Boosting Acetylcholine with Alpha BRAIN®

The importance of acetylcholine

Acetylcholine (Ach) transmission in the central nervous system plays a vital role in cognitive function, specifically in attention and memory. The entire cortex and the hippocampus receive cholinergic inputs from the basal forebrain, a structure responsible for cognitive awareness and alertness [1]. Ach, in effect, is the mediator of communication between important brain structures. Impaired cholinergic neurotransmission, either due to low levels of Ach or poorly functioning cholinergic neurons, has been implicated in the cognitive decline associated with aging. Furthermore, slightly elevating Ach levels can enhance working memory and focus [2, 3]. Alpha BRAIN® boosts Ach in two ways: by increasing Ach availability with αGPC and by preventing its degradation with Huperzine A.

The choline precursor α-GPC increases acetylcholine levels to enhance cognition

L- alpha glycerylphosphorylcholine (αGPC) is a phospholipid metabolite that resides in the neuronal membrane. During times of low Ach, membrane metabolites can be used to synthesize Ach. αGPC allows the passing of fatty acids through the membrane and can be used to directly synthesize Ach in the neuron [4]. Furthermore, αGPC provides membrane fluidity, allowing flexibility and changes in the neuron’s shape. Low density of αGPC in the membrane can cause rigidity, leading to decreased neuronal functionality.

αGPC supplements have been shown to directly cross the blood-brain barrier and be incorporated into the cell membrane. The compound can be utilized directly to synthesize choline in the neuron, which subsequently increases the biosynthesis of Ach [5]. In animal studies investigating the effects of αGPC, elevated concentrations of Ach were found in both the frontal cortex and hippocampus following αGPC supplementation. These findings were correlated with significant improvement in working memory and attention tasks [6].

Huperzine potentiates Ach by inhibiting degradation

Huperzine A is a well-described, competitive and reversible inhibitor of acetylcholinesterase (AchE), the enzyme responsible for degrading endogenous Ach neurotransmitter [7]. When compared to pharmacological AchE inhibitors, such as tacrine or donepezil, Huperzine A has been shown to have higher binding affinity, and preferentially inhibits a sub-type of AchE found predominately in mammalian brains [8]. This inhibition leads to elevated Ach levels in the synaptic cleft where Ach is released and subsequently binds to target receptors.

Huperzine A enhances memory and cognitive performance

More than ten large scale, double-blind, placebo controlled clinical trials from the past two decades support the significant increase in working memory and global cognition with Huperzine A supplementation [9]. Both patient and non-patient studies have evaluated the effects of Huperzine A. A 1999 study examined 68 adolescents given either Huperzine A or a placebo. Those who received a Huperzine A supplement showed significant improvement in their memory quotient and performance on the Weschler memory scale [10].

These studies have provided a framework to initiate U.S. clinical trials using Huperzine A to treat memory impairments. The efficacy of Huperzine A against age related degenerative conditions and trauma-related memory impairments, such as the recently documented brain injuries in ex-NFL players, is currently being investigated [11].

Alpha BRAIN® can boost Ach with combined supplements

Alpha BRAIN® includes both a precursor to Ach production and a potent AchE inhibitor to prevent Ach breakdown. In other words, Alpha BRAIN® provides both the building blocks for production of Ach neurotransmitter and potentiates the amount remaining after release by inhibiting its breakdown. Numerous peer-reviewed scientific studies support the cognitive benefits of αGPC and Huperzine A on an individual level. Combining both of these potent extracts into Alpha BRAIN® provides dual channels to support peak cognitive function in healthy adults.

References

  1. Amenta F, Tayebati SK: Pathways of acetylcholine synthesis, transport and release as targets for treatment of adult-onset cognitive dysfunction. Curr Med Chem 2008, 15:488-498.
  2. Furey ML, Pietrini P, Haxby JV: Cholinergic enhancement and increased selectivity of perceptual processing during working memory. Science 2000, 290:2315-2319.
  3. Parnetti L, Amenta F, Gallai V: Choline alphoscerate in cognitive decline and in acute cerebrovascular disease: an analysis of published clinical data. Mech Ageing Dev 2001, 122:2041-2055.
  4. Tayebati SK, Tomassoni D, Di Stefano A, Sozio P, Cerasa LS, Amenta F: Effect of choline-containing phospholipids on brain cholinergic transporters in the rat. J Neurol Sci, 302:49-57.
  5. Amenta F, Tayebati SK, Vitali D, Di Tullio MA: Association with the cholinergic precursor choline alphoscerate and the cholinesterase inhibitor rivastigmine: an approach for enhancing cholinergic neurotransmission. Mech Ageing Dev 2006, 127:173-179.
  6. Sigala S, Imperato A, Rizzonelli P, Casolini P, Missale C, Spano P: L-alpha-glycerylphosphorylcholine antagonizes scopolamine-induced amnesia and enhances hippocampal cholinergic transmission in the rat. Eur J Pharmacol 1992, 211:351-358.
  7. Li WM, Kan KK, Carlier PR, Pang YP, Han YF: East meets West in the search for Alzheimer’s therapeutics – novel dimeric inhibitors from tacrine and huperzine A. Curr Alzheimer Res 2007, 4:386-396.
  8. Cheng DH, Tang XC: Comparative studies of huperzine A, E2020, and tacrine on behavior and cholinesterase activities. Pharmacol Biochem Behav 1998, 60:377-386.
  9. Ha GT, Wong RK, Zhang Y: Huperzine a as potential treatment of Alzheimer’s disease: an assessment on chemistry, pharmacology, and clinical studies. Chem Biodivers, 8:1189-1204.
  10. Sun QQ, Xu SS, Pan JL, Guo HM, Cao WQ: Huperzine-A capsules enhance memory and learning performance in 34 pairs of matched adolescent students. Zhongguo Yao Li Xue Bao 1999, 20:601-603.
  11. Amen DG, Wu JC, Taylor D, Willeumier K: Reversing brain damage in former NFL players: implications for traumatic brain injury and substance abuse rehabilitation. J Psychoactive Drugs, 43:1-5.