The Alzheimer's plaques, tangles and memory deficits may have a common origin. Part II: therapeutic rationale.
In the previous papers, we hypothesized that there could be an intracellular calcium deficit in the early phase of Alzheimer's disease (AD). In the present study, we consider, from this point of view, several long-lasting questions about AD, which include: why plaques and tangles are only found in the brain; why aging is the primary risk factor; why presenilins are so vulnerable in the disease; and why AD only affects the most delicate function of the brain. Although discrepancies and alternative views exist in many aspects of AD, it came to our attention that our hypothesis perhaps could offer a reasonable and coherent explanation, at least in part, to several such questions by the known biochemical principles. Based on the analyses, we discuss some controversies in therapeutic strategies.
Chen
M
M
Department of Pharmacology and Therapeutics, University of South Florida, College of Medicine, Tampa, Florida 33612, USA. Florida michen@com1.med.usf.edu
D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000502:physiology; D003071:Cognition; D006801:Humans; D008565:Membrane Proteins / Q000502:physiology; D008569:Memory Disorders / Q000378:metabolism / Q000503:physiopathology*; D016874:Neurofibrillary Tangles / Q000378:metabolism / Q000502:physiology*; D058225:Plaque, Amyloid / Q000378:metabolism / Q000502:physiology*; D053764:Presenilin-1; D015398:Signal Transduction; D013569:Synapses / Q000473:pathology
D015220:Calcium Channels; D008565:Membrane Proteins; C508853:PSEN1 protein, human; D053764:Presenilin-1; D002118:Calcium