Hypothesis: Increased oxidative stress may accompany diseases of the centra
l nervous system either as a perpetrator or merely as the result of tissue
damage in the course of neurodegeneration. The brain is especially suscepti
ble to damage mediated by reactive oxygen species because it has a high rat
e of oxygen consumption and contains large amounts of readily oxidizable su
bstrates, such as polyunsaturated fatty acids. Indices of systemic oxidativ
e stress, including serum lipid-peroxidation products, may be greater in de
mentia than in normal aging.
Methods: Study groups consisted of 30 patients with dementia and 18 healthy
age-matched controls. All patients underwent neuropsychological testing an
d qualified for the study on the basis of history, physical examination, co
mplementary laboratory tests, and brain computed tomography scan. Serum lev
els were assessed for the following lipid-peroxidation products: conjugated
dienes, lipid peroxides, thiobarbituric acid reactive substances, and Schi
ff bases.
Results: There were two statistically significant differences in serum leve
ls of lipid-peroxidation products between the study groups. Lipid peroxides
were significantly lower (0.34 Angstrom 0.96 U532/mL versus 1.12 Angstrom
0.96 U532/mL, p = 0.000055), while Schiff bases were statistically higher (
589.4 Angstrom 267.3 AU/mL versus 329.0 Angstrom 107.5 AU/mL, p = 0.000282)
in the subject with dementia. There were statistically significant correla
tions between all measured products of lipid peroxidation in the controls a
nd between all products of lipid peroxidation except for Schiff bases in th
e subjects with dementia. Cognitive impairment did not correlate with level
s of lipid-peroxidation products. Age correlated negatively with Mini-Menta
l State Examination score and lipid peroxides in healthy controls.
Conclusion: More final fluorescent products of lipid peroxidation (Schiff b
ases) were found in subjects with dementia than in healthy controls, implyi
ng that oxidative stress is increased in dementia. Our data suggests a decr
ease in lipid peroxides during normal aging.