Hriday K. Das, Ph.D., and Harbans Lal, Ph.D.

Department of PharmacologyUniversity of North Texas Health Science Center at Fort Worth, Fort Worth, Texas 76107

Received 4/4/97; Accepted 5/28/97

TABLE OF CONTENTS

1. Abstract

2. Introduction

3. Discussion

3.1. Genes for Early-Onset Familial Alzheimer's Disease.

3.1.1. Hypothetical Function (s) of Presenilin 1 Gene.

3.1.2. Ttransgenic Mice Expressing Presenilin 1 Gene.

3.1.3. Possible Role of the PS1 Gene in the Development of Alzheimer's Disease.

3.1.4. Mutated PS2 Gene May Enhance Constitutive Programmed Cell Death in the Brain of Alzheimer's Patients.

3.2. Role of b-Amyloid Protein in Alzheimer's Disease.

3.2.1. A Transgenic Mouse Model with Mutated Amyloid Precursor Protein Gene of Alzheimer's Disease.

3.2.2. b-Amyloid Induces Alzheimer's Phenotype by Virtue of Altering Potassium Channels.

3.3 Alzheimer's disease; the Zinc connection.

3.4. Role of ApoE4 in the Pathophysiology of Alzheimer's Disease.

3.4.1. Binding Properties of ApoE4.

3.5. Role of Tau Protein in the Generation of Neurofibrillary Tangles in the Alzheimer's Disease.

4. References
5. Entire Manuscript

Keywords:Alzheimer's disease, presenilin genes, b- amyloid, tau, apolipoprotein E4, phosphorylation

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