[Frontiers in Bioscience, a32-37, June 8, 1998]

	[Frontiers in Bioscience, a32-37, June 8, 1998] Reprints PubMed CAVEAT LECTOR
	THE ALZHEIMER'S PLAQUES, TANGLES AND MEMORY DEFICITS MAY HAVE A COMMON ORIGIN - PART II: THERAPEUTIC RATIONALE 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 5/15/98 Accepted 5/24/98 2. INTRODUCTION Alzheimer's disease (AD) is a major cause of dementia affecting a large aged population. Amyloid plaques and neurofibrillary tangles in brain tissues are routinely used as prominent markers for diagnosing AD, even though other histological changes such as dystrophic neurites, synaptic and neuronal loss may correlate better with dementia (1-4). AD is clinically a multi-factorial disorder and its pathogenesis has been linked to several types of etiological factors including metabolic abnormalities, environmental toxins, genetic elements and social factors (1-5). A wealth of experimental data about AD has been accumulated over the past decades, which has provided a rich resource for developing working models pertaining to the disease origin. Any such models, however, will be subject to scrutinies against a number of the established or repeatedly observed AD features.

[Frontiers in Bioscience, a32-37, June 8, 1998]
Reprints
PubMed
CAVEAT LECTOR

THE ALZHEIMER'S PLAQUES, TANGLES AND MEMORY DEFICITS MAY HAVE A COMMON ORIGIN - PART II: THERAPEUTIC RATIONALE

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 5/15/98 Accepted 5/24/98

2. INTRODUCTION

Alzheimer's disease (AD) is a major cause of dementia affecting a large aged population. Amyloid plaques and neurofibrillary tangles in brain tissues are routinely used as prominent markers for diagnosing AD, even though other histological changes such as dystrophic neurites, synaptic and neuronal loss may correlate better with dementia (1-4). AD is clinically a multi-factorial disorder and its pathogenesis has been linked to several types of etiological factors including metabolic abnormalities, environmental toxins, genetic elements and social factors (1-5). A wealth of experimental data about AD has been accumulated over the past decades, which has provided a rich resource for developing working models pertaining to the disease origin. Any such models, however, will be subject to scrutinies against a number of the established or repeatedly observed AD features.