In this work, we will review the contributions to this field provided by transgenic mouse models, focusing on the role of nitric oxide (NO) and cyclooxygenase (COX) in cerebral cortex and/or cerebellum.
We have now studied CSF Aβ changes in three different APP transgenic mouse models, focusing our analysis on the time of the initial Aβ deposition in the brain, which differs significantly among the three mouse models.
To this end, we have studied CSF Aβ changes in three Aβ precursor protein transgenic mouse models, focusing our analysis on the initial Aβ deposition, which differs significantly among the models studied.
Use of structure activity (SAR) and structure property relationship (SPR) design criteria followed by in vivo evaluation of compounds in a mouse model focused on improving potency and establishing in vivo efficacy of analogues.
In case of the enigma of individual differences in antidepressant response, a mouse model focussing on extremes (i.e., good or early responder versus poor or non-responder) in response to treatment with the most commonly prescribed antidepressant compounds, that is, serotonin reuptake inhibitors and serotonine-norepinephrine reuptake inhibitors, could be considered a straightforward approach.
Current strategies in the mouse model focus on GM-CSF conjugation to enhance bioavailability, prolong half-life, and reduce systemic side-effects of administered GM-CSF [46].
Most of the investigations on these and other mouse models have focused on brain function since PrP is most abundant on neuronal cells and is therefore likely to alter brain function by its absence.
Studies on alcohol drinking behavior, intoxication, and addiction in human populations or in mouse models have focused primarily on QTL mapping [ 69– 72], candidate gene associations [ 73– 81], transcriptional profiling [ 45– 47, 65, 82– 84] and, most recently, on genome-wide associations [ 10, 12, 14, 20, 63, 85– 85].
This review will not attempt to cover all aspects of mouse models, rather focus on models of arterial injuries, vein grafts, and transplant arteriosclerosis, by which the major progress in understanding the mechanisms of the disease has been made.
Presently, existing NF2 mouse models primarily focus on merlin loss in Schwann cells.
