| First Author | Zampar S | Year | 2021 |
| Journal | Int J Mol Sci | Volume | 22 |
| Issue | 10 | PubMed ID | 34069029 |
| Mgi Jnum | J:311295 | Mgi Id | MGI:6753524 |
| Doi | 10.3390/ijms22105191 | Citation | Zampar S, et al. (2021) Characterization of a Mouse Model of Alzheimer's Disease Expressing Abeta4-42 and Human Mutant Tau. Int J Mol Sci 22(10) |
| abstractText | The relationship between the two most prominent neuropathological hallmarks of Alzheimer's Disease (AD), extracellular amyloid-beta (Abeta) deposits and intracellular accumulation of hyperphosphorylated tau in neurofibrillary tangles (NFT), remains at present not fully understood. A large body of evidence places Abeta upstream in the cascade of pathological events, triggering NFTs formation and the subsequent neuron loss. Extracellular Abeta deposits were indeed causative of an increased tau phosphorylation and accumulation in several transgenic models but the contribution of soluble Abeta peptides is still controversial. Among the different Abeta variants, the N-terminally truncated peptide Abeta4-42 is among the most abundant. To understand whether soluble Abeta4-42 peptides impact the onset or extent of tau pathology, we have crossed the homozygous Tg4-42 mouse model of AD, exclusively expressing Abeta4-42 peptides, with the PS19 (P301S) tau transgenic model. Behavioral assessment showed that the resulting double-transgenic line presented a partial worsening of motor performance and spatial memory deficits in the aged group. While an increased loss of distal CA1 pyramidal neurons was detected in young mice, no significant alterations in hippocampal tau phosphorylation were observed in immunohistochemical analyses. |
