Reduced TNF-α and increased IGF-I levels in the serum of Alzheimer's disease patients treated with the neurotrophic agent Cerebrolysin

被引:26
作者
Anton Alvarez, X. [1 ]
Sampedro, Carolina [1 ]
Cacabelos, Ramon [1 ]
Linares, Carlos [2 ]
Aleixandre, Manuel [3 ]
Garcia-Fantini, Manuel [4 ]
Moessler, Herbert [5 ]
机构
[1] EuroEspes Biomed Res Ctr, Dept Neuropharmacol, Bergondo 15166, A Coruna, Spain
[2] Clin Memoria, Malaga, Spain
[3] Univ Granada, Granada, Spain
[4] Hosp Univ A Coruna, La Coruna, Spain
[5] Ebewe Neuro Pharma, Unterach, Austria
关键词
Alzheimer's disease; Cerebrolysin; IGF-I; neuropsychiatric symptoms; TNF-alpha; GROWTH-FACTOR-I; INSULIN; BRAIN; PROGRESSION; DEMENTIA; PROTEIN; SCALE;
D O I
10.1017/S1461145709990101
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
According to current scientific knowledge, excess tumour necrosis factor-alpha (TNF-alpha) and low insulin-like growth factor-I (IGF-I) are pathogenic-risk factors that constitute therapeutic targets for Alzheimer's disease (AD). Changes in serum TNF-alpha, total and dissociable IGF-I levels were determined by ELISA in 207 AD patients completing a 24-wk, double-blind, placebo-controlled trial to evaluate the effects of the neurotrophic compound Cerebrolysin (Cere: 10, 30 or 60 ml for 12 wk). At week 24, Cere reduced TNF-alpha and enhanced dissociable IGF-I with respect to placebo in a dose-related manner. TNF-alpha decreased in parallel with behavioural disturbances. Increases in total IGF-I were induced by 60 ml Cere and correlated significantly with improvements in global function, disabilities and behaviour in late-onset AD patients. These results showing for the first time the opposite influence of one anti-dementia treatment on serum TNF-alpha and IGF-I suggest the contribution of both factors to the clinical effects of Cere, and probably other drugs.
引用
收藏
页码:867 / 872
页数:6
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