invasive assays to gain additional cognitive information, can easily be added.Ĭitation: Wolf A, Bauer B, Abner EL, Ashkenazy-Frolinger T, Hartz AMS (2016) A Comprehensive Behavioral Test Battery to Assess Learning and Memory in 129S6/Tg2576 Mice. Due to the modular nature of this test battery, more behavioral tests, e.g. Together, the non-invasive behavioral test battery presented here allows detecting cognitive impairment in scopolamine-treated 129S6/SvEvTac mice and in transgenic 129S6/Tg2576 mice. Both models showed distinctive patterns of cognitive impairment. We first established this behavioral test battery with the scopolamine-induced dementia model using 129S6/SvEvTac mice and then evaluated 129S6/Tg2576 mice using the same testing protocol. The test battery consisted of five tests to evaluate different aspects of cognitive impairment: a Y-Maze forced alternation task, a novel object recognition test, the Morris water maze, the radial arm water maze, and a Y-maze spontaneous alternation task. In this study, we used two dementia mouse models on a 129S6 background-scopolamine-treated 129S6/SvEvTac mice (3–5 month-old) and transgenic 129S6/Tg2576 mice (11–13 month-old)–to establish a behavioral test battery for assessing learning and memory. However, comprehensive studies on cognitive decline in 129S6/Tg2576 mice are limited. 129S6/Tg2576 mice do not develop retinal degeneration but still show Aβ accumulation in the brain that is comparable to the original B6 SJL/Tg2576 mouse. Therefore, B6 SJL/Tg2576 mice were systematically backcrossed with 129S6/SvEvTac mice resulting in 129S6/Tg2576 mice that lack the rd1 mutation. This can impair performance in behavioral tests that rely on visual cues, and thus, affect study results.
Tg2576 mice on a B6 SJL background strain carry a recessive rd1 mutation that leads to early retinal degeneration and visual impairment in homozygous carriers. Transgenic Tg2576 mice overexpressing human amyloid precursor protein (hAPP) are a widely used Alzheimer’s disease (AD) mouse model to evaluate treatment effects on amyloid beta (Aβ) pathology and cognition.
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