TY - JOUR
T1 - Disease-modifying therapies in Alzheimer's disease**EDITOR'S NOTE
T2 - The Journal intended to include this article in the January 2008 supplement, "Leon Thal Symposium on Prevention of Dementia."
AU - Salloway, Stephen
AU - Mintzer, Jacobo
AU - Weiner, Myron F.
AU - Cummings, Jeffrey L.
N1 - Funding Information:
Dr Salloway’s research is supported by the National Institutes of Health. Dr Mintzer’s research is supported by the National Institutes of Health/UNC School of Medicine, NIA Columbia University, Bristol-Myers Squibb, Eisai Inc, Forest Laboratories, NeuroChem, Novartis Pharmaceuticals Corp., Paraxel International Corp., Pfizer Inc., sanofi-aventis. Dr Weiner is supported by a National Institute on Aging grant (P50 AG123000), the Alzheimer’s Association and the King Foundation. Dr Cummings is supported by a National Institute on Aging Alzheimer’s Disease Research Center grant (P50 AG16570), an Alzheimer’s Research Center of California grant, the Sidell Kagan Foundation, and the Deane F. Johnson Alzheimer Research Foundation. Dr Salloway has received research support from Elan, Neurochem, Voyager, and Cephalon. He has served as a consultant and received research support and honoraria from Athena Diagnostics, Johnson & Johnson, Eisai, Pfizer, Forest and Myriad Pharmaceuticals. Dr Salloway has served as a consultant for Merck and sanofi-aventis. Dr Mintzer is a consultant and/or speaker and has received research support from Ono Pharma, for Bristol-Myers Squibb Co, Eisai Pharmaceuticals, Forest Laboratories, Inc, NeuroChem, Novartis Pharmaceuticals Corp, Otsuka America Pharmaceutical Inc, Otsuka Phamaceutical Co Ltd, Pfizer Inc, sanofi-synthelobo. and Myriad. Dr Weiner has received funding from sanofi-aventis, Myriad, and is a member of the speaker’s bureau for Pfizer/Eisai and Forest Laboratories. Dr Cummings has provided consultation to the following pharmaceutical companies: Abbott Laboratories, Astellas Acadia, Athenagen, Avanir, Eisai, EnVivo, Forest, Janssen, Lilly, Lundbeck, Merck, Merz, Myriad, Neurochem, Novartis, Ono Pharma, Pfizer, sanofi-aventis, and Takeda. The authors acknowledge Donna McGuire and Cindy van Dijk for editorial assistance that was funded by sanofi-aventis.
PY - 2008/3
Y1 - 2008/3
N2 - Alzheimer's disease (AD) is a chronic, progressive, neurodegenerative disorder that places a substantial burden on patients, their families, and society. The disease affects approximately 5 million individuals in the United States, with an annual cost of care greater than $100 billion. During the past dozen years, several agents have been approved that enhance cognition and global function of AD patients, and recent advances in understanding AD pathogenesis has led to the development of numerous compounds that might modify the disease process. A wide array of antiamyloid and neuroprotective therapeutic approaches are under investigation on the basis of the hypothesis that amyloid beta (Aβ) protein plays a pivotal role in disease onset and progression and that secondary consequences of Aβ generation and deposition, including tau hyperphosphorylation and neurofibrillary tangle formation, oxidation, inflammation, and excitotoxicity, contribute to the disease process. Interventions in these processes with agents that reduce amyloid production, limit aggregation, or increase removal might block the cascade of events comprising AD pathogenesis. Reducing tau hyperphosphorylation, limiting oxidation and excitotoxicity, and controlling inflammation might be beneficial disease-modifying strategies. Potentially neuroprotective and restorative treatments such as neurotrophins, neurotrophic factor enhancers, and stem cell-related approaches are also under investigation.
AB - Alzheimer's disease (AD) is a chronic, progressive, neurodegenerative disorder that places a substantial burden on patients, their families, and society. The disease affects approximately 5 million individuals in the United States, with an annual cost of care greater than $100 billion. During the past dozen years, several agents have been approved that enhance cognition and global function of AD patients, and recent advances in understanding AD pathogenesis has led to the development of numerous compounds that might modify the disease process. A wide array of antiamyloid and neuroprotective therapeutic approaches are under investigation on the basis of the hypothesis that amyloid beta (Aβ) protein plays a pivotal role in disease onset and progression and that secondary consequences of Aβ generation and deposition, including tau hyperphosphorylation and neurofibrillary tangle formation, oxidation, inflammation, and excitotoxicity, contribute to the disease process. Interventions in these processes with agents that reduce amyloid production, limit aggregation, or increase removal might block the cascade of events comprising AD pathogenesis. Reducing tau hyperphosphorylation, limiting oxidation and excitotoxicity, and controlling inflammation might be beneficial disease-modifying strategies. Potentially neuroprotective and restorative treatments such as neurotrophins, neurotrophic factor enhancers, and stem cell-related approaches are also under investigation.
KW - Alzheimer's disease
KW - Clinical trials
KW - Disease modification
KW - Neuroprotection
UR - http://www.scopus.com/inward/record.url?scp=40749160944&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=40749160944&partnerID=8YFLogxK
U2 - 10.1016/j.jalz.2007.10.001
DO - 10.1016/j.jalz.2007.10.001
M3 - Review article
C2 - 18631951
AN - SCOPUS:40749160944
SN - 1552-5260
VL - 4
SP - 65
EP - 79
JO - Alzheimer's and Dementia
JF - Alzheimer's and Dementia
IS - 2
ER -