Alzheimer's disease progresses as specific nerve cells in the brain, known as neurons, increasingly die off. Evidence suggests that in Alzheimer's, the brain is under increased oxidative stress and that this free radical attack may be an underlying source of neuronal damage.1
One specific type of free radical, lipid peroxides, which can damage the fatty layer of cell membranes, may play a key role in accelerating the process of cell aging in the brain.

A study by Swedish and Finnish scientists found that Alzheimer's patients produce more glutathione peroxidase, an enzyme that helps neutralize free radicals, as a defensive reaction against increased production of peroxides within the cells.2 Another recent study found that Alzheimer's patients with dementia often have "disturbance in antioxidant balance which may predispose to increased oxidative stress."3

Free radical damage has also been closely linked to the formation of plaque deposits in the brain, a hallmark of Alzheimer's disease. When free radicals injure the cell membrane, they can impair the cell's ability to regulate the passage of substances in and out of the cell. As a result, cells can be damaged or even destroyed by excess exposure to a normally healthy nutrient such as calcium.4

Numerous experimental studies show that increased oxidative stress can impair memory function in laboratory rodents.5-7 Clinical trials on elderly human populations also show that antioxidants are associated with improved memory and learning performance.8-10 The Alzheimer's Disease Cooperative Study, a preliminary double-blind placebo-controlled study of patients with moderate cases of Alzheimer's disease, found that supplementation with antioxidants (Vitamin E or selegiline) could significantly delay Alzheimer's-related complications. Dementia and inability to perform daily living tasks were, on the average, 25% slower to evolve in the patients who received either of these antioxidant supplements.11

Collectively, this evidence suggests that assessing and reducing oxidative damage may a beneficial clinical strategy to help prevent or retard the development and progression of Alzheimer's disease.

The Oxidative Stress Analysis (Blood and Urine) identifies urinary salicylate markers of hydroxyl radical activity, urine lipid peroxides, glutathione peroxidase, superoxide dismutase and reduced glutathione, revealing the sources of potential cellular damage underlying age-associated memory loss and Alzheimer's disease.

References:
1 Markesbery WR. Oxidative stress hypothesis in Alzheimer's disease. Free Rad Biol Med 1997;23(1):134-147.

2 Anneren G, Gardner A, Lundin T. Increased gluathione peroxidase activity in erythrocytes in patients with Alzheimer's disease/senile dementia of Alzheimer's type. Acta Neurol Scand 1986;73:586-589.

3 Sinclair AJ, Bayer AJ, Johnston J, Warner C, Maxweel SR. Altered plasma antioxidant status in subjects with Alzheimer's disease and vascular dementia. Int J Geriatr Psychiatr 1998;13(120:840-5.

4 Mark RJ, Lanc EM, Mattson MP. Amyloid beta-peptide and oxidative cellular injury in Alzheimer's disease. Mol Neurobiol 1996;12(3):211-224.

5 Bruce-Keller AJ, Li YJ, Lovell MA, Kraemer PJ, Gary DS, Grown RR, Markesbery WR, Mattson MP.
4-hydroxynonenal, a produce of lipid peroxidation, damages cholinergic neurons and impairs visuospatial memory in rats. J Neuropathol Exp Neurol 1998;57(3):257-67.

6 Rivas-Arancibia S, Vazquez-Sandoval R, Gonzalez-Kladiano D, Schneider-Rivas S, Lechuga-Guerrero A. Effects of ozone exposure in rats on memory and levels of brain and pulmonary superoxide dismutase. Environ Res 1998;76(1):33-9.

7 Shufitt-Hale B, Erat SA, Joseph JA. Spatial learning and memory deficits induced by dopamine administration with decreased glutathione. Free Radic Biol Med 1998;24(7-8):1149-58.

8 Perrig WJ, Perrig P, Stahelin HB. The relation between antioxidants and memory performance in the old and very old. J Am Geriatr Soc 1997;45(6):718-24.

9 Perkins AJ, Hendrie HC, Callahan CM, Gao S, Unversagt FW, Xu Y, Hall KS, Hui SL. Association of antioxidants with memory in a multiethnic elderly sample using the Third National Health and Nutrition Examination Survey. Am J Epidemiol 1999;150(1):37-44.

10 Sinclair AJ, Bayer AJ, Johnston J, Warner C, Maxwell, SR. Altered plasma antioxidant status in subjects with Alzheimer's disease and vascular dementia. Int J Geriatr Psychiatry 1998;13(12):840-5.

11 Sano M, Ernesto C, Thomas RG, Klauber MR, Schafer K, Grundman M, Woodbury P, Growdon J, Cotman CW, Pfeiffer E, Schneider LS, Thal LJ. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study. N Engl J Med 1997;336(17):1216-22.

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