Table 1.
Alzheimer transgenic model | Age of onset (senile plaques) | Tg-AD promoter/transgene | Senile plaque density | CNS-specific expression of amyloid | Synaptic pathology | Source reference |
---|---|---|---|---|---|---|
Tg2576 | 10 | Hamster prion promoter/human APP695 cDNA with KM670/671NL | ++++ | ++ | ++++ | [7,9] |
Tg-CRND8 | 3 | Hamster prion promoter/APPSwe/Ind (KM670/671NL + V717F) | ++ | + | − | [2] |
PSAPP | 6 | Tg2576 × PSEN1M146L | ++ | + | [6,10,27] | |
3xTg-AD | 6 | Thy1 promoter/APP695-Swedish/Tau isoform 4R0N(P301L mutation)/PSEN1M146L | ++ | ++++ | + | [18] |
5xFAD | 2 | Thy1 promoter/B6SJL-Tg(APPSwFlLon,PSEN1M146L*L286V)6799Vas/J | ++++ | ++++ | ++++ | [17] |
Symptomatic Tg-AD models exhibiting the highest senile plaque density (as seen anywhere within the CNS in aged Tg-AD models), and synaptic neuropathology (as determined by microscopic and molecular abundance measures; see text for further descriptions, unpublished observations) also displayed the highest levels of the inducible, inflammation-associated miRNA-146a species; + detected, ++ moderate abundance, ++++ extensive phenotype; see also Refs. [19,1,29,4,26,3,28,30]. The scoring system adapted from Ref. [19], also took into consideration additional Tg-AD characteristics listed at the Tg-AD website www.alzforum.org/res/com/tra/app/default.asp, in addition to consideration of deficits in the abundance of several important synaptic and cytoarchitectural support proteins, including synapsin-2, spectrin, syntenin, synaptophysin and neurofilament light chain (NF-L) protein assayed in these Tg-AD models (data not shown), and from observations made in the original source and supporting references for each Tg-AD type (rightmost column and text).