Active full-length DNA Aβ42immunization in 3xTg-AD mice reduces not only amyloid deposition but also tau pathology
- Roger N. Rosenberg,
- Min Fu and
- Doris Lambracht-WashingtonEmail authorView ORCID ID profile
Alzheimer’s Research & Therapy201810:115
https://doi.org/10.1186/s13195-018-0441-4
© The Author(s). 2018
- Received: 15 March 2018
- Accepted: 12 October 2018
- Published: 20 November 2018
Background
Alzheimer’s disease (AD) is the most well-known and most common type of age-related dementia. Amyloid deposition and hyperphosphorylation of tau protein are both pathological hallmarks of AD. Using a triple-transgenic mouse model (3xTg-AD) that develops plaques and tangles in the brain similar to human AD, we provide evidence that active full-length DNA amyloid-β peptide 1–42 […]