Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of Asp664

doi:10.1073/pnas.0509695103

Table 1

Summary of comparisons between four hAPP transgenic mouse lines

Measurement	PDAPP(J9)	PDAPP D664A(B21)	PDAPP(J20)	PDAPP D664A(B254)
Transgene	APP_Sw,ln	APP_Sw,ln D664A	APP_Sw,ln	APP_Sw,ln D664A
APP expression, OD/mm²	76	103	151	187
Aβ (ELISA), rank order	Fourth	Third	Second	First
Aβ plaques, rank order	Third	Second	First	ND
Brain weight (vs. control)	Normal	Normal	Normal	Normal
HSPD	Decreased^*	Normal	Decreased	Normal
Dentate gyral volume	Decreased	Normal	Decreased	Normal
fEPSP (CA3→CA1)	(Abnormal)^†	Normal	Abnormal	ND
Spatial memory	ND	Normal	Impaired	Normal
Working memory	ND	ND	Impaired	Normal
Novel object exploration	ND	ND	Abnormal	Normal
Neurogenesis (SGZ)	Increased^‡	Normal	Increased^‡	ND

ND, not determined.

*HSPDs in transgenic PDAPP(J9) mice have been shown to be decreased in refs. 2 and 9. In the present study, synaptic densities in transgenic PDAPP (J9) animals were reduced by 30% by 9-mo but reached statistical significance only at 12 mo.

^†fEPSPs in transgenic PDAPP(J9) mice have been shown to be impaired (2), and improvement in PDAPP(D664A)B21 was reported in abstract form (10,11).

^‡Transgenic and nontransgenic PDAPP(J9) and PDAPP(J20) mice were combined.