Animal Models of Alzheimer Disease

Abstract

Alzheimer Disease (AD) is the most common type of dementia. lts incidence progressively increases with ageing. it has a multifactorial etiology, and characterized by senile plaques in amygdale, hippocampus, and neocortex. in addition, neurofibriller tangles and evident atrophy in brain are seen histopathologically. Experimental models are based on producing lesions in cortex, hippocampus, and basal nucleus of Meyenert, neuronal destruction with toxins, and genetic manipulations. Cholinergic hypofunction is related to dementia and AD. Thus, destruction of cholinergic neurons by using methods such as electrocoagulation, kynolic acid, or 192 lgG-saporine, or by adding a choline derivative to the diets of rodent, which it leads to production of a false-neurotransmitter instead of acetylcholine. Because of the enhanced amyloid b (Ab) peptide deposition in the neuronal plaques, chronic Ab infusion to the ventricles via osmotic pumps proposed as an experimental model. Also by means of some genetic modifications Ab deposition can be induced in mice.
A Neuronal tangle related model could be produced by chronic intracerebroventricular (icv) infusion of ocadaic acid, a phosphatase 1/2A inhibitor. Transgenic mice model with mutations in presenilin gene (PS1 and PS2) is another tool for AD research. Other experimental models include investigation of aged primates, intoxication with aluminium, or organophosphate based pesticides, icv. streptozotacine infusion, and finally development of ethanol withdrawal syndrome. In the present workshop, it has been aimed to detailed investigation of experimental animal models of AD.