Table 1: Models of NAP protection against tau pathology or increased markers of apoptosis.

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]