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Disease modifying therapy for AD?1
Open accessAbstract
Alzheimer's disease (AD) is the most common form of dementia in industrialized nations. If more effective therapies are not developed that either prevent AD or block progression of the disease in its very early stages, the economic and societal cost of caring for AD patients will be devastating. Only two types of drugs are currently approved for the treatment of AD: inhibitors of acetyl cholinesterase, which symptomatically enhance cognitive state to some degree but are not disease modifying; and the adamantane derivative, memantine. Memantine preferentially blocks excessive NMDA receptor activity without disrupting normal receptor activity and is thought to be a neuroprotective agent that blocks excitotoxicty. Memantine therefore may have a potentially disease modifying effect in multiple neurodegenerative conditions. An improved understanding of the pathogeneses of AD has now led to the identification of numerous therapeutic targets designed to alter amyloid beta protein (Abeta) or tau accumulation. Therapies that alter Abeta and tau through these various targets are likely to have significant disease modifying effects. Many of these targets have been validated in proof of concept studies in preclinical animal models, and some potentially disease modifying therapies targeting Abeta or tau are being tested in the clinic. This review will highlight both the promise of and the obstacles to developing such disease modifying AD therapies.
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“AD disease-modifying strategies are designed to target abnormal Aβ aggregates, clear, and delay or prevent the formation of aggregates [33].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [33]
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Flagged first, then by citations
2 of the 250 references couldn’t be matched to a known paper.
Research works printed but not linked: 2
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Cited by
Sorted by citations
Parsons, C. G., Stöffler, A., & Danysz, W. (2007) · Neuropharmacology · doi:10.1016/j.neuropharm.2007.07.013 · Cited by 724
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Metadata
- Authors
- Golde, T. E.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Golde, Todd E.
- ORCID
- Golde, Todd E.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2006-10-02
- Volume
- 99
- Issue
- 3
- Pages
- 689-707
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2056442085
- Cited by
- 117
- References
- 250
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 2 · 2022: 2 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 3 · 2016: 5 · 2015: 3 · 2014: 3 · 2013: 5 · 2012: 6
- FWCI
- 2.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- National Institutes of Health
- National Institute on Aging
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Pharmacology (medical) › Cholinesterase and Neurodegenerative Diseases
- Keywords
- Alzheimer's disease, disease-modifying therapy, amyloid-beta, tau protein, acetylcholinesterase inhibitors, memantine, NMDA receptor, neuroprotection, excitotoxicity, therapeutic target, clinical trials, dementia
- MeSH terms
- Alzheimer Disease, Animals, Humans, Immunotherapy, Peptide Hydrolases, Phosphorylation, Protease Inhibitors, Amyloid beta-Peptides, Neurofibrillary Tangles, tau Proteins, Protein Folding, Molecular Chaperones, Alzheimer Vaccines
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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