Effects of human intravenous immunoglobulin on amyloid pathology and neuroinflammation in a mouse model of Alzheimer’s disease

Table 1 Amyloid pathology and microglial reactivity after 3 months of hIVIG treatment in APdE9 mice

Measured parameter	Treatments		Pvalue
Measured parameter	Saline	hIVIG	Pvalue
Serum Aβ40 (pg/μL)	0.56 ± 0.07	0.64 ± 0.07	0.67
Soluble Aβ42 (pg/mg)	0.36 ± 0.12	0.32 ± 0.05	0.74
Insoluble Aβ42 (ng/μL)	2.41 ± 0.25	2.43 ± 0.16	0.93
Aβ deposits (% 6E10 immunopositive area)	1.26 ± 0.08	1.20 ± 0.09	0.66
Fibrillar Aβ (% Congo red positive area)	0.10 ± 0.01	0.12 ± 0.01	0.12
Microglia (% CD45 immunopositive area)	0.84 ± 0.06	0.83 ± 0.06	0.90

Four-month-old APP/PS1dE9 mice were treated with once weekly intraperitoneal injection of either hIVIG (1 g/kg; n =16) or saline (n = 14) for 3 months. At the end of the treatment period, brains were extracted to assess amyloid and microglial pathology. Serum Aβ40, soluble and insoluble Aβ42 were measured by ELISA. Aβ deposits and microglial activity were quantitatively assessed from immunostainings whereas fibrillar amyloid was assessed by quantifying Congo red histological stain. Data are represented as mean ± SEM. Student’s t-test was employed to find treatment differences and P < 0.05 was considered statistically significant.

ISSN: 1742-2094