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Life Extension Magazine

LE Magazine September 2003
Quenching the flames of inflammatory brain aging
By Dale Kiefer

This particular phospholipid’s importance is underscored by the fact that the body manufactures it in order to insure its continual supply. Unfortunately, as with so many other vital functions, aging slows production of PS. Given that PS’s functions include everything from boosting vital acetylcholine levels, to reducing levels of the stress hormone cortisol and prompting the release of mood-regulating dopamine, PS is clearly an important player in brain health.

PS also helps the brain use its fuel more efficiently. By boosting blood glucose metabolism and stimulating production of acetylcholine, PS has been shown to improve the condition of patients in cognitive decline.20-23 Clinical trials involving small groups of presumed Alzheimer’s patients showed significant improvements with PS supplementation, especially among patients in the early stages of the disease. Positron emission tomography (PET) brain-imaging scans verified that patients taking PS experienced significant increases in glucose uptake compared to patients in the study who received social support or cognitive training, but no PS.

A large multi-center trial examined the use of PS to combat the effects of moderate to severe age-related cognitive decline. Patients were drawn from 23 general medicine or geriatric units. Compared to patients receiving placebo, PS patients demonstrated significant improvements in behavior, including increased socialization, motivation and initiative.

PS is generally safe and well tolerated, with no significant drug interactions reported.24 While there are no specific studies relating to the combined use of Coumadin® and PS, you should consult with your physician before taking PS, as it may enhance the anti-coagulant effect.

Vinpocetine — the brain cell oxygenator
Vinpocetine is a semi-synthetic derivative of the Vinca minor, or periwinkle plant. Developed more than two decades ago, vinpocetine has been hailed as an important neuroprotective agent with several key mechanisms of action. It has been widely used to treat symptoms of senility throughout Europe, where it is available only by prescription.

One of vinpocetine’s most powerful effects is its ability to increase blood circulation and enhance oxygen utilization in the brain. This is especially important, given that blood flow in the brain tends to diminish with advancing age. Vinpocetine improves cerebral blood flow by inhibiting an enzyme that degrades the cellular messenger cyclic GMP. The degradation of cyclic GMP causes blood vessel constriction. Preventing degradation, therefore, allows cerebral arteries to relax, improving blood flow.

Vinpocetine’s therapeutic effects may be mediated at the cellular level by its ability to enhance the electrical conductivity of cells comprising the neural network. It also protects the brain from damage caused by the excessive release of calcium ions intracellularly.

Vinpocetine’s effects on human subjects have been studied under controlled conditions in a variety of clinical trials. Vinpocetine has even been studied in newborn babies who suffered brain damage due to birth trauma. Vinpocetine significantly reduced or eradicated seizures and caused a decrease in abnormally high pressure within the brain.

These studies reveal that vinpocetine’s therapeutic effects compare favorably with prescription drugs of the acetylcholinesterase inhibitor class, such as Aricept®, which is used extensively in the United States and abroad to treat symptoms of Alzheimer’s disease and vascular dementia. Human trials, and others using rodent models, reveal that vinpocetine is safe, effective and well tolerated.25,26

Vinpocetine also exhibits some anti-clotting activity. While there are no specific studies relating to the combined use of Coumadin® and vinpocetine, you should consult with your physician before taking vinpocetine, as it may enhance the anti-coagulant effect.

Pregnenolone — the mother hormone
Pregnenolone is a powerful natural hormone that is synthesized by the body (in the mitochondria) directly from cholesterol. Mitochondria are important structures within the cells that function as “power plants.”

Pregnenolone has been called the “mother” hormone because the body converts it into a variety of other important hormones, including dehydroepiandrosterone (DHEA), estrogens, progesterone and testosterone. Aging causes a sharp decline in pregnenolone production. It stands to reason, then, that levels of its daughter hormones also decline with age.

Unfortunately, research into pregnenolone’s mechanisms of action and effects has been relatively scant. Because it is a naturally occurring substance, and thus cannot be patented, pharmaceutical companies have had little incentive to invest in costly human trials. However, intriguing studies in rodent models have suggested that enhanced levels of pregnenolone may play an important role in neuronal protection.16

Pregnenolone is not recommended for men with prostate cancer, as androgenizing hormones such as DHEA and testosterone may exacerbate this condition. Conversely, pregnenolone may actually confer some protection against other types of cancer by helping the body regulate estrogen levels. Pregnenolone has been credited with alleviating symptoms of menopause, reducing the incidence of osteoporosis and decreasing levels of “bad,” or LDL cholesterol.

Get proactive
The bad news is that a variety of factors conspire to rob us of mental acuity as we age. The good news is that modern science has worked hard to investigate and identify natural agents (some of which come to us from ancient herbal traditions) with potential to slow or even reverse the progression of this once-inevitable decline. They may represent the best available proactive option for maintaining or improving brain health as we age.


1. Burns A, Zaudig M. Mild cognitive impairment in older people. Lancet 2002; 360: 1963-1965.

2. Parnetti L et al. Choline alphoscerate in cognitive decline and in acute cerebrovascular disease: an analysis of published clinical data. Mech Ageing Dev 2001 Nov; 122(16): 2041-2055.

3. Klegeris A, McGeer P. Cyclooxygenase and 5-lipooxygenase inhibitors protect against mononuclear phagocyte neurotoxicity. Neurobiol Aging 2002; 23: 787-794.

4. Life Extension magazine, May 2001 pg.11., The Silent Stroke Epidemic.

5. Paris D, et al. AB vasoactivity: an inflammatory reaction. Ann NY Acad Sci 2000, Apr; 903: 97-109.

6. Bartus RT, et al. The cholinergic hypothesis of geriatric memory dysfunction. Science 1982; 217: 408-414.

7. Ritchie K, et al. Is senile dementia age- related or ageing-related? – evidence from a meta-analysis of dementia prevalence in the oldest old. Lancet 1995; 346: 931-934.

8. Ritchie K, Lovestone S. The dementias. Lancet 2002; 360: 1759-1766.

9. Hofman A, et al. The prevalence of dementia in Europe: a collaborative study of 1980-1990 findings. Int J Epidemiol 1991; 20: 736-748.

10. Jorm AF, et al. The prevalence of dementia: a quantitative integration of the literature. Acta Psychiatr Scand 1987; 76: 465-479.

11. Scali C, et al. The selective cyclooxygenase-2 inhibitor rofecoxib suppresses brain inflammation and protects cholinergic neurons from excitotoxic degeneration in vivo. Neuroscience 2003;117: 909-919.

12. Teismann P, et al. Cyclooxygenase-2 is instrumental in Parkinson’s disease neurodegeneration. PNAS 2003; 100 (9):5473-5478.

13. Pompl PN, et al. A therapeutic role for cyclooxygenase-2 inhibitors in a transgenic mouse model of amyotrophic lateral sclerosis. FASEB J. 2003; Apr;17(6):725-7.

14. Dennis and Company Research. Nexrutine® human trial report. Next Pharmaceuticals, Inc. 2002; 13.

15. Manev H, et al. Putative role of neuronal 5-lipoxygenase in an aging brain. FASEB J 2000; Jul;14(10):1464-9.

16. Pignatelli P, et al. The flavonoids quercetin and catechin synergistically inhibit platelet function by antagonizing the intracellular production of hydrogen peroxide. Am J Clin Nutr 2000;
72: 1150-1155.

17. Yamamoto K, et al. Plasminogen activator inhibitor-1 is a major stress- regulated gene: Implications for stress- induced thrombosis in aged individuals. Proc Natl Acad Sci 2002; 99 (2): 890-895.

18. Breteler M. Vascular involvement in cognitive decline and dementia: Epidemiologic evidence from the Rotterdam study and the Rotterdam scan study. Ann N Y Acad Sci 2000, Apr;903:457-465.

19. Iadecola C, Gorelick P.B. Converging pathogenic mechanisms in vascular and neurodegenerative dementia. Stroke 2003; 34: 335-337.

20. Schreiber S, et al. An open trial of plant- source derived Phosphatidylserine for the treatment of age-related cognitive decline. Isr J Psychiatry Relat Sci 2000;
37 (4): 302-307.

21. Palmieri G, et al. Double-blind controlled trial of phosphatidylserine in patients with senile mental deterioration. Clin Trials J 1987; 24:73-83.

22. Delwaide PJ, et al. Double-blind randomized controlled study of phosphatidylserine in senile demented patients. Acta Neurol Scand 1986; 73(2):136-40.

23. Fungfeld EW, et al. Double-blind study with Phosphatidylserine (PS) in parkinsonian patients with senile dementia of Alzheimer’s type (SDAT). Prog Clin Biol Res 1989;317: 1235-1246.

24. Van den Besselaar AM. Phosphatidylethanolamine and Phosphatidylserine synergistically promote heparin’s anticoagulant effect. Blood Coagul Fibrinolysis 1995; 6: 239-244.

25. Vas A, et al. Clinical and non-clinical investigations using positron emission tomography, near-infrared spectroscopy and transcranial Doppler methods on the neuroprotective drug vinpocetine: A summary of evidences. J Neurol Sci 2002; 203-204: 259-262.

26. Laszy J, Gyertyan I. Comparison of cognitive enhancer activity of acetylcholinesterase inhibitors and vinpocetine. Neurobiology of Aging; 2002 Jul-Aug, Suppl 1; 23(1):357.