Presenilin-2 Mutation Causes Early Amyloid Accumulation and Memory Impairment in a Transgenic Mouse Model of Alzheimer's Disease

Table 1

Characterization of amyloid accumulation in the mouse brain.

Genotype	Age (months)	Number of plaques (𝑛=3) (counts/section)	Insoluble fraction (𝑛=3-8)		Soluble fraction (𝑛=3-8)
			Aβ42 (ng/mg protein)	Aβ40 (ng/mg protein)	Aβ42 (pg/mg protein)	Aβ40 (pg/mg protein)
wild-type	2-3	ND	ND	0.2±0.0	ND	84.2±4.2
	4-5	ND	ND	0.2±0.0	ND	87.5±7.1
	6-7	ND	ND	0.3±0.0	ND	87.1±6.3
PS2	2-3	ND	ND	0.2±0.0	ND	68.6±4.7
	4-5	ND	ND	0.2±0.0	ND	93.8±5.3
	6-7	ND	ND	0.3±0.0	ND	86.4±8.3
Tg2576	2-3	ND	0.7±0.2	2.1±0.1 *	ND	82.5±23.0
	4-5	ND	0.7±0.1	2.2±0.1 *	ND	83.6±5.8
	6-7	0.0±0.0	0.6±0.1	2.2±0.1 *	3.5±1.0	81.1±5.1
PS2Tg2576	2-3	17.7±2.9	4.2±0.4^#	2.9±0.3^*, #	ND	70.7±5.1
	4-5	160.3±4.3	75.2±3.9^#	51.5±4.0^*, #	2.9±0.6	74.9±5.0
	6-7	645.7±98.6	411.8±19.0^#	380.1±18.5^*, #	7.1±0.7^#	151.4±11.8^*, #

The concentration of cerebral Aβ42 and Aβ40 in the TBS-insoluble and soluble fractions was measured with specific ELISA kits. Values represent the mean ± s.e.m. ND: not detectable. Statistical significance was assessed using the unpaired 𝑇-test and Welch's test: *𝑃<.05 compared with the wild-type mice at the same age; ^#𝑃<.05 compared with the Tg2576 mice at the same age.