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Increased glutathione peroxidase activity in erythrocytes in patients with Alzheimer's disease/senile dementia of Alzheimer's type
Author(s) -
Annerén G.,
Gardner A.,
Lundin T.
Publication year - 1986
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1986.tb04604.x
Subject(s) - alzheimer's disease , glutathione peroxidase , medicine , dementia , endocrinology , senile plaques , lipid peroxidation , glutathione , oxidative stress , chemistry , biochemistry , disease , enzyme , superoxide dismutase
Glutathione peroxidase (GSH‐Px) activity in erythrocytes was studied in 9 patients with Alzheimer's disease/senile dementia of Alzheimer's type (AD/SDAT) of ages 34–64 years and compared with that in 16 healthy controls of ages 21–66 years. The median GSH‐Px activity in erythrocytes from AD/SDAT patients was 408, μkat/1 (range 338–500 μkat/1) and that from healthy controls 348, μkat/1 (range 258–439 μkat). This difference was significant ( p < 0.005) Wilcoxon rank test. Since there are great clinical and pathological similarities between AD/SDAT and the dementia of Down's syndrome (DS) patients and since both these groups of patients have increased activity of the selenium‐dependent enzyme GSH‐Px, it is suggested that there could be a similar metabolic background of the dementia. Many findings in the oxidative metabolism of DS suggest increased oxidative damage with an elevation of the turnover of superoxides to peroxides within cells and with a secondary biochemical modification such as increase in tissual GSH‐Px activity. A similar mechanism with elevated peroxidation within cells might be responsible for the present finding of increased GSH‐Px activity in erythocytes and for the development of dementia in AD/SDAT.