Choline Donors

Active forms of choline donors that work through different pathways in the peripheral and central nervous system to support acetylcholine levels, along with the other synergistically stacked cholinergics (e.g., acetyl donors, acetylcholinesterase inhibitors, racetamic compounds).

Alpha GPC

Scientific Name:


Alpha-GPC | Glycerophosphocholine | Choline alphoscerate | L-alpha-glycerophosphocholine


Supports cognitive function*

Supports exercise performance* 


Alpha-glycerophosphocholine (alpha-GPC) is a choline-containing phospholipid that can be used to augment the body and brain choline pool. In this role it serves as a precursor for both acetylcholine and phosphatidylcholine biosynthesis. Alpha-GPC and citicoline (i.e., CDP-choline) are considered the nootropic forms of choline, with both forms able to increase brain choline levels, act as building blocks for acetylcholine, and support choline-dependent neurotransmission.[1–4]* However, of the two, alpha-GPC contains a higher proportion of choline, so a lower dose of alpha-GPC gives greater choline support than a similar dose of citicoline.[5–7] This means that by weight alpha-GPC is the more efficient choline precursor. Following an oral dose, alpha-GPC metabolizes into choline and the phospholipid glycerophosphate. The choline can be used for acetylcholine synthesis and neurotransmission.[3,8–14] Acetylcholine is central to brain neurotransmission; it’s also used in both the fight or flight and rest and relax parts of the autonomic nervous system; and it is a signaling molecule for activating muscles. Because alpha-GPC is a precursor in the biosynthesis of acetylcholine, it plays a supportive role in a variety of cognitive functions, including attention, concentration, mental focus, and memory formation and recall.[15]* Alpha-GPC also supports aspects of muscle performance, and is involved in maintaining organs and tissues.* And, because alpha-GPC can be readily metabolized into phosphatidylcholine, it can be used to support the structure and function of cell membranes. Alpha-GPC is found in low amounts in a variety of foods[16] and in breast milk.[17,18] 


Alpha-glycerophosphocholine (Alpha-GPC) is a source of choline; it is able to influence both systemic and brain concentrations of choline.

Alpha-GPC is derived from soy.

Neurohacker uses an Alpha-GPC that is sourced to be non-GMO, gluten-free, and vegan.


Alpha-glycerophosphocholine (Alpha-GPC) is by weight one of the best sources of choline. While alpha-GPC is often treated as if it’s dose-dependent (i.e., a higher dose is better) and doses of 1200 mg/day have been used in some clinical studies, Neurohacker believes the evidence suggests a threshold response (see Neurohacker Dosing Principles) when alpha-GPC is given to healthy people. This means that more might not be better under all circumstances. As an example, in a study of healthy college-aged men, while the higher dose (500 mg/day) of alpha-GPC did a better job increasing free choline levels, the lower dose (250 mg/day) produced a better peak muscle force response.[19] In general, Neurohacker’s experience with alpha-GPC (as well as citicoline) indicate that when used as part of comprehensive nootropic formulations, a more modest dose is often sufficient. Alpha-GPC is a useful choline source in liquids because of its taste and solubility. In general, the best time to take alpha-GPC is early in the day.


Augments choline pool

Alpha-GPC is part of the CDP-choline (or Kennedy) pathway, which has a central role in choline homeostasis [13,14]

Supports plasma choline levels [20]

Precursor for phosphatidylcholine synthesis [3]

Precursor for acetylcholine synthesis [2,3]

Brain function

Supports memory and learning [7,27,36]

Supports attention [7,36]

Supports cognition [2,3,15,36,37]

Supports acetylcholine synthesis and release [2,3,21]

Supports vesicular acetylcholine transporter levels [21,22]

Supports high affinity choline uptake transporter levels [22]

Protects from age-related changes in cholinergic neurotransmission [23]

Supports dopamine synthesis and release [1,24]

Supports dopamine plasma membrane transporter (DAT) levels [24]

Supports serotonin synthesis [24]

Supports GABA release [25]

Supports phospholipid synthesis [9,26]

Supports phosphoinositide synthesis [26,27]

Supports protein kinase C (PKC) activation [28–30]

Supports growth hormone secretion from the pituitary gland [10,20,31]

Counters some age-related brain microstructural changes [32–35]

Supports neuroprotective functions [2,3]

Exercise Performance

Supports isometric force production [38]

Supports maximum power and velocity in jump movements [19]


CDP-choline, Uridine Monophosphate, Huperzine A, Bacopa monnieri, Celastrus paniculatus, Coleus forskohlii, Vitamin B5 in supporting cholinergic neurotransmission


[1]M. Trabucchi, S. Govoni, F. Battaini, Farmaco Sci. 41 (1986) 325–334.
[2]C.M. Lopez, S. Govoni, F. Battaini, S. Bergamaschi, A. Longoni, C. Giaroni, M. Trabucchi, Pharmacol. Biochem. Behav. 39 (1991) 835–840.
[3]S. Sigala, A. Imperato, P. Rizzonelli, P. Casolini, C. Missale, P. Spano, Eur. J. Pharmacol. 211 (1992) 351–358.
[4]N. Canal, Others, Le Basi Raz Ter 23 (1993) 102.
[5]R. Di Perri, G. Coppola, L.A. Ambrosio, A. Grasso, F.M. Puca, M. Rizzo, J. Int. Med. Res. 19 (1991) 330–341.
[6]G. Gatti, N. Barzaghi, G. Acuto, G. Abbiati, T. Fossati, E. Perucca, Int. J. Clin. Pharmacol. Ther. Toxicol. 30 (1992) 331–335.
[7]L. Parnetti, F. Mignini, D. Tomassoni, E. Traini, F. Amenta, J. Neurol. Sci. 257 (2007) 264–269.
[8]I.H. Ulus, R.J. Wurtman, C. Mauron, J.K. Blusztajn, Brain Res. 484 (1989) 217–227.
[9]G. Abbiati, T. Fossati, G. Lachmann, M. Bergamaschi, C. Castiglioni, Eur. J. Drug Metab. Pharmacokinet. 18 (1993) 173–180.
[10]G.P. Ceda, G.P. Marzani, V. Tontodonati, E. Piovani, A. Banchini, M.T. Baffoni, G. Valenti, A.R. Hoffman, in: Growth Hormone II, Springer New York, 1994, pp. 328–337.
[11]J.P. Fernández-Murray, C.R. McMaster, J. Biol. Chem. 280 (2005) 38290–38296.
[12]F. Amenta, S.K. Tayebati, D. Vitali, M.A. Di Tullio, Mech. Ageing Dev. 127 (2006) 173–179.
[13]Z. Li, D.E. Vance, J. Lipid Res. 49 (2008) 1187–1194.
[14]F. Gibellini, T.K. Smith, IUBMB Life 62 (2010) 414–428.
[15]N. Canal, M. Franceschi, M. Alberoni, C. Castiglioni, P. De Moliner, A. Longoni, Int. J. Clin. Pharmacol. Ther. Toxicol. 29 (1991) 103–107.
[16]S.H. Zeisel, M.-H. Mar, J.C. Howe, J.M. Holden, The Journal of Nutrition 133 (2003) 1302–1307.
[17]M.Q. Holmes-McNary, W.L. Cheng, M.H. Mar, S. Fussell, S.H. Zeisel, Am. J. Clin. Nutr. 64 (1996) 572–576.
[18]Y.O. Ilcol, R. Ozbek, E. Hamurtekin, I.H. Ulus, J. Nutr. Biochem. 16 (2005) 489–499.
[19]L. Marcus, J. Soileau, L.W. Judge, D. Bellar, J. Int. Soc. Sports Nutr. 14 (2017) 39.
[20]T. Kawamura, T. Okubo, K. Sato, S. Fujita, K. Goto, T. Hamaoka, M. Iemitsu, Nutrition 28 (2012) 1122–1126.
[21]S.K. Tayebati, D. Tomassoni, A. Di Stefano, P. Sozio, L.S. Cerasa, F. Amenta, J. Neurol. Sci. 302 (2011) 49–57.
[22]D. Tomassoni, A. Catalani, C. Cinque, M.A. Di Tullio, S.K. Tayebati, A. Cadoni, I.E. Nwankwo, E. Traini, F. Amenta, Curr. Alzheimer Res. 9 (2012) 120–127.
[23]F. Amenta, F. Franch, A. Ricci, J.A. Vega, Ann. N. Y. Acad. Sci. 695 (1993) 311–313.
[24]S.K. Tayebati, D. Tomassoni, I.E. Nwankwo, A. Di Stefano, P. Sozio, L.S. Cerasa, F. Amenta, CNS & Neurological Disorders - Drug Targets 12 (2013) 94–103.
[25]L. Ferraro, S. Tanganelli, L. Marani, C. Bianchi, L. Beani, A. Siniscalchi, Neurochem. Res. 21 (1996) 547–552.
[26]G. Aleppo, F. Nicoletti, M.A. Sortino, G. Casabona, U. Scapagnini, P.L. Canonico, Pharmacol. Toxicol. 74 (1994) 95–100.
[27]G. Schettini, C. Ventra, T. Florio, M. Grimaldi, O. Meucci, A. Scorziello, A. Postiglione, A. Marino, Pharmacol. Biochem. Behav. 43 (1992) 139–151.
[28]S. Govoni, F. Battaini, L. Lucchi, A. Pascale, M. Trabucchi, Ann. N. Y. Acad. Sci. 695 (1993) 307–310.
[29]L. Lucchi, A. Pascale, F. Battaini, S. Govoni, M. Trabucchi, Life Sci. 53 (1993) 1821–1832.
[30]S. Govoni, L. Lucchi, F. Battaini, M. Trabucchi, Life Sci. 50 (1992) PL125–8.
[31]G.P. Ceda, G. Ceresini, L. Denti, G. Marzani, E. Piovani, A. Banchini, E. Tarditi, G. Valenti, Horm. Metab. Res. 24 (1992) 119–121.
[32]F. Amenta, M. Del Valle, J.A. Vega, D. Zaccheo, Mech. Ageing Dev. 61 (1991) 173–186.
[33]A. Ricci, E. Bronzetti, J.A. Vega, F. Amenta, Mech. Ageing Dev. 66 (1992) 81–91.
[34]F. Amenta, F. Ferrante, J.A. Vega, D. Zaccheo, Prog. Neuropsychopharmacol. Biol. Psychiatry 18 (1994) 915–924.
[35]G. Muccioli, G.M. Raso, C. Ghé, R. Di Carlo, Prog. Neuropsychopharmacol. Biol. Psychiatry 20 (1996) 323–339.
[36]L. Parnetti, F. Amenta, V. Gallai, Mech. Ageing Dev. 122 (2001) 2041–2055.
[37]F. Amenta, A. Carotenuto, A.M. Fasanaro, R. Rea, E. Traini, J. Neurol. Sci. 322 (2012) 96–101.
[38]D. Bellar, N.R. LeBlanc, B. Campbell, J. Int. Soc. Sports Nutr. 12 (2015) 42.

Cognizin Citicoline

Scientific Name:
Cytidine diphosphocholine

CDP Choline is a compound made up of choline and cytidine with neuroprotective and nootropic activity. CDP Choline decreases age-related memory impairment and cognitive decline, and enhances attention, learning and memory.

Scientific Name:
Cytidine diphosphocholine


  • After ingestion, CDP Choline originates choline and cytidine, the latter then being converted into uridine[1]
  • Both choline and uridine are neuroprotective[1]
  • Choline is a nicotinic Acetylcholine receptor agonist[2]
  • Increases the production of acetylcholine, adrenalin and noradrenalin[1]
  • Increases the release of Dopamine by acting on dopamine transporters[3]
  • Increases phosphatidylcholine production in the brain – an important component of cell membranes[4]
  • Maintains neuronal membrane integrity and reduces neuronal death[4,5]

[1] Weiss GB1 (1995). Metabolism and actions of CDP-choline as an endogenous compound and administered exogenously as citicoline. Life Sci. 1995;56(9):637-60. doi: 10.1016/0024-3205(94)00427-T
[2] Levin ED (2013). Complex relationships of nicotinic receptor actions and cognitive functions. Biochem Pharmacol, 86(8):1145-52. doi: 10.1016/j.bcp.2013.07.021
[3] Tayebati SK, et al (2013). Modulation of monoaminergic transporters by choline-containing phospholipids in rat brain. CNS Neurol Disord Drug Targets, 12(1):94-103. doi: 10.2174/1871527311312010015
[4] Fagone P & Jackowski S (2012). Phosphatidylcholine and the CDP-choline cycle. Biochim Biophys Acta, 1831(3):523-32. doi: 10.1016/j.bbalip.2012.09.009
[5] Dempsey RJ & Raghavendra Rao VL (2003). Cytidinediphosphocholine treatment to decrease traumatic brain injury-induced hippocampal neuronal death, cortical contusion volume, and neurological dysfunction in rats. J Neurosurg, 98(4):867-73. doi: 10.3171/jns.2003.98.4.0867


Scientific Name:

Centrophenoxine is a cholinergic compound with long-term neuroprotective and nootropic activity. Studies indicate that centrophenoxine can improve working memory and be a general memory enhancer.

Scientific Name:


  • Increases the levels of Acetylcholine in the brain[1]
  • Anti-aging effects[2]
  • Decreases the accumulation of cellular waste and toxins in the brain[3]
  • Antioxidant effect – decreases lipid peroxidation
  • Increases RNA and protein synthesis in the brain[4]
  • Increases glucose uptake in neurons and glia[5]
  • Decreases cognitive decline by reducing cellular dehydration[6]
  • Increases synaptic connections – improved neuronal communication[7]

[1] Wood PL & Péloquin A (1982). Increases in choline levels in rat brain elicited by meclofenoxate. Neuropharmacology, 21(4):349-54. doi: 10.1016/0028-3908(82)90099-5
[2] Bhalla P & Nehru B (2005). Modulatory effects of centrophenoxine on different regions of ageing rat brain. Exp Gerontol, 40(10):801-6. doi: 10.1016/j.exger.2005.06.016
[3] Nehru B1 & Bhalla P (2006). Reversal of an aluminium induced alteration in redox status in different regions of rat brain by administration of centrophenoxine. Mol Cell Biochem, 290(1-2):185-91. doi: 10.1007/s11010-006-9186-7
[4] Sharma D, et al (1993). Age-related decline in multiple unit action potentials of CA3 region of rat hippocampus: correlation with lipid peroxidation and lipofuscin concentration and the effect of centrophenoxine. Neurobiol Aging, 14(4):319-30. doi: 10.1016/0197-4580(93)90117-T
[5] Watanabe S, et al (1975). Effects of various cerebral metabolic activators on glucose metabolism of brain. Folia Psychiatr Neurol Jpn, 29(1):67-76. doi: 10.1111/j.1440-1819.1975.tb02324.x
[6] Zs-Nagy I (1989). On the role of intracellular physicochemistry in quantitative gene expression during aging and the effect of centrophenoxine. A review. Arch Gerontol Geriatr, 9(3):215-29. doi: 10.1016/0167-4943(89)90042-3
[7] Bertoni-Freddari C, et al (1982). The effect of acute and chronic centrophenoxine treatment on the synaptic plasticity of old rats. Arch Gerontol Geriatr, 1(4):365-73. doi: 10.1016/0167-4943(82)90036-X