1 개요
Lesser periwinkle라는 식물에서 추출된 성분. 1975년 헝가리 화학자에 의해 처음으로 추출되었다.
2 특징
이는 혈류개선에 영향을 주어 알츠하이머 병의 개선을 위해서 쓰여지기도 했으나 식약청에서 투약금지 요청을 한 바 있다. 관련기사
부작용으로 백혈구 감소증이 유발될 수도 있으며 이로인해 폐혈증등에 걸릴 수 있거나, DOPAC등의 증가를 유발할 수 있으며 이는 도파민의 대사에 영향을 끼칠 수 있다. 도파민이 불균형해지면 파킨슨병에 걸릴 수 있다.
3 인용문
Vinpocetine (ethyl apovincaminate) is a synthetic derivative of the alkaloid vincamine (from the periwinkle plant vinca minor) and has cerebral blood-flow enhancing (1) and voltage sensitive Na+ channel inhibiting properties (2), leading to it's use as a drug in Hungary, Germany and Russia in the treatment of cerebrovascular dementia and Alzheimer's disease (3). Vinpocetine has also become popular supplement in the United States, and is often marketed to otherwise healthy individuals for improvement of memory and self-treatment of age-associated memory decline. Though the specific mechanism of action of vinpocetine has not been fully elucidated, effects on the dopaminergic system have been scarcely investigated.
Trejo F et al, 2001 reported on the "Characterization of vinpocetine effects on DA and DOPAC release in striatal isolated nerve endings" and found that vinpocetine increases DOPAC release, while simultaneously decreasing vesicular dopamine storage in a similar fashion as reserpine - an indole alkaloid with antipsychotic and antihypertensive properties with some structural similarities to vinpocetine (4). The authors report in the results section that "vinpocetine at increasing concentrations progressively decreases internal DA and increases DOPAC release" and "markedly inhibits DAT-mediated release of endogenous DA." (5)
The effects of vinpocetine on DA and DOPAC levels are not believed to be related to the well-demonstrated inhibitory effects on voltage sensitive Na+ channels, as "vinpocetine increases DOPAC release independently of the state of presynaptic VSSC." A possible MAO-A enhancing mechanism is ruled out "as vinpocetine fails to modify the inhibition of DOPAC formation caused by clorgyline" - a potent inhibitor of MAO-A, "indicating that a reserpine-like mechanism is involved in the vinpocetine-induced increase in DOPAC formation." (6)
If vinpocetine does indeed act in a "reserpine-like" fashion in striatal dopaminergic neurons, one could legitimately raise concern over the use of vinpocetine in otherwise healthy individuals for "cognitive enhancement," as side effects may manifest consistent with reserpine-like side effects, including depression and cognitive dysfunction (7, 8). Because resperine inhibits VMAT-2, the protein primarily responsible for the transportation of monoamines from the cytosol to synaptic vesicles, the amount of dopamine, norepinephrine and serotonin stored in neurons may be substantially decreased pre-synaptically by vinpocetine, leading to a downregulation of monoaminergic tone.
In other words, while vinpocetine may be neuroprotective under some experimental and clinical conditions, it may also interfere with monoamine storage, and affect the way in which the brain responds to drugs acting through dopaminergic, adrenergic, or serotonergic pathways (e.g. amphetamine, modafinil, methylphenidate, cocaine, SSRIs, bupropion, etc). Serious consideration should be given before taking vinpocetine, as it is a highly active pharmacological agent that interacts and interferes with a wide array of brain systems and functions.
1. Szilágyi G, Nagy Z, Balkay L, Boros I, Emri M, Lehel S, Márián T, Molnár T, Szakáll S, Trón L, Bereczki D, Csiba L, Fekete I, Kerényi L, Galuska L, Varga J, Bönöczk P, Vas A, Gulyás B. "Effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke patients: a PET study." Journal of Neurological Sciences 2005 Mar 15;229-230:275-84. Epub 2005 Jan 8. PMID: 15760651. [abstract]
2. Sitges M, Galván E, Nekrassov V. "Vinpocetine blockade of sodium channels inhibits the rise in sodium and calcium induced by 4-aminopyridine in synaptosomes." Neurochemistry International 2005 Jun;46(7):533-40. PMID: 15843047. [abstract]
3. "Vinpocetine. Monograph." Alternative Medicine Review 2002 Jun;7(3):240-3, pp. 240. PMID: 12126465. [full text]
4. Trejo F, Nekrassov V, Sitges M. "Characterization of vinpocetine effects on DA and DOPAC release in striatal isolated nerve endings." Brain Research 2001 Aug 3;909(1-2):59-67. PMID: 11478921. [abstract]
5. Ibid, pp. 61.
6. Ibid, pp. 64.
7. Huffman JC, Stern TA. "Neuropsychiatric consequences of cardiovascular medications." Dialogues in Clinical Neuroscience 2007;9(1):29-45. PMID: 17506224. [abstract]
8. Cai JX, Ma YY, Xu L, Hu XT. "Reserpine impairs spatial working memory performance in monkeys: reversal by the alpha 2-adrenergic agonist clonidine." Brain Research 1993 Jun 18;614(1-2):191-6. [abstract]