NIH Public Access Author Manuscript Ann N Y Acad Sci. Author manuscript; available in PMC 2011 June 2.
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Published in final edited form as: Ann N Y Acad Sci. 2010 April ; 1191(Suppl 1): E1–15. doi:10.1111/j.1749-6632.2010.05532.x.
Therapeutics for cognitive aging Diana W. Shineman1, Timothy A. Salthouse2, Lenore J. Launer3, Patrick R. Hof4, George Bartzokis5, Robin Kleiman6, Victoria Luine7, Jerry J. Buccafusco8, Gary W. Small5, Paul S. Aisen9, David A. Lowe10, and Howard M. Fillit1 1The
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Alzheimer’s Drug Discovery Foundation, New York, New York 2Department of Psychology, University of Virginia, Charlottesville, Virginia 3Laboratory of Epidemiology, Demography, and Biometry, National Institute on Aging, Bethesda, Maryland 4Department of Neurology, Mount Sinai School of Medicine, New York, New York 5Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, California 6Pfizer Global Research and Development, Groton, Connecticut 7Department of Psychology, Hunter College, New York, New York 8Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 9Department of Neurosciences, University of California San Diego, La Jolla, California 10Memory Pharmaceutical Corporation, Montvale, New Jersey
Abstract This review summarizes the scientific talks presented at the conference “Therapeutics for Cognitive Aging,” hosted by the New York Academy of Sciences and the Alzheimer’s Drug Discovery Foundation on May 15, 2009. Attended by scientists from industry and academia, as well as by a number of lay people—approximately 200 in all—the conference specifically tackled the many aspects of developing therapeutic interventions for cognitive impairment. Discussion also focused on how to define cognitive aging and whether it should be considered a treatable, tractable disease.
Introduction
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One of the difficulties in developing therapies for cognitive aging is that the syndrome is not well defined clinically, pathologically, or mechanistically. While some consider cognitive aging to be a prodromal phase to dementia or Alzheimer’s disease (AD), others consider it a separate clinical syndrome. Cognitive aging can significantly affect productivity and quality of life, and while effective symptomatic or preventative treatments could provide many benefits to individuals and society, defining and differentiating the syndrome of cognitive aging from “normal” and “diseased” is a crucial first step. It is becoming clear that many of the same neural network abnormalities found in AD (as discussed below) may be functionally impaired in cognitive aging; this fact supports the hypothesis that cognitive aging may be a prodromal phase to AD. On the other hand, many individuals exhibit symptoms of cognitive aging and never go on to develop AD. It is clear that individual differences in many factors (e.g., diet, lifestyle, stress, genetic factors) can play a major role in the aging process, adding to the complexity of distinguishing between
© 2010 New York Academy of Sciences. Address for correspondence: Howard M. Fillit, Alzheimer’s Drug Discovery Foundation, 1414 Avenue of the Americas, Suite 1502, New York, NY 10019. hfillit@alzdiscovery.org. Conflicts of interest The authors declare no conflicts of interest.