|
| Models of tau pathology detecting protective effects when treated with NAP |
|
| (i) Transgenic ADNP heterozygous mouse [4] |
| (ii) Transgenic human double-mutant tau mouse [5] |
| (iii) Triple transgenic mice expressing the amyloid (Aβ) precursor protein APP(Swe), presenilin PS1 (M146V), and tau (P301L) [45, 46] |
| (iv) Mixed neuroglial primary cultures treated with Aβ (1–42, 2.5 μM) [3] |
| (v) Primary cultures of astrocytes [47] |
|
| Models of apoptosis detecting protective effects when treated with NAP |
|
| (i) A stroke model using spontaneously hypertensive rats which underwent permanent middle cerebral artery occlusion [48] |
| (ii) A rat model of diabetes (streptozocin toxicity) [7] |
| (iii) A rat model of epilepsy [49] |
| (iv) PC-12 cells exposed to H2O2 [50] |
| (v) Primary neuronal cultures subjected to ischemia/ reperfusion schedule of 3 h/3 h [39] |
|