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To: scaram(o)uche who wrote (264)	11/15/1999 2:28:00 PM
From: RWReeves	Read Replies (2) \| Respond to of 673

Old news, but see highlighted part of the quote: KENSINGTON, Md.--(BUSINESS WIRE)--Oct. 25, 1999--Nymox Pharmaceutical Corp. (Nasdaq:NYMX.O) today announced that a method for treating Alzheimer's Disease to which it has certain rights has shown promise in early studies conducted by Dr. Ben Wolozin, M.D., Ph.D., of the Loyola University Medical Center in Chicago, IL. Dr. Wolozin has licensed the commercial rights to his discoveries in this area to Nymox. Dr. Wolozin presented the results of a study tracking the rates of Alzheimer's Disease among some 50,000 patients at three major U.S. medical centers at the annual meeting of the Society for Neuroscience in Miami Beach, FL, on October 24, 1999. "We found that the rate of Alzheimer's Disease for patients taking two kinds of a type of an anti-cholesterol known as statin -- lovastatin (Mevacor) and pravastatin (Pravachol) -- was reduced by 60 percent to 73 percent compared to a total patient population or compared to patients taking other medications typically used to treat cardiovascular disease or hypertension," said Dr. Wolozin. "Our studies suggests that these two drugs may protect against Alzheimer's Disease." Dr. Michael Munzar, M.D., medical director of Nymox, said that "while these findings need to be further verified, they might offer a potentially new and exciting approach to the treatment of this dread disease, which is now the fourth-leading cause of death among the elderly in the U.S. "This appears to be the first time that a statin drug has been demonstrated in a large study to be associated with reduced Alzheimer's Disease incidence. >>>>>>>The reduction in the rate of Alzheimer's Disease among the patients taking these two drugs is greater than other proposed therapeutics for the disease investigated to date. <<<<<<< An additional positive feature is that these drugs are FDA approved, in common medical use, and well-tolerated by patients," Dr. Munzar added. Nymox Pharmaceutical Corp. pioneers in the research and development of products for the diagnosis and treatment of Alzheimer's disease, an affliction for more than 20 million people around the world. Nymox offers the world's only accurate, non-invasive test to aid in the diagnosis of the disease, and is developing proprietary Spheron-based drug therapies that could lead to effective treatment of Alzheimer's disease. Nymox also is developing unique drug therapies to treat E. coli infections and urinary tract infections, which have become highly resistant to conventional antibiotic treatments. RWR

To: scaram(o)uche who wrote (264)	11/15/1999 8:50:00 PM
From: scaram(o)uche	Read Replies (1) \| Respond to of 673

J Neurosci 1999 Oct 1;19(19):8487-97 Fibroblast growth factor-2 activates a latent neurogenic program in neural stem cells from diverse regions of the adult CNS. Palmer TD, Markakis EA, Willhoite AR, Safar F, Gage FH The Salk Institute, Laboratory of Genetics, La Jolla, California 92037, USA. During development of the mammalian brain, both neurons and glia are generated from multipotent neural stem cells. Although neurogenesis ceases in most areas at birth, stem cells continue to generate neurons within the subventricular zone and hippocampal dentate gyrus throughout adult life. In this work, we provide the first demonstration that precursors native to regions of the adult brain that generate only glia can also generate neurons after exposure to FGF-2 in vitro. When progenitors isolated from hippocampal tissue were directly compared with cells isolated from the neocortex, both populations were able to initiate a program of proliferative neurogenesis. Genetic marking and lineage analysis showed that a majority of the cells able to generate neurons were multipotent precursors; however, progeny from these precursors acquired the competence to differentiate into neurons only after exposure to FGF-2. The recruitment of similar FGF-2-responsive cells from the adult optic nerve, a structure well isolated from the neurogenic zones within the brain, confirmed that neuron-competent precursors naturally exist in widely divergent tissues of the adult brain. Proc Natl Acad Sci U S A 1999 Sep 14;96(19):10893-8 Age-associated neuronal atrophy occurs in the primate brain and is reversible by growth factor gene therapy. Smith DE, Roberts J, Gage FH, Tuszynski MH Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093-0626, USA. The effects of normal aging on the primate brain are incompletely understood. Although both human and nonhuman primates demonstrate clear functional declines in selective attention, "executive" functions, and some components of declarative memory with aging, most studies have failed to demonstrate extensive neuronal atrophy or loss as a substrate for these degenerative changes in primates. In particular, extensive age-related neuronal loss in memory-related brain regions such as the hippocampus and entorhinal cortex has not been found. However, it is possible that neuronal loss or atrophy might occur in subcortical nuclei that modulate the activity of neocortical regions, thereby accounting for altered cognitive function with aging. In the present study, we describe, to our knowledge for the first time, a significant and extensive decline in the number and size of immunolabeled neurons in subcortical cholinergic basal forebrain regions of aged rhesus monkeys, the best animal model of human aging, by using stereological methods. Notably, the loss of subcortical cholinergic neuronal markers in aged monkeys was nearly completely reversed by human nerve growth factor gene delivery. These findings (i) identify reversible cellular atrophy as a potential mechanism contributing to age-related cognitive decline in primates, (ii) suggest, when considered with other studies, that subcortical brain regions exhibit greater vulnerability to the effects of aging than cortical regions, and (iii) indicate that neurotrophin gene transfer may be an effective means of preventing neuronal atrophy or degeneration in age-related neurodegenerative disorders.