Table 1.

Various neuropathological characteristics of transgenic AD (Tg-AD) mouse models derived from previous studies and unpublished data. Genotype and phenotype are further described in detail in the original ‘source’ references provided for these Tg-AD models.

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neuropathology (as determined by microscopic and molecular abundance measures; see text for further descriptions, unpublished observations) also displayed the highest levels of the inducible, inflammation-associated miRNA-146a species; + detected, ++ moderate abundance, ++++ extensive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).