THE ALZHEIMER'S PLAQUES, TANGLES AND MEMORY DEFICITS MAY HAVE A COMMON ORIGIN - PART III: ANIMAL MODEL

Ming Chen

Department of Pharmacology and Therapeutics, University of South Florida , College of Medicine, Tampa, Florida 33612, and Medical Research Service (151), Bay Pines VA Medical Center, St. Petersburg, Florida 33744

Received 6/9/98 Accepted 6/17/98

2. INTRODUCTION

Alzheimer's disease (AD) is characterized by memory loss, the presence of amyloid plaques, neurofibrillary tangles, synapse losses and neuronal death as hallmark lesions (1-4). Despite that enormous research efforts have been devoted to the disease, the mechanism of its pathological origin has remained elusive. A major obstacle that has limited the progress of AD research and drug development is the absence of animal models that mimic the full spectrum of the disease pathologies. Several strategies have been attempted to create animal models, including overexpression of the wild-type gene of ß-amyloid precursor protein (APP), infusion of ß-amyloid protein (Aß) and other components of the amyloid plaques, and insertion of mutant APP and presenilin genes (for reviews, see Refs. 1,5,6). Despite considerable efforts devoted in this area and current models have developed some AD lesions, a fully successful animal model, especially for sporadic AD, the vast majority of all AD cases, has yet to be developed (1,5,6). In this context, it is necessary to explore other avenues to achieve this goal.