[Frontiers in Bioscience 3, a27-31, May 11, 1998]

	[Frontiers in Bioscience 3, a27-31, May 11, 1998] Reprints PubMed CAVEAT LECTOR
	THE ALZHEIMER'S PLAQUES, TANGLES AND MEMORY DEFICITS MAY HAVE A COMMON ORIGIN; PART I; A CALCIUM DEFICIT HYPOTHESIS Ming Chen Department of Pharmacology and Therapeutics, University of South Florida, College of Medicine, Tampa, Florida 3361 and Medical Research Service (151), Bay Pines VA Medical Center, St. Petersburg, Florida 33744 Received 4/27/98 Accepted 5/1/98 1. ABSTRACT Review of the literature reveals that several biochemical events implicated in the pathology of Alzheimer's disease (AD) are calcium dependent processes. These processese include normal processing of b-amyloid precursor protein, dephosphorylation and degradation of tau, neurotransmitter release and memory formation. Since all of these processes appear to be inactivated during progression of AD, we propose that a "deficit" of intracellular calcium levels may occur in the early phase of the disease. We also propose several experiments to test this hypothesis. The hypothesis predicts that presenilins most likely act as calcium channels in vivo and that their gene mutations may cause the disease by diminishing the Ca²⁺ channeling function.

[Frontiers in Bioscience 3, a27-31, May 11, 1998]
Reprints
PubMed
CAVEAT LECTOR

THE ALZHEIMER'S PLAQUES, TANGLES AND MEMORY DEFICITS MAY HAVE A COMMON ORIGIN; PART I; A CALCIUM DEFICIT HYPOTHESIS

Ming Chen

Department of Pharmacology and Therapeutics, University of South Florida, College of Medicine, Tampa, Florida 3361 and Medical Research Service (151), Bay Pines VA Medical Center, St. Petersburg, Florida 33744

Received 4/27/98 Accepted 5/1/98

1. ABSTRACT

Review of the literature reveals that several biochemical events implicated in the pathology of Alzheimer's disease (AD) are calcium dependent processes. These processese include normal processing of b-amyloid precursor protein, dephosphorylation and degradation of tau, neurotransmitter release and memory formation. Since all of these processes appear to be inactivated during progression of AD, we propose that a "deficit" of intracellular calcium levels may occur in the early phase of the disease. We also propose several experiments to test this hypothesis. The hypothesis predicts that presenilins most likely act as calcium channels in vivo and that their gene mutations may cause the disease by diminishing the Ca²⁺ channeling function.