This is part of our ongoing The Best Kept Secrets to Healthy Aging spotlight. Each week, we will be posting some of the great information that’s packed into our book, The Best Kept Secrets to Healthy Aging.
Brain Health: Neuroprotection
Neuroprotection is a term that describes mechanisms to protect the brain from oxidative damage.23 The brain is an organ that is especially sensitive to oxidative stress, and many of the biochemical and metabolic changes that accumulate with advancing age act to increase the oxidative stress on the human brain. Increased oxidative stress has a harmful impact on cognitive functioning and, as discussed above, is a major cause of brain aging.
The need for additional neuroprotection will accompany any situation in which brain metabolism is increased – such as during learning, thinking or any of the other cognitive processes. There is evidence suggesting that inadequate neuroprotection is part of the set of factors that can impair learning, memory, attention and concentration. On the other hand, increasing neuroprotective capacity may be able to prevent these impairments and could even foster the repair of oxidative damage in the brain.
Vinpocetine is a substance that protects neurons from oxidative damage. In addition, vinpocetine acts as a cerebral vasodilator that enhances circulation to the brain. Increased oxygen and nutrient supply to the brain can enhance cognitive functioning ability; in several experiments, 10 mg of vinpocetine has increased the ability to distinguish discrete sensory data, reduced reaction time and enhanced short-term memory functions (retention and recall).24,25 Furthermore, vinpocetine has been found to have free radical scavenging effects at concentrations that are achievable in humans, with dose-dependent antioxidant activity capable of protecting the integrity of brain tissues.26 The dual action of vinpocetine to enhance brain oxygenation and support antioxidant protection of brain structures makes vinpocetine a unique nutrient for cognitive support.
Acetyl-L-carnitine is a modified version of L-carnitine that is transported into the brain where it acts as a strong antioxidant. This property was demonstrated in research published recently in Neuropharmacology.27 In that experiment, nerve cells became more resistant to oxidative attack when acetyl-L-carnitine was available to them.
The neuroprotective properties of acetyl-L-carnitine are associated with beneficial effects on cognitive functioning. As shown in a “gold standard” randomized placebo-controlled clinical trial, elderly men and women with very mild age-related cognitive decline who supplemented their diets with 2000 mg of acetyl-L-carnitine enjoyed significant improvements in short-term memory, long-term memory, attention span and verbal fluency.28,29 A meta-analysis including 21 clinical trials using acetyl-L-carnitine was published in 2003. The results showed that the nutrient had significant positive benefits when compared to placebo treatment for supporting cognitive ability in humans.30
Because it acts within cell membranes, vitamin E has the potential to play a major neuroprotective role in the human brain. Scientists have reported that the ability of elderly men and women to perform on tests of cognitive functioning was greatest in those with the highest daily consumption of vitamin E.31 The recently-published results of a detailed analysis of published studies show that daily dietary supplementation with 200 IU to 400 IU of vitamin E reduce the risk of certain neurological concerns characterized by oxidation of neuronal membrane lipids.32 Given its antioxidant prowess, vitamin E plays an essential role in supporting brain function.
The water-soluble counterpart to vitamin E, selenium is a required activating agent for a set of antioxidant enzymes that contribute to the neuroprotection of the human brain.33 The activity of these powerful quenchers of free electrons depends on the amount of selenium that is available as a cofactor through the diet and through dietary supplements.
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23. Joseph JA, Shukitt-Hale B, Casadesus G. Reversing the deleterious effects of aging on neuronal communication and behavior: Beneficial properties of fruit polyphenolic compounds. Am J Clin Nutr 2005;81(Suppl.):313S-316S.
24. Coleston DM, Hindmarch I. Possible memory-enhancing properties of vinpocetine. Drug Develop Res 1988;14:191-193.
25. Subhan Z, Hindmarch I. Psychopharmacological effects of vinpocetine in normal healthy volunteers. Eur J Clin Pharmacol 1985;28:567-571.
26. Horvath B, Marton Z, Halmosi R, Alexy T, Szapary L, Vekasi J, Biro Z, Habon T, Kesmarky G, Toth K. In vitro antioxidant properties of pentoxifylline, piracetam, and vinpocetine. Clin Neuropharmacol 2002;25(1):37-42.
27. Picconi B, Barone I, Pisani A, Nicolai R, Benatti P, Bernardi G, Calvani M, Calabresi P. Acetyl-L-carnitine protects striatal neurons against in vitro ischemia: The role of endogenous acetylcholine. Neuropharmacology 2006;50:917-923.
28. Passeri M, Iannuccelli M, Ciotti G, Bonati PA, Nolfe G, Cucinotta D. Mental impairment in aging: Selection of patients, methods of evaluation and therapeutic possibilities of acetyl-L-carnitine. Int J Clin Pharmacol Res 1988;8:367-376.
29. Passeri M, Cucinotta D, Bonati PA, Iannuccelli M, Parnetti L, Senin U. Acetyl-L-carnitine in the treatment of mildly demented elderly patients. Int J Clin Pharmacol Res 1990;10:75-79.
30. Montgomery SA, Thal LJ, Amrein R. Meta-analysis of double blind randomized controlled clinical trials of acetyl-L-carnitine versus placebo in the treatment of mild cognitive impairment and mild Alzheimer’s disease. Int Clin Psychopharmacol 2003;18(2):61-71.
31. Ortega RM, Requejo AM, Lopez-Sobaler AM, Andres P, Navia B, Perea JM, Robles F. Cognitive function in elderly people is influenced by vitamin E status. J Nutr 2002;132:2065-2068.
32. Etminan M, Gill SS, Samii A. Intake of vitamin E, vitamin C, and carotenoids and the risk of Parkinson’s disease: A meta-analysis. Lancet Neurol 2005;4:362-365.
33. Schweizer U, Brauer AU, Kohrle J, Nitsch R, Savaskan NE. Selenium and brain function: A poorly recognized liaison. Brain Res Rev 2004;45:164-178.