Serum copper in Alzheimer's disease and vascular dementia

被引:28
作者
Agarwal R. [1 ]
Kushwaha S.S. [2 ]
Tripathi C.B. [3 ]
Singh N. [1 ]
Chhillar N. [1 ]
机构
[1] Department of Neurochemistry, Institute of Human Behaviour and Allied Sciences, Delhi
[2] Department of Neurology, Institute of Human Behaviour and Allied Sciences, Delhi
[3] Department of Biostatistics, Institute of Human Behaviour and Allied Sciences, Delhi
基金
英国科研创新办公室;
关键词
Alzheimer's disease; Ceruloplasmin; Copper; Neurodegeneration; Oxidative stress; Vascular dementia;
D O I
10.1007/s12291-008-0081-8
中图分类号
学科分类号
摘要
Alzheimer's disease is the most common form of dementia in the elderly and it's prevalence is rapidly rising. Oxidative stress plays important role in the pathophysiology of Alzheimer's disease. Metals like copper, iron derived through diet can act as pro-oxidant under oxidative stress. In the present study, serum copper levels were evaluated in 50 patients with Alzheimer's disease, 24 patients with Vascular Dementia and 30 controls. All the groups were also investigated for serum ceruloplsmin levels. The mean copper levels in Alzheimer's disease and Vascular Dementia were significantly raised compared to controls. An attempt has been made to study the relationship of serum copper with ceruloplasmin. Our study found weak correlation between copper and ceruloplasmin levels in Alzheimer's disease and Vascular Dementia.
引用
收藏
页码:369 / 374
页数:5
相关论文
共 26 条
[1]  
Bush A.I., The metallobiology of Alzheimer's disease, Trends Neurosci, 26, pp. 207-214, (2003)
[2]  
Atwood C.S., Huang X., Moir R.D., Tanzi R.E., Bush A.I., Role of free radicals and metal ions in the pathogenesis of Alzheimer's disease, Met Ions Biol Syst, 36, pp. 309-364, (1999)
[3]  
Squitti R., Lupoi D., Pasqualetti P., Dal Forno G., Vernieri F., Chiovenda P., Et al., Elevation of serum copper levels in Alzheimer's disease, Neurology, 59, pp. 1153-1161, (2002)
[4]  
Markesbery W.R., Oxidative stress hypothesis in Alzheimer's disease, Free Radic Biol Med, 23, pp. 134-147, (1997)
[5]  
Pratico D., Uryu K., Leight S., Trojanoswki J.Q., Lee V.M., Increased lipid peroxidation precedes amyloid plaque formation in an animal model of Alzheimer's amyloidosis, J Neurosci, 21, pp. 4183-4187, (2001)
[6]  
Opazo C., Huang X., Cherny R.A., Moir R.D., Roher A.E., White A.R., Et al., Metalloenzyme- like activity of Alzheimer's disease β-amyloid: Cu-dependent catalytic conversion of dopamine, cholesterol and biological reducing agents to neurotoxic H<sub>2</sub>O<sub>2</sub>, J Biol Chem, 277, pp. 40302-40308, (2002)
[7]  
Huang X., Atwood C.S., Hartshorn M.A., Multhaup G., Goldstein L.E., Scarpa R.C., Et al., The Aβ peptide of Alzheimer's disease directly produces hydrogen peroxide through metal ion, Experimental Gerontology, 4, 1, pp. 445-451, (2000)
[8]  
Huang X., Cuajungco M.P., Atwood C.S., Hartshorn M.A., Tyndall J.D., Hanson G.R., Et al., Cu (II) potentiation of Alzheimer A β neurotoxicity: Correlation with cell- free hydrogen peroxide production and metal reduction, J Biol Chem, 274, pp. 37111-37116, (1999)
[9]  
Lovell M.A., Robertson J.D., Teesdale W.J., Campbell J.L., Markesbery W.R., Copper, iron and zinc in Alzheimer's disease senile plaques, J Neurol Sci, 158, pp. 47-52, (1998)
[10]  
Sayre L.M., Perry G., Harris P.L., Liu Y., Schubert K.A., Smith M.A., In situ catalysis by neurofibrillary tangles and senile plques in Alzheimer's disease: A central role for bound transition metal, J Neurochem, 74, pp. 270-279, (2000)