Table 1.
The phenotypes of double mutants by crossing AD model mice with mice lacking IRS2, IGF1R, or IR
AD mouse model | Deletion of IRS2, IGF1R, or IR in mice | Phenotypes | References |
---|---|---|---|
Tg2576 | Systemic IRS2 KO–/– (diabetes) | Cognitive improvement; decreased amyloid deposition; preventing premature mortality (with normal level of blood glucose) | Killick et al. (2009), Freude et al. (2009) |
Neuronal IGF1 receptor KO+/– | Reducing premature mortality; no decrease in amyloid deposition | Stöhr et al. (2013) | |
Neuronal IGF1 receptor KO–/– | Cognitive improvement; decreased β-amyloid aggregation; reducing premature mortality | Freude et al. (2009), Cohen et al. (2009) | |
Neuronal Insulin receptor KO–/– | Decreased amyloid deposition; premature mortality | Stöhr et al. (2013) |
AD: Alzheimer’s disease; IRS: insulin receptor substrate; IGF1R: insulin-like growth factor-1 receptor; IR: insulin receptor.