Copyright
©The Author(s) 2020.
World J Biol Chem. Sep 27, 2020; 11(2): 62-75
Published online Sep 27, 2020. doi: 10.4331/wjbc.v11.i2.62
Published online Sep 27, 2020. doi: 10.4331/wjbc.v11.i2.62
Strain | Promoter used | Proteins expressed | Pathogeny | Ref. |
3xTG–AD | Thy1 and mPS1 | Mutant of APP (hAPP695, Swedish mutation), PS1 (PSEN1, M146V) and tau (hTau-4R0N, P301L) | Mice containing these mutations develop β-amyloid plaques and NFTs resembling the brain with AD | [36,60,96,97] |
CK-p25 | tetO (tet operator) | These mice overexpress the truncated form of p35, p25 | p25 activates CDK5 (cyclin-dependent kinase 5), implicated in AD. CK-p25 mice develop neuronal loss, β-amyloid accumulation and loss of synaptic terminations in the hippocampus and cortex as well as memory deficits | [57,98,99] |
APPPS 1-21 /HDAC6–/– crossbred | Thy1 | Mutated APP (KM670/671NL) and the mutated presenilin 1 (L166P) | Mice develop β-amyloid plaques leading to cerebral amyloidosis, dystrophic synaptic boutons, hyper-phosphorylated tau, inflammatory responses and the impairment of cognitive function | [64,100,101] |
TgCRND8 | Hamster PrP | hAPP695 Swe/Ind | The brain of mice contains plaques formed by depositions of β-amyloid, leading to inflammation and cognitive impairments. There is also neuronal loss, accumulation of NFTs, and neuritic changes similar to those observed in AD | [93,102,103] |
Tg19959 | Hamster PrP | hAPP695 with two familial mutations (Swedish and Indiana mutations: K670N/M671L and V717F, respectively). (FVB X 129S6F1 background) | Mice overexpress β-amyloid 1-42 peptide and Bace1 forming plaques | [5,93,102,104] |
Tg2576-APPswe crossbred | Hamster PrP and Mouse PrP | The Swedish mutation (hAPP695) and m/hAPP6953 (extra and intracellular regions of mouse β-amyloid, a human β-amyloid sequence and the Swedish mutations of β-amyloid, K594N/M595L) | These mice develop β-amyloid plaques deposition and memory deficits | [94,105,106] |
APP/PSI | Thy | Mutated APP (KM670/671 NL) and mutated presenilin 1 (L166P) | Mice show dystrophic synaptic, hyperphosphorylation of tau, gliosis, and neuronal loss in the dentate gyrus as well as impairment in reversal learning | [95,101] |
- Citation: Tecalco-Cruz AC, Ramírez-Jarquín JO, Alvarez-Sánchez ME, Zepeda-Cervantes J. Epigenetic basis of Alzheimer disease. World J Biol Chem 2020; 11(2): 62-75
- URL: https://www.wjgnet.com/1949-8454/full/v11/i2/62.htm
- DOI: https://dx.doi.org/10.4331/wjbc.v11.i2.62