An amino acid that is naturally produced in the body which helps produce energy and can help increase energy production in the mitochondria. This acetylated version of carnitine is able to cross the blood-brain barrier. Its primary effect is on the production of acetylcholine which is one of the main neurotransmitters involved in memory, learning, computation, analysis and many other cognitive processes.†
“Dietary supplementation with acetyl-l-carnitine counteracts age-related alterations of mitochondrial biogenesis, dynamics and antioxidant defenses in brain of old rats.”
Results: Overall, our findings indicate a systemic positive effect of ALCAR dietary treatment and a tissue specific regulation of mitochondrial homeostasis in brain of old rats. Moreover, it appears that ALCAR acts as a nutrient since in most cases its effects were almost completely abolished one month after treatment suspension. Dietary supplementation of old rats with this compound seems a valuable approach to prevent age-related mitochondrial dysfunction and might ultimately represent a strategy to delay age-associated negative consequences in mitochondrial homeostasis.
Exp Gerontol. 2017 Nov;98:99-109. doi: 10.1016/j.exger.2017.08.017. Epub 2017 Aug 12.
Nicassio L1, Fracasso F1, Sirago G1, Musicco C2, Picca A3, Marzetti E3, Calvani R3, Cantatore P1, Gadaleta MN2, Pesce V4.https://doi.org/10.1016/j.exger.2017.08.017
“L-Carnitine and Acetyl-L-carnitine Roles and Neuroprotection in Developing Brain.”
Results: There is compelling evidence from preclinical studies that L-carnitine and ALCAR can improve energy status, decrease oxidative stress and prevent subsequent cell death in models of adult, neonatal and pediatric brain injury. ALCAR can provide an acetyl moiety that can be oxidized for energy, used as a precursor for acetylcholine, or incorporated into glutamate, glutamine and GABA, or into lipids for myelination and cell growth. Administration of ALCAR after brain injury in rat pups improved long-term functional outcomes, including memory. Additional studies are needed to better explore the potential of L-carnitine and ALCAR for protection of developing brain as there is an urgent need for therapies that can improve outcome after neonatal and pediatric brain injury.
Neurochem Res. 2017 Jun;42(6):1661-1675. doi: 10.1007/s11064-017-2288-7. Epub 2017 May 16.
Ferreira GC1,2, McKenna MC3,4.https://link.springer.com/article/10.1007%2Fs11064-017-2288-7
“Acetyl-l-carnitine protects dopaminergic nigrostriatal pathway in 6-hydroxydopamine-induced model of Parkinson's disease in the rat.”
Results: The results of this study clearly suggest the neuroprotective effect of ALC in 6-OHDA-induced model of PD through abrogation of neuroinflammation, apoptosis, astrogliosis, and oxidative stress and it may be put forward as an ancillary therapeutic candidate for controlling PD.
Biomed Pharmacother. 2017 May;89:1-9. doi: 10.1016/j.biopha.2017.02.007. Epub 2017 Feb 12.
Afshin-Majd S1, Bashiri K2, Kiasalari Z3, Baluchnejadmojarad T4, Sedaghat R5, Roghani M6.https://doi.org/10.1016/j.biopha.2017.02.007
“Functional proteomics of synaptic plasma membrane ATP-ases of rat hippocampus: effect of l-acetylcarnitine and relationships with Dementia and Depression pathophysiology.”
Results: These results have been discussed considering the pathophysiology and treatment of Dementias and Depression because, although referred to normal healthy animals, they support the notion that l-acetylcarnitine may have positive effects in these pathologies.
Eur J Pharmacol. 2015 Jun 5;756:67-74. doi: 10.1016/j.ejphar.2015.03.011. Epub 2015 Mar 19.
Ferrari F1, Gorini A1, Villa RF2https://doi.org/10.1016/j.ejphar.2015.03.011
“Chronic acetyl-L-carnitine alters brain energy metabolism and increases noradrenaline and serotonin content in healthy mice.”
Results: These findings are consistent with decreased metabolism of glucose to lactate but not via the TCA cycle. Higher amounts of the sum of adenosine nucleotides, phosphocreatine and the phosphocreatine/creatine ratio found in the cortex of ALCAR-treated mice are indicative of increased energy levels. Furthermore, ALCAR supplementation increased the levels of the neurotransmitters noradrenaline in the HF and serotonin in cortex, consistent with ALCAR’s potential efficacy for depressive symptoms. Other ALCAR-induced changes observed included reduced amounts of GABA in the HF and increased myo-inositol. In conclusion, chronic ALCAR supplementation decreased glucose metabolism to lactate, resulted in increased energy metabolite and altered monoamine neurotransmitter levels in the mouse brain.
Neurochem Int. 2012 Jul;61(1):100-7. doi: 10.1016/j.neuint.2012.04.008. Epub 2012 Apr 23.
Smeland OB1, Meisingset TW, Borges K, Sonnewald U.https://doi.org/10.1016/j.neuint.2012.04.008
Cognizin® delivers a patented form of citicoline. Citicoline is a brain health ingredient that provides support for attention, focus and recall. Clinical studies have shown Cognizin to help improve attention, focus, motor speed and increase brain activity. †
“Dietary CDP-choline supplementation prevents memory impairment caused by impoverished environmental conditions in rats.”
Results: These findings indicate that long-term dietary CDP-choline supplementation can ameliorate the hippocampal-dependent memory impairment caused by impoverished environmental conditions in rats, and suggest that its actions result, in part, from a long-term effect such as enhanced membrane phosphatide synthesis, an effect shown to require long-term dietary supplementation with CDP-choline.
Learn Mem. 2005 Jan-Feb;12(1):39-43. Epub 2005 Jan 12.
Teather LA1, Wurtman RJ.http://www.learnmem.org/cgi/doi/10.1101/lm.83905.
“Improvements in concentration, working memory and sustained attention following consumption of a natural citicoline-caffeine beverage.”
Results: Overall, these findings suggest that the beverage significantly improved sustained attention, cognitive effort and reaction times in healthy adults. Evidence of improved P450 amplitude indicates a general improvement in the ability to accommodate new and relevant information within working memory and overall enhanced brain activation.
Int J Food Sci Nutr. 2014 Dec;65(8):1003-7. doi: 10.3109/09637486.2014.940286. Epub 2014 Jul 21.
Bruce SE1, Werner KB, Preston BF, Baker LM.https://doi.org/10.3109/09637486.2014.940286
“Short-term administration of uridine increases brain membrane phospholipid precursors in healthy adults: a 31-phosphorus magnetic resonance spectroscopy study at 4T.”
Results: This is the first study to report a direct effect of uridine on membrane phospholipid precursors in healthy adults using (31) P-MRS. Sustained administration of uridine appears to increase PME in healthy subjects. Further investigation is required to clarify the effects of uridine in disorders with altered phospholipid metabolism such as bipolar disorder.
Bipolar Disord. 2010 Dec;12(8):825-33. doi: 10.1111/j.1399-5618.2010.00884.x.
Agarwal N1, Sung YH, Jensen JE, daCunha G, Harper D, Olson D, Renshaw PF.https://doi.org/10.1111/j.1399-5618.2010.00884.x
(Hericium Erinaceus) 216mg
Hericium Erinaceus (also called Lion's Mane) is an edible and medicinal mushroom. Lion's Mane can induce Nerve Growth Factor synthesis in nerve cells which is essential for the maintenance of the basal forebrain cholinergic system. A double-blind placebo-controlled clinical trial study showed increased cognitive function scores for people who took Lion's Mane vs a placebo group. †
“Neurotrophic properties of the Lion's mane medicinal mushroom, Hericium erinaceus (Higher Basidiomycetes) from Malaysia"
Results: 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.
Int J Med Mushrooms. 2013;15(6):539-54.
Lai PL1, Naidu M, Sabaratnam V, Wong KH, David RP, Kuppusamy UR, Abdullah N, Malek SN.
Evid Based Complement Alternat Med. 2017;2017:3864340. doi: 10.1155/2017/3864340. Epub 2017 Jan 1.
Brandalise F1, Cesaroni V2, Gregori A3, Repetti M2, Romano C2, Orrù G4, Botta L2, Girometta C5, Guglielminetti ML6, Savino E6, Rossi P7.
Results: Intriguingly other neurobiological effects have recently been reported like the effect on neurite outgrowth and differentiation in PC12 cells. Until now no investigations have been conducted to assess the impact of this dietary supplementation on brain function in healthy subjects. Therefore, we have faced the problem by considering the effect on cognitive skills and on hippocampal neurotransmission in wild-type mice. In wild-type mice the oral supplementation with H. erinaceus induces, in behaviour test, a significant improvement in the recognition memory and, in hippocampal slices, an increase in spontaneous and evoked excitatory synaptic current in mossy fiber-CA3 synapse. In conclusion, we have produced a series of findings in support of the concept that H. erinaceus induces a boost effect onto neuronal functions also in non-pathological conditions.https://doi.org/10.1155/2017/3864340
“Improving effects of the mushroom Yamabushitake (Hericium erinaceus) on mild cognitive impairment: a double-blind placebo-controlled clinical trial.”
Results: The results obtained in this study suggest that Yamabushitake is effective in improving mild cognitive impairment.
Phytother Res. 2009 Mar;23(3):367-72. doi: 10.1002/ptr.2634.
Mori K1, Inatomi S, Ouchi K, Azumi Y, Tuchida T.https://doi.org/10.1002/ptr.2634
“Reduction of depression and anxiety by 4 weeks Hericium erinaceus intake.”
Results: Our results show that HE intake has the possibility to reduce depression and anxiety and these results suggest a different mechanism from NGF-enhancing action of H. erinaceus.
Biomed Res. 2010 Aug;31(4):231-7.
Nagano M1, Shimizu K, Kondo R, Hayashi C, Sato D, Kitagawa K, Ohnuki K.