Objective: Active or passive immunisation can mitigate plaque pathology in mur ine models of Alzheimers disease (AD). Recently, it has been shown that antibo dies against β amy loid (Aβ) are present in human immun...Objective: Active or passive immunisation can mitigate plaque pathology in mur ine models of Alzheimers disease (AD). Recently, it has been shown that antibo dies against β amy loid (Aβ) are present in human immunoglobulin preparation s (IVIgG), which specifically recognise and inhibit the neurotoxic effects of A β. This study reports the results from a pilot study using IVIgG in patients wi th AD. Methods: Five patients with AD were enrolled and received monthly IVIgG o ver a 6 month period. Efficacy assessment included total Aβ/Aβ1 42measured in the CSF/serum as well as effects on cognition (ADAS cog; CERAD) at baseline an d at 6 months following IVIgG. Results: Following IVIgG, total Aβ.levels in the CSF decreased by 30.1%(17.3 43.5%) compared to baseline (p < 0.05). Total A β.increased in the serum by 233%(p < 0.05). No significant change was found in Aβ1 42 levels in the CSF/serum. Using ADAS cog, an improvement of 3.7±2.9 p oints was detected. Scores in the MMSE were essentially unchanged (improved in f our patients, stable in one patient) following IVIgG compared to baseline. Concl usion: Although the sample size of this pilot study is too small to draw a clear conclusion, the results of this pilot study provide evidence for a more detaile d investigation of IVIgG for the treatment of AD.展开更多
文摘Objective: Active or passive immunisation can mitigate plaque pathology in mur ine models of Alzheimers disease (AD). Recently, it has been shown that antibo dies against β amy loid (Aβ) are present in human immunoglobulin preparation s (IVIgG), which specifically recognise and inhibit the neurotoxic effects of A β. This study reports the results from a pilot study using IVIgG in patients wi th AD. Methods: Five patients with AD were enrolled and received monthly IVIgG o ver a 6 month period. Efficacy assessment included total Aβ/Aβ1 42measured in the CSF/serum as well as effects on cognition (ADAS cog; CERAD) at baseline an d at 6 months following IVIgG. Results: Following IVIgG, total Aβ.levels in the CSF decreased by 30.1%(17.3 43.5%) compared to baseline (p < 0.05). Total A β.increased in the serum by 233%(p < 0.05). No significant change was found in Aβ1 42 levels in the CSF/serum. Using ADAS cog, an improvement of 3.7±2.9 p oints was detected. Scores in the MMSE were essentially unchanged (improved in f our patients, stable in one patient) following IVIgG compared to baseline. Concl usion: Although the sample size of this pilot study is too small to draw a clear conclusion, the results of this pilot study provide evidence for a more detaile d investigation of IVIgG for the treatment of AD.
