There are several lines of Alzheimer's disease (AD) model mice as you know: i) genetically engineered models, ii) amyloid injection models and iii) drug-induced models (scopolamine etc.).

The third one does not evoke inflammation.

The second one (Abeta injection) can induce inflammation. You can easily and quickly induce inflammation by optimising the conditions. The model, however, is more artificial and injection itself can induce inflammation.

As to the first one, most AD models are based on the over expression of causative genes of familial AD. We and other groups established knock-in models, which express the causative genes at physiological levels in physiological places. The knock-in models develop only a few amyloid plaques at the age of more than 18 months.

Generally, brain pathology of AD can not be fully reproduced by single mutant gene related to familial AD. And the highest degree of inflammation can be achieved by triple transgenic mice (APPSweTg + tauP301L Tg + PS1M146V knock-in). They are available at Jackson lab (http://jaxmice.jax.org/strain/004807.html, 3xTg-AD developed by Dr. LaFerla). They develop amyloid plaques as early as 6 months of age.

5xFAD mice (APPswe/florida/london + PS1[M146L/L286V]) developed by Dr. Vassar) also evoke massive inflammation as early as 2-4 months of age.

If you want to see inflammation related to Abeta, you can take 5xFAD because they develop plaques earlier. If you want to see inflammation related to Abeta and neuronal death related to Abeta and tau, you may choose 3xTg-AD mice.