura et al. 2006). In patients with Alzheimer’s disease, administration of medium-chain triglycerides improved memory and the degree of improvement correlated with blood levels of β -hydroxybutyrate (Reger et al. 2004). Further, direct application of β -hydroxybutyrate protected cultured hippocampal neurons against Aβ  toxicity (Kashiwaya et al. 2000). Finally, exogenous administration of either β -hydroxybutyrate or acetoacetate reduced neuronal loss and improved neuronal function in animal models of hypoxia, hypoglycemia and focal ischemia (Suzuki et al. 2001, 2002; Massieu et al. 2001, 2003; Masuda et al. 2005). The Neuroprotective Properties of Calorie Restriction, the Ketogenic Diet, and Ketone Bodies.. Maalouf, et al. Brain Res Rev. 2009 March ; 59(2): 293–315. doi:10.1016/j.brainresrev.2008.09.002

 

  • A combination of β -hydroxybutyrate and acetoacetate (1 mM each) increased the survival of acutely dissociated rat neocortical neurons exposed to glutamate or hydrogen peroxide for 10 min or more (Kim et al. 2007; Maalouf et al. 2007b). Increased survival was associated with the inhibition of electrophysiological signs of neuronal injury, specifically, irreversible depolarization associated with a significantly decreased membrane resistance. Acetoacetate (also in millimolar concentrations) had a similar effect in primary hippocampal cultures (Noh et al. 2006a). In addition, the combination of β -hydroxybutyrate and acetoacetate prevented oxidative impairment of long-term potentiation in the CA1 region of the hippocampus, indicating that ketone bodies not only limited neuronal loss but also preserved synaptic function (Maalouf et al. 2007a). The Neuroprotective Properties of Calorie Restriction, the Ketogenic Diet, and Ketone Bodies.. Maalouf, et al. Brain Res Rev. 2009 March ; 59(2): 293–315. doi:10.1016/j.brainresrev.2008.09.002

 

  • A combination of β – hydroxybutyrate and acetoacetate (1 mM each) decreased the production of reactive oxygen species by complex I of the mitochondrial respiratory chain (Maalouf et al. 2007b). Specifically, in acutely isolated rat neocortical neurons, increases in the intracellular levels of superoxide following prolonged exposure to glutamate were inhibited by pretreatment with ketone bodies. Ketone bodies also decreased reactive oxygen species concentrations in isolated mitochondria overloaded with calcium. In a similar study, increased survival of HT22 hippocampal cell lines treated with acetoacetate was associated with decreased production of reactive oxygen species (Noh et al. 2006a). The Neuroprotective Properties of Calorie Restriction, the Ketogenic Diet, and Ketone Bodies.. Maalouf, et al. Brain Res Rev. 2009 March ; 59(2): 293–315. doi:10.1016/j.brainresrev.2008.09.002

 

  • In the study by Maalouf et al. (2007b), ketone bodies decreased NADH levels in intact neurons and in isolated mitochondria but did not affect glutathione levels. Furthermore, ketone bodies prevented the inhibition of mitochondrial respiration by calcium in the presence of pyruvate and malate but not succinate. Given that NADH oxidation correlates with decreased mitochondrial formation of reactive oxygen species (Duchen, 1992; Kudin et al, 2004; Sullivan et al, 2004a) and that pyruvate and malate drive mitochondrial respiration through complex I, the source of reactive oxygen species in neurons (Turrens 2003), these findings strongly suggested that ketone bodies decreased the production of reactive oxygen species by enhancing complex I-driven mitochondrial respiration rather than increase antioxidant factors such as glutathione. The Neuroprotective Properties of Calorie Restriction, the Ketogenic Diet, and Ketone Bodies.. Maalouf, et al. Brain Res Rev. 2009 March ; 59(2): 293–315. doi:10.1016/j.brainresrev.2008.09.002

 

  • Ketone bodies prevented neuronal injury and death caused by hydrogen peroxide or by the glutathione oxidant diamide (Kim et al. 2007). Their neuroprotective effect was replicated by inhibitors of mitochondrial permeability transition. In addition, ketone bodies elevated the threshold for calcium-induced mitochondrial permeability transition in isolated brain mitochondria. Mitochondrial permeability transition can be triggered by various pathological menchanisms, most notably oxidative stress, causing the cytoplasmic release of cytochrome c and the subsequent induction of caspase-mediated apoptosis (Mattson et al. 2003; Nicholls 2004; Balaban et al. 2005). In support of these data, ketone bodies blocked the activation of the apoptotic enzyme serine/threonine phosphatase 2A by oxidative stress (Maalouf et al. 2007a). The Neuroprotective Properties of Calorie Restriction, the Ketogenic Diet, and Ketone Bodies.. Maalouf, et al. Brain Res Rev. 2009 March ; 59(2): 293–315. doi:10.1016/j.brainresrev.2008.09.002

 

  • Ketone bodies were recently shown to prevent oxidative impairment of long-term potentiation, an effect that was associated with inhibition of protein phosphatase 2A (Maalouf et al. 2007a). The Neuroprotective Properties of Calorie Restriction, the Ketogenic Diet, and Ketone Bodies.. Maalouf, et al. Brain Res Rev. 2009 March ; 59(2): 293–315. doi:10.1016/j.brainresrev.2008.09.002

 

  • Ketosis and neuroprotection are linked through metabolic regulation via four mechanisms: 1) the “glucose sparing” effect which suggests that a decrease in glucose utilization and oxidation may be beneficial for brain function during recovery from neurological damage (LaManna et al. 2009; Zhang et al. 2013b), 2) the presence of brain ketone bodies in the reduction of glutamate neurotoxicity and promotion of GABA synthesis (Noh et al. 2006), 3) brain adaptation to chronic ketosis by induction of molecular regulatory proteins, such as monocarboxylate transporters (MCT) (Leino et al. 2001;Vannucci and Simpson 2003) and hypoxia-inducible factor (HIF1-α) that accounts for angiogenesis (Puchowicz et al. 2008), and 4) the reduction of reactive oxygen species (ROS) and subsequent oxidative stress in mitochondria (Bough and Eagles 1999; Maalouf et al. 2009; Sullivan et al. 2004). Decreased carbon shunting from glucose towards oxidative metabolism in diet-induced ketotic rat brain.  Yifan Zhang, Ph.D, Shenghui Zhang, M.S, Isaac Marin-Valencia, M.D and Michelle A. Puchowicz, Ph.D. J Neurochem. 2015 February;132(3):301–312. doi:10.1111

 

  • Ketones maintain brain metabolism and are neuroprotective during severe hypoglycemia. Effects of exogenous ketone supplementation on blood ketone, glucose, triglyceride, and lipoprotein levels in Sprague–Dawley rats. Shannon L. Kesl, et al. Kesl et al. Nutrition & Metabolism (2016) 13:9 DOI 10.1186/s12986-016-0069-y

 

  • BHB offers protection from ABeta toxicity. Ketone Bodies as a Therapeutic for Alzheimer’s Disease. Samuel T. Henderson. Accera, Inc., Broomfield, Colorado 80021. Neurotherapeutics: The Journal of the American Society for Experimental NeuroTherapeutics

 

  • Infusion of KB into rodents protects them from glutamate toxicity, ischemia, and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity. Ketone Bodies as a Therapeutic for Alzheimer’s Disease. Samuel T. Henderson. Accera, Inc., Broomfield, Colorado 80021. Neurotherapeutics: The Journal of the American Society for Experimental NeuroTherapeutics

 

  • BHB induces AgRP expression while increasing ATP and inhibiting AMPK phosphorylation (Cheng et al., 2008). Moreover, Laeger and colleagues have recently demonstrated that under physiological conditions BHB decreases AMPK phosphorylation and AgRP mRNA expression in GT1-7 hypothalamic cells. Ketosis,ketogenic diet and food intake control: a complex relationship AntonioPaoli1*, GerardoBosco1, et al. Frontiers in Psychology. published: 02 February 2015 doi: 10.3389/fpsyg.2015.00027

 

  • (D)-3-hydroxybutyrate, a metabolite also subject to gut microbial regulation, was recently shown to antagonize GPR41-mediated SNS activation. Metabolic tinkering by the gut microbiome : Implications for brain development and function. Joel Selkrig, et al. Gut Microbes 5:3, 369-380. May/June 2014. Landes Bioscience.

 

  • BHB decreases hypoglycemia and glutamate-mediated lipoperoxidation in the rat brain. The physiologic and the nonphysiologic isomers of BHB (D- and L-BHB, respectively) scavenge OH in a free-cell system and reduce neuronal death and ROS production induced by glycolysis inhibition in cultured hippocampal neurons and hypoglycemia-induced lipoperoxidation in vivo. These observations support the potential of KB to prevent oxidative stress and cell death induced during energy limiting conditions or overexcitation. Protection of hypoglycemia-induced neuronal death by β-hydroxybutyrate involves the preservation of energy levels and decreased production of reactive oxygen species. Alberto Julio-Amilpas, et al. Journal of Cerebral Blood Flow & Metabolism (2015) 35, 851–860

 

  • Present observations suggest that D-BHB can substitute for glucose in an in vivo model of noncoma hypoglycemia and effectively prevent ROS generation and cell death in all affected cortical areas, regardless their differential production of ROS and vulnerability to cell death. In vitro results suggest that the metabolic activity of D-BHB in combination with its antioxidant action contributes to the effective protective action of this KB, and that these actions can take place during the recovery period in the presence of glucose. These observations support the therapeutic potential of D-BHB against ischemic and traumatic insults, which are associated with energy impairment and oxidative stress and which require treatments that can be effective when administered after the insult. Protection of hypoglycemia-induced neuronal death by β-hydroxybutyrate involves the preservation of energy levels and decreased production of reactive oxygen species. Alberto Julio-Amilpas, et al. Journal of Cerebral Blood Flow & Metabolism (2015) 35, 851–860

 

  • In vitro data show that D-BHB notably prevents neuronal death when incubated during glucose deprivation and glucose reperfusion, but is also effective when incubated only during glucose deprivation or only during glucose reperfusion. Consistently, ATP levels recover to the same extent when D-BHB is present only during glucose deprivation, only during glucose reperfusion or during both periods. According to these data preserving ATP concentrations at levels 30% to 40% below control values is sufficient to significantly prevent neuronal death. These observations also indicate that D-BHB can stimulate ATP production during glucose deprivation but also during glucose reperfusion likely through its metabolism by the tricarboxylic acid cycle. The present results agree with other studies showing protection by the ketogenic diet or BHB infusion against ischemic and traumatic brain injury. The improvement of mitochondrial function and ATP production has been suggested by several studies as the main mechanism involved in the neuroprotective action of KB. According to the present data, besides the stimulation of ATP production, D-BHB also reduces ROS levels. Similar results have been previously reported in cultured and isolated neurons as well as in isolated mitochondria, and this effect has been implicated in the protective action of KB against excitotoxic neuronal death. Protection of hypoglycemia-induced neuronal death by β-hydroxybutyrate involves the preservation of energy levels and decreased production of reactive oxygen species. Alberto Julio-Amilpas, et al. Journal of Cerebral Blood Flow & Metabolism (2015) 35, 851–860

 

  • Some studies have suggested that there may be a bioenergetics shift taking place within neuronal metabolism prior to the onset of clinical signs of neurodegeneration, where glucose uptake and utilization become progressively reduced. This glucose hypometabolism may reflect a decline in mitochondrial function. The shift has been observed to occur long before the onset of clinical signs of neurodegeneration, suggesting the possibility that glucose hypometabolism may be the initial step leading to axonal atrophy and neuronal loss through a reduction in ATP availability. The bioenergetics shift appears to specifically affect the metabolism of glucose. No such shift is seen with ketone body metabolism. The Therapeutic Potential of the Ketogenic Diet in Treating Progressive Multiple Sclerosis. Mithu Storoni and Gordon T. Plant. Hindawi Publishing Corporation. Multiple Sclerosis International. Volume 2015, Article ID 681289, 9 pages.

 

  • Ketone bodies play a neuroprotective role in animal models of neurodegeneration. ATP-sensitive potassium channels (K ATP channels) located on the cell surface of neurons stabilize neuronal excitability. Ketones promote an “open state” of these channels and confer neuronal stability. K ATP channels also play a role in mitochondrial function and in cell death. The “open state” of K ATP channels located on the inner mitochondrial membrane prevents the formation of mitochondrial permeability transition pores (MPTPs) that can lead to mitochondrial swelling and cell death. Acetoacetate and beta-hydroxybutyrate have been shown to increase the threshold for calcium-induced MPTP formation. The Therapeutic Potential of the Ketogenic Diet in Treating Progressive Multiple Sclerosis. Mithu Storoni and Gordon T. Plant. Hindawi Publishing Corporation. Multiple Sclerosis International. Volume 2015, Article ID 681289, 9 pages.

 

  • Acetone and BHB enhanced inhibitory glycine receptors, whereas BHB alone was able to enhance GABAA -receptor mediated currents – but all of these actions were observed at highly supratherapeutic (i.e., anesthetic) concentrations, not seen during KD treatment. Mechanisms of Ketogenic Diet Action. Susan A. Masino, Jong M. Rho. Jasper’s Basic Mechanisms of the Epilepsies, Fourth Ed.

 

  • More recent work has demonstrated that BHB decreases GABA degradation, and thus could increase the available pool of GABA. Mechanisms of Ketogenic Diet Action. Susan A. Masino, Jong M. Rho. Jasper’s Basic Mechanisms of the Epilepsies, Fourth Ed.

 

  • Late treatment with choline alfoscerate (l-alpha glycerylphosphorylcholine, α-GPC) increases hippocampal neurogenesis and provides protection against seizure-induced neuronal death and cognitive impairment. Brain Res. 2017 Jan 1;1654(Pt A):66-76. doi: 10.1016/j.brainres.2016.10.011. Epub 2016 Oct 17

 

  • Neuroprotective Effects of Agomelatine and Vinpocetine Against Chronic Cerebral Hypoperfusion Induced Vascular Dementia. Curr Neurovasc Res. 2015;12(3):240-52.

 

  • Neuroprotective, Neurotrophic and Anti-oxidative Role of Bacopa monnieri on CUS Induced Model of Depression in Rat. Neurochem Res. 2016 Nov;41(11):3083-3094. Epub 2016 Aug 10.

 

  • Efficacy of Standardized Extract of Bacopa monnieri (Bacognize®) on Cognitive Functions of Medical Students: A Six-Week, Randomized Placebo-Controlled Trial. Evid Based Complement Alternat Med. 2016;2016:4103423. Epub 2016 Oct 10.

 

  • Elucidation of Molecular Mechanism(s) of Cognition Enhancing Activity of Bacomind®: A Standardized Extract of Bacopa Monnieri. Pharmacogn Mag. 2016 Jul;12(Suppl 4):S482-S487.

 

  • Cognitive training and Bacopa monnieri: Evidence for a combined intervention to alleviate age associated cognitive decline. Med Hypotheses. 2016 Oct;95:71-76. doi: 10.1016/j.mehy.2016.09.002. Epub 2016 Sep 7.

 

  • The Ayurvedic plant Bacopa monnieri inhibits inflammatory pathways in the brain. J Ethnopharmacol. 2016 Jul 26. pii: S0378-8741(16)30495-0. doi: 10.1016/j.jep.2016.07.073. [Epub ahead of print]

 

  • Acetyl-L-Carnitine via Upegulating Dopamine D1 Receptor and Attenuating Microglial Activation Prevents Neuronal Loss and Improves Memory Functions in Parkinsonian Rats. Mol Neurobiol. 2016 Dec 14. [Epub ahead of print]
Neurostim for Cognition
  • The single administration of MCT led to a significant correlation between performance on the paragraph recall task and serum BHB concentration, with those subjects presenting the highest BHB levels showing the most improvement. In addition, there was significant improvement in ADAS-Cog scores. The rapid (90 min) improvement seen in cognitive tasks suggests that the effect is driven by enhanced neuronal metabolism. Ketone Bodies as a Therapeutic for Alzheimer’s Disease. Samuel T. Henderson. Accera, Inc., Broomfield, Colorado 80021. Neurotherapeutics: The Journal of the American Society for Experimental NeuroTherapeutics

 

  • Vinpocetine Improves Scopolamine Induced Learning and Memory Dysfunction in C57 BL/6J Mice. Biol Pharm Bull. 2016 Sep 1;39(9):1412-8. doi: 10.1248/bpb.b15-00881. Epub 2016 Jun 21.

 

  • Bacopa monnieri (Brahmi) improved novel object recognition task and increased cerebral vesicular glutamate transporter type 3 in sub-chronic phencyclidine rat model of schizophrenia. Clin Exp Pharmacol Physiol. 2016 Dec;43(12):1234-1242. doi: 10.1111/1440-1681.12658.

 

  • Cognition-enhancing properties of subchronic phosphatidylserine (PS) treatment in middle-aged rats: comparison of bovine cortex PS with egg PS and soybean PS. Nutrition. 1999 Oct;15(10):778-83.

 

  • The influence of soy-derived phosphatidylserine on cognition in age-associated memory impairment. Nutr Neurosci. 2001;4(2):121-34.