To determine whether the Aβ toxicity–limiting effects of p38γ were tau-dependent, we crossed APP23.p38γ−/− with tau−/− mice.
The basic question for Fig. 2: Is the protective effect that p38y has against Amyloid beta toxicity only seen in mice that have tau proteins. Experiments were ran on mice that had various combinations of p38y and tau.
To test whether p38γ−/− augments Aβ-induced deficits, we crossed p38γ−/− with Aβ-forming APP23 mice.
Fig 1 C-J experiments are testing to see if the abscence of p38y increases amyloid beta deficiets. Mice that have amyloid beta deficets were bred with mice that did not have p38y kinase. Amyloid beta - forming APP23 mice have amyloid beta induced deficits.
We used mice with individual deletion of p38α, p38β, p38γ, or p38δ
Each mouse had one isoform of the p38 kinase eliminated from its cellular biology. All other forms are present.
To understand the roles of p38 kinases in AD, we induced excitotoxic seizures with pentylenetetrazole (PTZ), an approach widely used for studying excitotoxicity in AD mouse models
The basic goal of the research was to understand the role of p38 kinases in AD mice. The experiment used mice that were made to have excitotoxic seizures through injection of pentylenetetrazole (PTZ). Injection of PTZ has been used in the past to study excitotoxicity in AD mice models.
EDA (ectodysplasin A)
This is a protein involved in cell signalling between two layers of skin (ectoderm and mesoderm) , which is especially important in embryo formation.
This allows the formation of hair follicles, sweat glands, and teeth.