Nootropic Mushroom Formula

CLINICAL STUDIES ON THE FOLLOWING INGREDIENTS:

Lion’s Mane Mushroom (Hericium erinaceus)

Neurotrophic properties of the Lion's mane medicinal mushroom, Hericium erinaceus (Higher Basidiomycetes) from Malaysia*

Abstract

Neurotrophic factors are important in promoting the growth and differentiation of neurons. Nerve growth factor (NGF) is essential for the maintenance of the basal forebrain cholinergic system. Hericenones and erinacines isolated from the medicinal mushroom Hericium erinaceus can induce NGF synthesis in nerve cells. In this study, we evaluated the synergistic interaction between H. erinaceus aqueous extract and exogenous NGF on the neurite outgrowth stimulation of neuroblastoma-glioma cell NG108-15. The neuroprotective effect of the mushroom extract toward oxidative stress was also studied. Aqueous extract of H. erinaceus was shown to be non-cytotoxic to human lung fibroblast MRC-5 and NG108-15 cells. The combination of 10 ng/mL NGF with 1 μg/mL mushroom extract yielded the highest percentage increase of 60.6% neurite outgrowth. The extract contained neuroactive compounds that induced the secretion of extracellular NGF in NG108-15 cells, thereby promoting neurite outgrowth activity. However, the H. erinaceus extract failed to protect NG108-15 cells subjected to oxidative stress when applied in pre-treatment and co-treatment modes. In conclusion, the aqueous extract of H. erinaceus contained neuroactive compounds which induced NGF-synthesis and promoted neurite outgrowth in NG108-15 cells. The extract also enhanced the neurite outgrowth stimulation activity of NGF when applied in combination. The aqueous preparation of H. erinaceus had neurotrophic but not neuroprotective activities.

Source: Puei-Lene Lai, Murali Naidu, Vikineswary Sabaratnam, Kah-Hui Wong, Rosie Pamela David, Umah Rani Kuppusamy, Noorlidah Abdullah, and Sri Nurestri A Malek. “Neurotrophic properties of the Lion's mane medicinal mushroom, Hericium erinaceus (Higher Basidiomycetes) from Malaysia '' International Journal of Medicinal Mushrooms (2013): 15(6):539-54.

Chaga Mushroom (Inonotus obliquus)

Inhibitory effects of a polysaccharide extract from the Chaga medicinal mushroom, Inonotus obliquus (higher Basidiomycetes), on the proliferation of human neurogliocytoma cells*

Abstract

This study aimed to investigate the inhibitory roles of a polysaccharide extract from Inonotus obliquus on U251 human neurogliocytoma cells cultured in vitro. After administering the polysaccharide extract from I. obliquus to U251 cells cultivated in vitro, methyl thiazolyl tetrazoliym assay was performed to measure the inhibitory effects of the extract on tumor cell proliferation. The expression of the apoptosis-related proteins Bcl-2 and caspase-3 were determined by Western blotting. Different concentrations of I. obliquus extract (25, 50, 100, 200, and 500 µg/mL) were added to U251 cells at 24, 48, and 72 hours. Methyl thiazolyl tetrazoliym assay showed that the inhibition ratio increased with increased extract concentration and prolonged treatment duration. The I. obliquus extract sharply decreased the expression of Bcl-2 but dramatically increased the expression of caspase-3. This function was gradually enhanced with increased drug concentration and prolonged treatment duration. The I. obliquus extract can inhibit the proliferation of tumor cells. This inhibition function is closely related to the downregulation of Bcl-2 and the upregulation of caspase-3.

Source: Xianbin Ning, Qi Luo, Chuang Li, Zhaoyi Ding, Jinfeng Pang, and Changfu Zhao. “Inhibitory effects of a polysaccharide extract from the Chaga medicinal mushroom, Inonotus obliquus (higher Basidiomycetes), on the proliferation of human neurogliocytoma cells'' International Journal of Medicinal Mushrooms (2014)16(1):29-36.

Shiitake Mushroom (Lentinula edodes)

β-Glucan from Lentinula edodes prevents cognitive impairments in high-fat diet-induced obese mice: involvement of colon-brain axis*

Abstract

Background: Long-term high fat (HF) diet intake can cause neuroinflammation and cognitive decline through the gut-brain axis. (1, 3)/(1, 6)-β-glucan, an edible polysaccharide isolated from medical mushroom, Lentinula edodes (L. edodes), has the potential to remodel gut microbiota. However, the effects of L. edodes derived β-glucan against HF diet-induced neuroinflammation and cognitive decline remain unknown. This study aimed to evaluate the neuroprotective effect and mechanism of dietary L edodes β-glucan supplementation against the obesity-associated cognitive decline in mice fed by a HF diet.

Methods: C57BL/6J male mice were fed with either a lab chow (LC), HF or HF with L. edodes β-glucan supplementation diets for 7 days (short-term) or 15 weeks (long-term). Cognitive behavior was examined; blood, cecum content, colon and brain were collected to evaluate metabolic parameters, endotoxin, gut microbiota, colon, and brain pathology.

Results: We reported that short-term and long-term L. edodes β-glucan supplementation prevented the gut microbial composition shift induced by the HF diet. Long-term L. edodes β-glucan supplementation prevented the HF diet-induced recognition memory impairment assessed by behavioral tests (the temporal order memory, novel object recognition and Y-maze tests). In the prefrontal cortex and hippocampus, the β-glucan supplementation ameliorated the alteration of synaptic ultrastructure, neuroinflammation and brain-derived neurotrophic factor (BDNF) deficits induced by HF diet. Furthermore, the β-glucan supplementation increased the mucosal thickness, upregulated the expression of tight junction protein occludin, decreased the plasma LPS level, and inhibited the proinflammatory macrophage accumulation in the colon of mice fed by HF diet.

Conclusions: This study revealed that L. edodes β-glucan prevents cognitive impairments induced by the HF diet, which may occur via colon-brain axis improvement. The finding suggested that dietary L. edodes β-glucan supplementation may be an effective nutritional strategy to prevent obesity-associated cognitive decline.

Source: Wei Pan, Pengfei Jiang, Jinxiu Zhao, Hongli Shi, Peng Zhang, Xiaoying Yang, Joanna Biazik, Minmin Hu, Hui Hua, Xing Ge, Xu-Feng Huang, and Yinghua Yu. “β-Glucan from Lentinula edodes prevents cognitive impairments in high-fat diet-induced obese mice: involvement of colon-brain axis” Journal of Translational Medicine (2021): 19(1):54.

Reishi Mushroom (Ganoderma lucidium)

Polysaccharide from Ganoderma lucidum ameliorates cognitive impairment by regulating the inflammation of the brain-liver axis in rats*

Abstract

Ganoderma lucidum (G. lucidum) polysaccharide-1 (GLP-1) is one of the polysaccharides isolated from the fruiting bodies of G. lucidum. Inflammation in the brain-liver axis plays a vital role in the progress of cognitive impairment. In this study, the beneficial effect of GLP-1 on d-galactose (d-gal) rats was carried out by regulating the inflammation of the brain-liver axis. A Morris water maze test was used to assess the cognitive ability of d-gal rats. ELISA and/or western blot analysis were used to detect the blood ammonia and inflammatory cytokines levels in the brain-liver axis. Metabolomic analysis was used to evaluate the changes of small molecule metabolomics between the brain and liver. As a result, GLP-1 could obviously ameliorate the cognitive impairment of d-gal rats. The mechanism was related to the decreasing levels of TNF-α, IL-6, phospho-p38MAPK, phospho-p53, and phospho-JNK1 + JNK2 + JNK3, the increasing levels of IL-10 and TGF-β1, and the regulation of the metabolic disorders of the brain-liver axis. Our study suggests that G. lucidum could be exploited as an effective food or health care product to prevent and delay cognitive impairment and improve the quality of life.

Source: Yan Zhang, Haitao Li, Lianlian Song, Jianfei Xue, Xinyan Wang, Shuang Song, and Shuang Wang. “Polysaccharide from Ganoderma lucidum ameliorates cognitive impairment by regulating the inflammation of the brain-liver axis in rats” Food and Function (2021): 12(15):6900-6914.

Bacopa Monnieri

Neuropharmacological Review of the Nootropic Herb Bacopa monnieri*

Abstract

This review synthesizes behavioral research with neuromolecular mechanisms putatively involved with the low-toxicity cognitive enhancing action of Bacopa monnieri (BM), a medicinal Ayurvedic herb. BM is traditionally used for various ailments, but is best known as a neural tonic and memory enhancer. Numerous animal and in vitro studies have been conducted, with many evidencing potential medicinal properties. Several randomized, double-blind, placebo-controlled trials have substantiated BM's nootropic utility in humans. There is also evidence for potential attenuation of dementia, Parkinson's disease, and epilepsy. Current evidence suggests BM acts via the following mechanisms—antioxidant neuroprotection (via redox and enzyme induction), acetylcholinesterase inhibition and/or choline acetyltransferase activation, β-amyloid reduction, increased cerebral blood flow, and neurotransmitter modulation (acetylcholine [ACh], 5-hydroxytryptamine [5-HT], dopamine [DA]). BM appears to exhibit low toxicity in model organisms and humans; however, long-term studies of toxicity in humans have yet to be conducted. This review will integrate molecular neuroscience with behavioral research.

Conclusions: BM demonstrates immense potential in the amelioration of cognitive disorders, as well as prophylactic reduction of oxidative damage, NT modulation, and cognitive enhancement in healthy people. Biomedical research on BM is still in its infancy, but preliminary results such as these have begun to open the research floodgates. It is critical that much longer-term studies be conducted BM in combination with other substances, as is prescribed by the Ayurvedic system, may result in synergistic effects and should also be investigated.145–148 The social implications of cognition-enhancing drugs are promising but must be appropriately tempered with ethical consideration as researchers enter the brave new world of neural enhancement.

Source: Sebastian Aguiar and Thomas Borowski. “Neuropharmacological Review of the Nootropic Herb Bacopa monnieri” Rejuvenation Research (2013): 16(4): 313–326.

Rhodiola rosea

***Rhodiola rosea* Extract Protects Human Cortical Neurons against Glutamate and Hydrogen Peroxide-induced Cell Death Through Reduction in the Accumulation of Intracellular Calcium***

Abstract

The aim of this study was to investigate the neuroprotective effects of a titolated extract from Rhodiola rosea L. (RrE) and of salidroside (Sa), one of the major biologically active compounds extracted from this medicinal plant, against oxidative stressor hydrogen peroxide (H₂O₂) and glutamate (GLU)-induced cell apoptosis in a human cortical cell line (HCN 1-A) maintained in culture. The results obtained indicate that exposure of differentiated HCN 1-A neurons to GLU or H₂O₂ resulted in concentration-dependent cell death. A 24 h pre-treatment with RrE significantly increased cell survival and significantly prevented the plasma membrane damage and the morphological disruption caused by GLU or H₂O₂, indicating that neurons treated with RrE were protected from the neurotoxicity induced by the oxidative stressor used. In addition, RrE significantly reduced H₂O₂ or GLU-induced elevation of intracellular free Ca²⁺ concentration. The results obtained have also shown that Sa caused similar effects in all experimental models used; however, the potency of the action was lower than that of the extract containing corresponding quantities of Sa. These findings indicate that RrE has a neuroprotective effect in cortical neurons and suggest that the antioxidant activity of the RrE, due to the structural features of the synergic active principles they contain, may be responsible for its ability to stabilize cellular Ca²⁺ homeostasis.

Source; Dora Rita Palumbo, Francesco Occhiuto, Federica Spadaro, and Clara Circosta. “Rhodiola rosea Extract Protects Human Cortical Neurons against Glutamate and Hydrogen Peroxide-induced Cell Death Through Reduction in the Accumulation of Intracellular Calcium” Phytotherapy Research (2012): Vol. 26, Issue 6, pp 878-883.

Ginkgo biloba

Botanicals as Modulators of Neuroplasticity: Focus on BDNF*

Abstract

The involvement of brain-derived neurotrophic factor (BDNF) in different central nervous system (CNS) diseases suggests that this neurotrophin may represent an interesting and reliable therapeutic target. Accordingly, the search for new compounds, also from natural sources, able to modulate BDNF has been increasingly explored. The present review considers the literature on the effects of botanicals on BDNF. Botanicals considered were Bacopa monnieri (L.) Pennell, Coffea arabica L., Crocus sativus L., Eleutherococcus senticosus Maxim., Camellia sinensis (L.) Kuntze (green tea), Ginkgo biloba L.,Hypericum perforatum L., Olea europaea L. (olive oil), Panax ginseng C.A. Meyer, Rhodiola rosea L., Salvia miltiorrhiza Bunge, Vitis vinifera L., Withania somnifera (L.) Dunal, and Perilla frutescens (L.) Britton. The effect of the active principles responsible for the efficacy of the extracts is reviewed and discussed as well. The high number of articles published (more than one hundred manuscripts for 14 botanicals) supports the growing interest in the use of natural products as BDNF modulators. The studies reported strengthen the hypothesis that botanicals may be considered useful modulators of BDNF in CNS diseases, without high side effects. Further clinical studies are mandatory to confirm botanicals as preventive agents or as useful adjuvant to the pharmacological treatment.
6. Ginkgo biloba L. Ginkgo biloba is an ancient Chinese tree belonging to the family of Ginkgoaceae, cultivated for its health-promoting properties. Although both leaves and seeds are currently used as herbal medicine in China, in many countries, leaves are considered the unique source of active principles and dried green leaves are used for supplying pharmaceutical formulations or extracts as ingredients of food supplements. Ginkgo biloba and its constituents were evaluated on BDNF in three in vitro, eight in vivo, and one clinical studies.
6.1. In Vitro Studies Ginkgo biloba leaf extract (EGb761, 100 μg/mL) restored the levels of BDNF protein (both pro and mature form) in cells stimulated with appropriate medium able to induce amyloid β-peptide Aβ expression. Administration of individual EGb761 constituents, namely, ginkgolides A (GA), B (GB), C (GC), and J (GJ) and 10 μg/mL bilobalide, increased the levels of BDNF by following a similar pattern. Accordingly, flavonol-enriched extract containing quercetin, kaempferol, and isorhamnetin (50 μg/mL) significantly restored BDNF protein expression in double transgenic APP/PS1 primary neurons.Moreover, 100 μg/mL of YY162, a patented formula consisting of terpenoid-strengthened Ginkgo bilobaand ginsenoside Rg3, prevented the reduction of BDNF protein levels induced by 48 h of Aroclor 1254 in SH-SY5Y neuroblastoma cell line.
6.2. In Vivo Studies Ginkgo flavonols (50 mg/kg, per os, daily for 4 months) significantly normalized the deficit of BDNF protein levels in the hippocampus of transgenic APP/PS1 mice and improved spatial learning similar to the administration of the antidepressant SSRI (serotonin selective reuptake inhibitor) fluoxetine (10 mg/kg), while exerting an antidepressant effect on wild-type animals.
YY162 (200 mg/kg, per os, from PND 21 to PND 35) significantly attenuated the reduction of BDNF protein in the prefrontal cortex and ameliorated the ADHD- (attention deficit hyperactivity disorder-) like behavioral phenotype induced by Aroclor 1254.
Intravenous (i.v.) injections of EGb761 (45 mg/kg), just before ischemia-reperfusion, induced a significant increase in BDNF positive neurons in the hippocampus with respect to the control group; the treatment significantly reduced the behavior grade measured by a postural reflex test at 24 h after reperfusion. The effect exerted by EGb761 was comparable to that exerted by the antihypertensive nimodipine (2 mg/kg).
Chronic treatment with EGb761 (100 mg/kg/day via oral gavage for 30 days) increased the BDNF levels in plasma of both young and aged (18 months) rats, but the effect was not statistically significant; on the opposite, in the aged female group, treatment significantly increased the number of platform crossings in the aged female group in the open field test (OFT).
Pretreatment with EGb761 (100 or 150 mg/kg/day, per os for 10 days) significantly inhibited the reduction of hippocampal BDNF protein due to LPS (lipopolysaccharide) injections (0.83 mg/kg, i.p.) and showed an antidepressant effect. Furthermore, EGb761 treatment (50 mg/kg/day, by oral gavage for 5 weeks) normalized the reduction of BDNF protein levels induced by the first-generation antipsychotic haloperidol injection (2 mg/kg/day, i.p., 5 weeks) in the prefrontal cortex, striatum, substantia nigra, and globus pallidus and reduced the vacuous chewing movement scores over the withdrawal period. Finally, 28 days of treatment with EGb761 (40 mg/kg) increased the expression of BDNF and explored the behavior in stressed rats. The effect was comparable to that of the SNRI (serotonin noradrenaline reuptake inhibitor) antidepressant venlafaxine (15 mg/kg). Administration of bilobalide (10 mg/kg, i.p.) for 10 days enhanced the hippocampal protein levels in normal mice more efficiently than that of fluoxetine (10 mg/kg).
Taken together, these preclinical results suggest that Ginkgo biloba L. administration may be efficacious in restoring BDNF in pathologies characterized by neurotrophin deficits. The main problem is that studies take into consideration different animal models mimicking different kinds of diseases, from Alzheimer's disease to stroke, thus making further results mandatory to confirm the supposed effect on BDNF.
6.3. Clinical Studies In the unique clinical study, one hundred fifty-seven patients affected by tardive dyskinesia (TD) associated with long-term neuroleptic treatment were randomized to either EGb761 80 mg three times a day or placebo treatment. EGb761 significantly increased the BDNF protein plasma levels compared with placebo at week 12 in TD patients.

Source: Enrico Sangiovanni, Paola Brivio, Mario Dell'Agli, and Francesca Calabrese. “Botanicals as Modulators of Neuroplasticity: Focus on BDNF” Neural Plasticity (2017): 5965371.

Panax ginseng

Cognition enhancing effect of panax ginseng in Korean volunteers with mild cognitive impairment: a randomized, double-blind, placebo-controlled clinical trial*

Abstract

This study aimed to investigate the cognition-enhancing effect of Panax ginseng. A randomized, double-blind, placebo-controlled clinical trial was conducted to address the cognition-enhancing effects of Panax ginseng. A total of 90 Korean volunteers with mild cognitive impairment participated in this study. All subjects were allocated randomly into ‘Ginseng’ group or ‘Placebo’ group. All subjects were administered 3g of Panax ginseng powder or starch (placebo) for 6 months. The Korean version of the Mini-Mental Status Examination (K-MMSE), Korean version of Instrumental Activities of Daily Living (K-IADL), and Seoul Neuropsychological Screening Battery (SNSB) were used to assess the changes in cognitive function at the end of the 6 month study period. The subjects of the ‘Ginseng’ group improved significantly on the Rey Complex Figure Test (RCFT) immediate recall (P = 0.0405 and P = 0.0342 in per-protocol (PP) and intention-to-treat (ITT) analysis, respectively) and on the RCFT 20-min delayed recall (P = 0.0396 and P = 0.0355 in PP and ITT analysis, respectively) compared with ‘placebo’ group throughout the 6 months of Panax ginseng administration. There were no serious adverse events. These results suggest that Panax ginseng has a cognition-enhancing effect.

Conclusions: In conclusion, we found that the oral administration of ginseng for 6 months has a positive effect on cognitive improvement, particularly on visual memory function in Korean subjects with MCI. Our results provide clinical evidence of Panax ginseng as a cognition-enhancing medicine.

Source: Key-Chung Park, Hui Jin, Renhua Zheng, Sehyun Kim, Seung-Eun Lee, Bo-Hyung Kim, and Sung-Vin Yim. “Cognition enhancing effect of panax ginseng in Korean volunteers with mild cognitive impairment: a randomized, double-blind, placebo-controlled clinical trial” Translation of Clinical Pharmacology (2019): 27(3): 92–97.

Gingko biloba & Panax gingseng

The memory enhancing effects of a Ginkgo biloba/Panax ginseng combination in healthy middle-aged volunteers*

Abstract

The effects of capsules containing 60 mg of a standardised extract of Ginkgo biloba (GK501) and 100 mg of a standardised extract of Panax ginseng (G115) on various aspects of cognitive function were assessed in healthy middle-aged volunteers. A double blind, placebo controlled, 14-week, parallel group, repeated assessment, multi-centre trial of two dosing regimens, 160 mg b.i.d. and 320 mg o.d. was conducted. Two hundred and fifty-six healthy middle-aged volunteers successfully completed the study. On various study days (weeks 0, 4, 8, 12 and 14) the volunteers performed a selection of tests of attention and memory from the Cognitive Drug Research computerised cognitive assessment system prior to morning dosing and again, at 1, 3 and 6 h later. The volunteers also completed questionnaires about mood states, quality of life and sleep quality. The Ginkgo/ginseng combination was found significantly to improve an Index of Memory Quality, supporting a previous finding with the compound. This effect represented an average improvement of 7.5% and reflected improvements to a number of different aspects of memory, including working and long-term memory. This enhancement to memory was seen throughout the 12-week dosing period and also after a 2-week washout. This represents the first substantial demonstration of improvements to the memory of healthy middle-aged volunteers produced by a phytopharmaceutical.

Source: K. A. Wesnes, T. Ward, A. McGinty, and O. Petrini. “The memory enhancing effects of a Ginkgo biloba/Panax ginseng combination in healthy middle-aged volunteers” Pharmacology (Clinical trial) (2000): 152(4):353-61.

CDP Choline (citicoline)

Cytidinediphosphocholine (CDP-choline) for cognitive and behavioural disturbances associated with chronic cerebral disorders in the elderly*

Abstract

Background: CDP-choline (cytidine 5'-diphosphocholine) is a precursor essential for the synthesis of phosphatidylcholine, one of the cell membrane components that is degraded during cerebral ischaemia to free fatty acids and free radicals. Animal studies suggest that CDP-choline may protect cell membranes by accelerating resynthesis of phospholipids. CDP-choline may also attenuate the progression of ischaemic cell damage by suppressing the release of free fatty acids. CDP-choline is the endogenous compound normally produced by the organism. When the same substance is introduced as a drug it can be called citicoline. CDP-choline is mainly used in the treatment of disorders of a cerebrovascular nature. The many years of its presence in the clinical field have caused an evolution in dosage, method of administration, and selection criteria of patients to whom the treatments were given. Modalities of the clinical studies, including length of observation, severity of disturbance, and methodology of evaluation of the results were also heterogeneous. In spite of uncertainties about its efficacy due to these complexities, CDP-choline is a frequently prescribed drug for cognitive impairment in several European countries, especially when the clinical picture is predominantly one of cerebrovascular disease, hence the need for this review. Due to its effects on the adrenergic and dopaminergic activity of the CNS, CDP-choline has also been used as an adjuvant in the treatment of Parkinson's disease.

Source: M. Fioravanti, and M. Yanagi. “Cytidinediphosphocholine (CDP-choline) for cognitive and behavioural disturbances associated with chronic cerebral disorders in the elderly” The Cochrane Database of Systemic Reviews (2005): (2):CD000269.

Huperzine A (Huperzia serrata)

Neuroprotective effects of huperzine A. A natural cholinesterase inhibitor for the treatment of Alzheimer's disease*

Abstract

Huperzine A (HupA), isolated from Chinese herb Huperzia serrata, is a potent, highly specific and reversible inhibitor of acetylcholinesterase. It has been found to reverse or attenuate cognitive deficits in a broad range of animal models. Clinical trials in China have demonstrated that HupA significantly relieves memory deficits in aged subjects, patients with benign senescent forgetfulness, Alzheimer's disease (AD) and vascular dementia (VD), with minimal peripheral cholinergic side effects compared with other AChEIs in use. HupA possesses the ability to protect cells against hydrogen peroxide, beta-amyloid protein (or peptide), glutamate, ischemia and staurosporine-induced cytotoxicity and apoptosis. These protective effects are related to its ability to attenuate oxidative stress, regulate the expression of apoptotic proteins Bcl-2, Bax, P53 and caspase-3, protect mitochondria, and interfere with APP metabolism. Antagonizing effects on NMDA receptors and potassium currents may contribute to the neuroprotection as well. It is also possible that the non-catalytic function of AChE is involved in neuroprotective effects of HupA. The therapeutic effects of HupA on AD or VD are probably exerted via a multi-target mechanism.

Source: Rui Wang, and Xi Can Tang. “Neuroprotective effects of huperzine A. A natural cholinesterase inhibitor for the treatment of Alzheimer's disease” Neuro-Signals (2005)14(1-2):71-82.

Vitamin B6 (pyridoxine hydrochloride)

Vitamin B6 deficiency decreases the glucose utilization in cognitive brain structures of rats*

Abstract

The effects of vitamin B(6) deficiency on metabolic activities of brain structures were studied. Male Sprague-Dawley weanling rats received one of the following diets: (1) 7 mg pyridoxine HCl/kg (control group); (2) 0 mg pyridoxine HCl/kg (vitamin B(6)-deficient group); or (3) 7 mg pyridoxine HCl/kg with food intake restricted in quantity to that consumed by the deficient group (pair-fed control group). After 8 weeks of dietary treatment, rats in all three groups received an intravenous injection of 2-deoxy-[(14)C] glucose (100 microCi/kg). Vitamin B(6) status was evaluated by plasma pyridoxal 5'-phosphate concentrations. The vitamin B(6)-deficient group had significantly lower levels of plasma pyridoxal 5'-phosphate than did the control and pair-fed groups. The local cerebral glucose utilization rates in structures of the limbic system, basal ganglia, sensory motor system, and hypothalamic system were determined. The local cerebral glucose utilization rates in each of the four brain regions in the deficient animals were approximately 50% lower (P < 0.05) than in the control group. Results of the present study suggest that serious cognitive deficit may occur in vitamin B(6)-deficient animals.

Source; I. L. Wei, Y. H. Huang, and G. S. Wang. Vitamin B6 deficiency decreases the glucose utilization in cognitive brain structures of rats” The Journal of Nutritional Biochemistry (1999): 10(9):525-31.

Vitamin B12 (methylcobalamin)

Vitamin B-12 concentration, memory performance, and hippocampal structure in patients with mild cognitive impairment*

Abstract

Background: Low-normal concentrations of vitamin B-12 (VitB12) may be associated with worse cognition. However, previous evidence has been mixed, and the underlying mechanisms remain unclear.

Objective: We determined whether serum VitB12 concentrations within the normal range were linked to memory functions and related neuronal structures in patients with mild cognitive impairment (MCI).

Design: In a cross-sectional design, we assessed 100 amnestic MCI patients (52 women; age range: 50-80 y) with low- and high-normal VitB12 concentration (median split: 304 pmol/L) for memory functions with the use of the Auditory Verbal Learning Test. MRI was performed at 3 tesla (n= 86) for the estimation of the volume and microstructure of the hippocampus and its subfields as indicated by the mean diffusivity on diffusion-weighted images. With the use of a mediation analysis, we examined whether the relation between VitB12 and memory performance was partially explained by volume or microstructure.

Results: MCI patients with low-normal VitB12 showed a significantly poorer learning ability (P= 0.014) and recognition performance (P= 0.008) than did patients with high-normal VitB12. Also, the microstructure integrity of the hippocampus was lower in patients with low-normal VitB12, mainly in the cornu ammonis 4 and dentate gyrus region (P= 0.029), which partially mediated the effect of VitB12 on memory performance (32-48%). Adjustments for age, sex, education, apolipoprotein E e4 status, and total homocysteine, folate, and creatinine did not attenuate the effects.

Conclusions: Low VitB12 concentrations within the normal range are associated with poorer memory performance, which is an effect that is partially mediated by the reduced microstructural integrity of the hippocampus. Future interventional trials are needed to assess whether supplementation of VitB12 may improve cognition in MCI patients even in the absence of clinically manifested VitB12 deficiency. This trial was registered at clinicaltrials.gov as NCT01219244.

Source: Theresa Köbe, A. Veronica Witte, Ariane Schnelle, Ulrike Grittner, Valentina A. Tesky, Johannes Pantel, Jan Philipp Schuchardt, Andreas Hahn, Jens Bohlken, Dan Rujescu, and Agnes Flöel. “Vitamin B-12 concentration, memory performance, and hippocampal structure in patients with mild cognitive impairment” The American Journal of Clinical Nutrition (2016): 103(4):1045-54.

Nootropic Mushroom Formula

CLINICAL STUDIES ON THE FOLLOWING INGREDIENTS:

Lion’s Mane Mushroom (Hericium erinaceus)

Neurotrophic properties of the Lion's mane medicinal mushroom, Hericium erinaceus (Higher Basidiomycetes) from Malaysia*

Abstract

Chaga Mushroom (Inonotus obliquus)

Inhibitory effects of a polysaccharide extract from the Chaga medicinal mushroom, Inonotus obliquus (higher Basidiomycetes), on the proliferation of human neurogliocytoma cells*

Abstract

Shiitake Mushroom (Lentinula edodes)

β-Glucan from Lentinula edodes prevents cognitive impairments in high-fat diet-induced obese mice: involvement of colon-brain axis*

Abstract

Reishi Mushroom (Ganoderma lucidium)

Polysaccharide from Ganoderma lucidum ameliorates cognitive impairment by regulating the inflammation of the brain-liver axis in rats*

Abstract

Bacopa Monnieri

Neuropharmacological Review of the Nootropic Herb Bacopa monnieri*

Abstract

Rhodiola rosea

Rhodiola rosea Extract Protects Human Cortical Neurons against Glutamate and Hydrogen Peroxide-induced Cell Death Through Reduction in the Accumulation of Intracellular Calcium*

Abstract

Ginkgo biloba

Botanicals as Modulators of Neuroplasticity: Focus on BDNF*

Abstract

Panax ginseng

Cognition enhancing effect of panax ginseng in Korean volunteers with mild cognitive impairment: a randomized, double-blind, placebo-controlled clinical trial*

Abstract

Gingko biloba & Panax gingseng

The memory enhancing effects of a Ginkgo biloba/Panax ginseng combination in healthy middle-aged volunteers*

Abstract

CDP Choline (citicoline)

Cytidinediphosphocholine (CDP-choline) for cognitive and behavioural disturbances associated with chronic cerebral disorders in the elderly*

Abstract

Huperzine A (Huperzia serrata)

Neuroprotective effects of huperzine A. A natural cholinesterase inhibitor for the treatment of Alzheimer's disease*

Abstract

Vitamin B6 (pyridoxine hydrochloride)

Vitamin B6 deficiency decreases the glucose utilization in cognitive brain structures of rats*

Abstract

Vitamin B12 (methylcobalamin)

Vitamin B-12 concentration, memory performance, and hippocampal structure in patients with mild cognitive impairment*

Abstract

References:

***Rhodiola rosea* Extract Protects Human Cortical Neurons against Glutamate and Hydrogen Peroxide-induced Cell Death Through Reduction in the Accumulation of Intracellular Calcium***