From: BACE1 inhibitor drugs in clinical trials for Alzheimer’s disease
| Phenotype | Putative Substrate | References |
|---|---|---|
| Astrogenesis increase; neurogenesis decrease | Jag1 | [46] |
| Axon guidance defects | CHL1 | [36]-[38] |
| Hyperactivity | NRG1 | [29],[48] |
| Hypomyelination | NRG1 | [39]-[41] |
| Memory deficits | Unknown | [17],[30],[32],[42],[43] |
| Insulin sensitivity enhanced | Unknown | [29],[51],[52] |
| Muscle spindle reduction | NRG1 | [44] |
| Neurochemical deficits | Unknown | [45] |
| Neurodegeneration with age | Unknown | [47] |
| Postnatal lethality, growth retardation | Unknown | [29] |
| Retinal abnormalities | VEGFR1 | [49] |
| Schizophrenia endophenotypes | NRG1 | [48] |
| Seizures | Navβ2 | [42],[47],[50],[53] |
| Spine density reduction | NRG1 | [48] |
| BACE2 knockout mouse phenotypes | ||
| Phenotype | Putative Substrate | References |
| Normal | --- | [29] |
| Pancreatic β cell increase | Tmem27 | [54] |
| Pigmentation abnormalities | PMEL | [55] |
| BACE1/2 double knockout mouse phenotypes | ||
| Phenotype | References | |
| Similar to BACE1 knockout, except postnatal lethality is enhanced | [29] | |