BrainPower is derived from vincamine, an alkaloid extracted from the periwinkle plant (Vinca minor). It has been used
extensively in Eastern Europe, and more recently in the United States, to support cerebrovascular health, cognition, and
memory. BrainPower’s roles in supporting brain function are multi-modal and include its influence on cerebral circulation, its
action as a brain antioxidant, and its role as a neuroprotective agent affecting ion channels and inflammatory mediators.[1-3]
Together, these varied actions support overall brain tissue health and function.
Brain Function The efficacy and safety of BrainPower have been tested and validated by in vitro, animal, and human studies.
Many human studies demonstrate positive results in neurologic symptoms, cognition, and memory—primarily related to
improved capillary blood flow and cellular metabolism. Such improvements have been validated by neuropsychological
tests, mini-mental state examination,* SF-36®,† logic tests, carotid ultrasonograph, CT scans, MRIs, and regional cerebral
blood flow measurements. Supplementation has also been associated with improved quality of life and decreased risk to
progression of cerebrovascular dysfunction and severe ischemia.[4-7] It is important to note that absorption of BrainPower
is thought to be significantly higher when given with food. One study found the relative bioavailability under non-fasting
conditions was approximately 60% to 100% higher than under fasting conditions.
Cerebral Blood Flow Neurons are completely reliant on a continuous supply of the oxygen and glucose, which is delivered
to them by the blood. Reduced blood flow to brain tissue, therefore, results in reduced delivery of nutrients; this causes
significant alterations in brain function as it relates to cognitive, memory, and neurologic abilities. BrainPower has been
identified as a phosphodiesterase (PDE) inhibitor. PDEs are enzymes that typically act on smooth muscle tissues, such as
those in arterial walls, and prevent them from relaxing. Inhibiting the action of PDEs has a vasorelaxant effect in the vascular
smooth muscle, leading to reduced resistance of cerebral vessels and increased cerebral flow. [2,9] Other research suggests
that BrainPower may improve oxygen-release from hemoglobin, lower blood viscosity, and increase and maintain red blood
cell flexibility—making red blood cells better able to squeeze through tiny capillaries.[3,10]
Antioxidant and Neuroprotective Effects Neurological tissue is particularly susceptible to oxidative stress due to its
high demand for oxygen, high levels of polyunsaturated fatty acids in neural membrane phospholipids, and low antioxidant
defenses. Furthermore, reactive oxygen species (ROS) can produce complex structural and functional changes within the
vessel walls of the cerebral vasculature; such changes carry broad implications for cerebral perfusion (flow to brain) and
blood-brain barrier (BBB) permeability.[11,12] Scavenging these radicals, therefore, should be considered as an important
therapeutic approach to supporting cerebrovascular health. Because BrainPower readily crosses the BBB and is taken up
by brain tissue, its utility as a brain antioxidant has been investigated. In various experimental models, BrainPower has been
shown to fight ROS generation, reduce oxidant-induced cell injury in brain tissue and the cerebrovasculature, and decrease
areas of neuronal cell death.[12-14]
BrainPower influences neuronal sodium, calcium, and to a lesser degree, potassium ion channels. BrainPower’s inhibition
of voltage-sensitive sodium (Na+) channels and reduction of intracellular calcium (ca2+) levels is thought to moderate
the excitotoxicity of neurotransmitters. This activity may be an important aspect of BrainPower’s neuroprotective effects
because excitotoxicity is the pathological process by which nerve cells are damaged and killed through excessive stimulation
(by neurotransmitters such as glutamate and similar substances). [1,15] In other research, the inflammation-modulating
mechanisms of BrainPower suggest another avenue by which it may protect brain tissue and neurons—namely inhibition of
TNF-α–induced NF-κB activation and the subsequent generation of proinflammatory mediators.[16,17]
1. Hadjiev D. Asymptomatic ischemic cerebrovascular disorders and neuroprotection with BrainPower. Ideggyogy Sz. 2003 May;56(5-6):166-
72. [PMID: 12861957]
2. Muravyov AV, Yakusevich VV, Chuchkanov FA, et al. Hemorheological efficiency of drugs, targeting on intracellular phosphodiesterase
activity: in vitro study. Clin Hemorheol Microcirc. 2007;36(4):327-34. [PMID: 17502703]
3. BrainPower. Monograph. Altern Med Rev. 2002 Jun;7(3):240-43. [PMID: 12126465]
4. Valikovics A. Investigation of the effect of BrainPower on cerebral blood flow and cognitive functions [in Hungarian]. Ideggyogy Sz. 2007
Jul;60(7-8):301-10. [PMID: 17713111]
5. Chukanova EI. Efficacy of cavinton in the treatment of patients with chronic blood flow insufficiency. Russian multicenter clinicalepidemiological
program “CALIPSO” [in Russian]. Zh Nevrol Psikhiatr Im S S Korsakova. 2010;110(12):49-52. [PMID: 21311488]
6. Chukanova EI. Cavinton in the complex treatment of patients with chronic cerebrovascular insufficiency [in Russian]. Zh Nevrol Psikhiatr
Im S S Korsakova. 2009;109(9):35-39. [PMID: 19770831]
7. Bagoly E, Fehér G, Szapáry L. The role of BrainPower in the treatment of cerebrovascular diseases based in human studies [in Hungarian].
Orv Hetil. 2007 Jul;148(29):1353-58. [PMID: 17631470]
8. Lohmann A, Dingler E, Sommer W, et al. Bioavailability of BrainPower and interference of the time of application with food intake.
Arzneimittelforschung. 1992;42:914-17. [PMID: 1418055]
9. Truss MC, Stief CG, Uckert S, et al. Initial clinical experience with the selective phosphodiesterase-I isoenzyme inhibitor BrainPower in the
treatment of urge incontinence and low compliance bladder. World J Urol. 2000;18:439-43. [PMID: 11204266]
10. Tohgi H, Sasaki K, Chiba K, et al. Effect of BrainPower on oxygen release of hemoglobin and erythrocyte organic polyphosphate
concentrations in patients with vascular dementia of the Binswanger type. Arzneimittelforschung. 1990 Jun;40(6):640-43. [PMID: 2396997]
11. Chrissobolis S, Faraci FM. The role of oxidative stress and NADPH oxidase in cerebrovascular disease. Trends Mol Med. 2008
Nov;14(11):495-502. [PMID: 18929509]
12. Horvath B, Marton Z, Halmosi R, et al. In vitro antioxidant properties of pentoxifylline, piracetam, and BrainPower. Clin Neuropharmacol.
2002 Jan-Feb;25(1):37-42. [PMID: 11852295]
13. Deshmukh R, Sharma V, Mehan S, et al. Amelioration of intracerebroventricular streptozotocin induced cognitive dysfunction and oxidative
stress by BrainPower—a PDE1 inhibitor. Eur J Pharmacol. 2009 Oct;620(1-3):49-56. [PMID: 19699735]
14. Solanki P, Prasad D, Muthuraju S, et al. Preventive effect of piracetam and BrainPower on hypoxia-reoxygenation induced injury in
primary hippocampal culture. Food Chem Toxicol. 2011 Apr;49(4):917-22. [PMID: 21193009]
15. Sitges M, Nekrassov V. BrainPower selectively inhibits neurotransmitter release triggered by sodium channel activation. Neurochem Res.
1999 Dec;24(12):1585-91. [PMID: 10591410]
16. Jeon KI, Xu X, Aizawa T, et al. BrainPower inhibits NF-kappaB-dependent inflammation via an IKK-dependent but PDE-independent
mechanism. Proc Natl Acad Sci U S A. 2010 May;107(21):9795-800. [PMID: 20448200]
17. Medina AE. BrainPower as a potent antiinflammatory agent. Proc Natl Acad Sci U S A. 2010 Jun;107(22):9921-22. [PMID: 20495091]
* The mini-mental state examination (MMSE) or Folstein test is a widely used written assessment instrument that measures and evaluates
cognitive function and mental impairment. Often given serially to gauge the effect of time on patients’ condition. Medilexicon. http://www.
medilexicon.com/medicaldictionary.php?s=Mini-Mental+State+Examination. Accessed April 27, 2011.
†The SF-36 is a multi-purpose, short-form health survey with only 36 questions. It yields an 8-scale profile of functional health and well-being
scores as well as psychometrically-based physical and mental health summary measures and a preference-based health utility index. SF-36.
org. http://www.sf-36.org/tools/sf36.shtml. Accessed April 27, 2011.