| First Author | Takahashi RH | Year | 2010 |
| Journal | Neurobiol Aging | Volume | 31 |
| Issue | 7 | Pages | 1145-52 |
| PubMed ID | 18771816 | Mgi Jnum | J:161990 |
| Mgi Id | MGI:4462134 | Doi | 10.1016/j.neurobiolaging.2008.07.021 |
| Citation | Takahashi RH, et al. (2010) Co-occurrence of Alzheimer's disease beta-amyloid and tau pathologies at synapses. Neurobiol Aging 31(7):1145-52 |
| abstractText | Although beta-amyloid (Abeta) plaques and tau neurofibrillary tangles are hallmarks of Alzheimer's disease (AD) neuropathology, loss of synapses is considered the best correlate of cognitive decline in AD, rather than plaques or tangles. How pathological Abeta and tau aggregation relate to each other and to alterations in synapses remains unclear. Since aberrant tau phosphorylation occurs in amyloid precursor protein (APP) Swedish mutant transgenic mice, and since neurofibrillary tangles develop in triple transgenic mice harboring mutations in APP, tau and presenilin 1, we utilized these well-characterized mouse models to explore the relation between Abeta and tau pathologies. We now report that pathological accumulation of Abeta and hyperphosphorylation of tau develop concomitantly within synaptic terminals. |
