The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
Disease‐modifying therapies in Alzheimer's disease
Abstract
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.
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1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer's Disease
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Cited by
Lannfelt, L., Blennow, K., Zetterberg, H., Batsman, S., Ames, D., Harrison, J., Masters, C. L., Targum, S., Bush, A. I., Murdoch, R., et al. (2008) · The Lancet Neurology · doi:10.1016/s1474-4422(08)70167-4 · Cited by 725
Natural products as a source of Alzheimer's drug leads
Williams, P., Sorribas, A., & Howes, M.-J. R. (2011) · Nat. Prod. Rep. · doi:10.1039/c0np00027b · Cited by 404
Anti-Aβ Therapeutics in Alzheimer's Disease: The Need for a Paradigm Shift
Golde, T. E., Schneider, L. S., & Koo, E. H. (2011) · Neuron · doi:10.1016/j.neuron.2011.01.002 · Cited by 382
Fagan, A. M., Mintun, M. A., Shah, A. R., Aldea, P., Roe, C. M., Mach, R. H., Marcus, D., Morris, J. C., & Holtzman, D. M. (2009) · EMBO Molecular Medicine · doi:10.1002/emmm.200900048 · Cited by 353
Agrawal, M., Ajazuddin, Tripathi, D. K., Saraf, S., Saraf, S., Antimisiaris, S. G., Mourtas, S., Hammarlund-Udenaes, M., & Alexander, A. (2017) · Journal of Controlled Release · doi:10.1016/j.jconrel.2017.05.019 · Cited by 356
Metadata
- Authors
- Salloway, S., Mintzer, J., Weiner, M. F., & Cummings, J. L.
- Venue
- Alzheimer's & Dementia
- Publisher
- Wiley
- Published
- 2008-02-18
- Volume
- 4
- Issue
- 2
- Pages
- 65-79
- ISSN
- 1552-5260 (ISSN-L)
- 1552-5279
- OpenAlex
- W2007377859
- Cited by
- 161
- References
- 35
- FWCI
- 14.07
- Type
- journal article
- Language
- en
- Open access
- closed
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- Salloway, S., Mintzer, J., Weiner, M. F., & Cummings, J. L. (2008). Disease‐modifying therapies in Alzheimer's disease. Alzheimer's & Dementia. https://doi.org/10.1016/j.jalz.2007.10.001
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
