[Frontiers in Bioscience E4, 214-229, January 1, 2012]

[Frontiers in Bioscience E4, 214-229, January 1, 2012]

Chronic psychosocial stress exposes Alzheimer's disease phenotype in a novel at-risk model

1Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. The symptom-free at-risk Ab rat model of AD
4. Treatments and animal groups: 4.1. Chronic psychosocial stress
5. Behavioral tests: the radial arm water maze task: 5.1. Learning trials; 5.2. Short-term memory trial; 5.3. Long-term memory trial; 5.4. Summary
6. Synaptic plasticity: 6.1. Early-phase long-term potentiation (E-LTP); 6.2. Late-phase long-term potentiation (L-LTP); 6.3. Long-term depression (LTD); 6.4. Summary
7. Basal levels of memory- and synaptic plasticity-related signaling molecules essential: 7.1. Basal Levels of CaMKII; 7.2. Basal Levels of calcineurin; 7.3. Basal levels of cAMP response element binding (CREB) protein; 7.4. Basal levels of brain derived neurotropic factor (BDNF); 7.5. Summary
8. Possible mechanisms of the effects of stress
9. Acknowledgement
10. References

1. ABSTRACT

Because of the extensive individual variations in the time of onset and severity of the prevalent sporadic form of Alzheimer's disease (AD), a patient-related external factor must be assumed to play a significant role in the development of the disease. Since stress is increasingly recognized as an external factor in the development of AD, a number of labs, including this lab, have shown that chronic stress or corticosterone administration worsens the AD phenotype in both transgenic and non-transgenic models of the disease. Recently we develop a novel at-risk model that correlates with seemingly normal individuals who are predisposed to develop AD. This review is a summarized recount of the findings we have reported on the effect of chronic psychosocial stress in this at-risk model of AD. Behavioral (learning and memory tests), electrophysiological and molecular findings indicated that even mild chronic psychosocial stress clearly transforms this seemingly normal rat model to a full-fledge AD phenotype.