To print: Select File and then Print from your browser's menu --------------------------------------------------------------------------------------- Title: Gene May Play Key Role in Brain Cell Death and Alzheimer's Disease URL: http://www.pslgroup.com/dg/E9BA.htm Doctor's Guide December 6, 1996
CHICAGO, Dec. 6, 1996 -- A gene that prompts damaged cells to kill themselves may play a role in the development of Alzheimer's disease -- a finding that could someday lead to effective treatments for the disorder, reports a researcher at Loyola University Medical Center, Chicago. The gene, presenilin 2, codes for a protein that creates a natural defense against cancer with abnormal or damaged DNA, a process known as "programmed cell death." DNA, found in every cell, is biological substance that serves as the natural building block for all life forms. Under normal circumstances, this presenilin protein remains inactive until stimulated by hormonal changes or DNA damage that occurs to cells in the body. However, a mutation that occasionally occurs in this presenilin gene can keep its cell-death switch in the "on" position, said Benjamin Wolozin, an associate professor of pharmacology at Loyola. In his study, published in the Dec. 6 issue of Science, Wolozin discovered that this gene mutation becomes particularly troublesome as the body ages and seemingly contributes to familial Alzheimer's disease, a form of the brain disorder that is inherited and usually develops before the age of 65. Familial Alzheimer's disease represents about 15 percent of the Alzheimer's cases. Abnormalities in both presenilin 2 and a similar gene, presenilin 1, account for most of the cases of familial Alzheimer's disease. "Our results offer the first scientific evidence of the function of presenilin genes, especially the presenilin 2 gene, in initiating and controlling 'programmed cell death'" Wolozin said. The researcher theorizes that the mutated genes create a cycle of unending brain cell death, starting with an increase of beta-amyloids in the brain. These chemicals, which are peptides that build up in the brain as a person ages, are toxic to brain cells, damaging them and their DNA. The heightened presence of cells with damaged DNA excites the abnormal presenilin genes into accelerating the process of programmed cell death, thereby killing more and more brain cells. "Past studies have associated the abnormal presenilin genes with prompting an increase of beta-amyloids in the brain. What we did not know until now is the role that these genes play in accelerating the process of brain cell death," Wolozin said. "In short, persons with abnormal presenilin genes are more likely to experience programmed cell death due to the damage that occurs to brain cells as a part of the aging process," he said. Further research based on this finding could eventually lead to the development of medications that block the activities of these genes, Wolozin stated. Although Wolozin's work focused on genes known to be involved in the familial form of Alzheimer's disease, the scientific community generally accepts the notion that even seemingly sporadic cases of Alzheimer's disease -- cases that seemingly occur sporadically within a family -- have some type of genetic basis, he said. In conducting his study, Wolozin first took neuronal cells derived from rodent adrenal glands and stimulated the cells with the hormone, nerve growth factor. Once the cells became used to the nerve growth factor, he withdrew the hormone and noted that the cells underwent programmed cell death. By inserting presenilin 2 gene into the cells, this programmed death process was accelerated significantly. By blocking the activity of the gene, programmed cell death ceased. "The presence of presenilin 2 gene was necessary for the process to occur," he said. --------------------------------------------------------------------------------------------- Copyright © 1999 P\S\L Consulting Group Inc. All rights reserved. Republication or redistribution of P\S\L content is expressly prohibited without the prior written consent of P\S\L. P\S\L shall not be liable for any errors, omissions or delays in this content or any other content on its sites, newsletters or other publications, nor for any decisions or actions taken in reliance on such content. --------------------------------------------------------------------------------------------- This news story was printed from *Doctor's Guide to the Internet* located at http://www.docguide.com --------------------------------------------------------------------------------------- Return to News Story Page This site is maintained by webmaster@pslgroup.com Please contact us with any comments, problems or bugs. All contents Copyright (c) 1998 P\S\L Consulting Group Inc. All rights reserved.