Neurological Disorders – Alzheimer’s Disease
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APP/PS1 Double Transgenic Model
Double transgenic mice from the cross between Tg 2576 (mutant APP) and a mutant presenilin (PS1) line develop large numbers of fibrillar amyloid α (Aα) deposits in the cerebral cortex and in the hippocampus and express memory deficits as early as 8 - 12 weeks of age. Tests used to characterize cognitive deficits in this model include, Spontaneous Alternation, Trace Fear Conditioning and Morris Water Maze.
For this model obtaining a license may be necessary.
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Aged Mice
PsychoGenics has colonies of aged mice, natural models for the study of age-associated cognitive impairment and memory deficits. Aged animals are advantageous when the aim of the study is to look at global memory deficits or to test compounds that can reverse age-related neuronal degeneration. The aged mice can be used in any of our cognition models. Typically, access to aged colonies has been limited, and requires significant investment of time after purchasing animals at 8-10 weeks of age and aging them over a 12 - 18 month period. The availability of aged animals from existing colonies at PsychoGenics offers a great advantage and immediate initiation of studies without the need to wait for months until the animals have aged sufficiently.
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Scopolamine-induced cognitive deficit
One of the mechanisms thought to play a role in dementia involves the forebrain acetylcholine system. Pharmacological blockade of muscarinic acetylcholine receptors in the brain results in a variety of effects on cognitive functions. Because of global impairment and neurochemical correspondence with Alzheimer’s disease scopolamine administration may be an attractive model of cognitive decline.
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The total number of errors (including reference memory and working memory errors) decreases over 4 days of training.
