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Toward the Treatment and Prevention of Alzheimer's Disease: Rational Strategies and Recent Progress
Open accessAbstract
Alzheimer's disease (AD) is the major cause of late-life brain failure. In the past 25 years, autosomal dominant forms of AD were found to be primariy attributable to mutations in one of two presenilins, polytopic proteins that contain the catalytic site of the γ-secretase protease that releases the amyloid beta (Aβ) peptide. Some familial AD is also due to mutations in the amyloid precursor protein (APP), but recently a mutation in APP was discovered that reduces Aβ generation and is protective against AD, further implicating amyloid metabolism. Prion-like seeding of amyloid fibrils and neurofibrillary tangles has been invoked to explain the stereotypical spread of AD within the brain. Treatment trials with anti-Aβ antibodies have shown target engagement, if not significant treatment effects. Attention is increasingly focused on presymptomatic intervention, because Aβ mismetabolism begins up to 25 years before symptoms begin. AD trials deriving from new biological information involve extraordinary international collaboration and may hold the best hope for success in the fight against AD.
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“Cognitive decline and memory loss from neurodegeneration are linked to deposition of extracellular amyloid β (Aβ) and intracellular accumulation of neurofibrillary tangles of phospho-tau2.”
From Regulation of cell distancing in peri-plaque glial nets by Plexin-B1 affects glial activation and amyloid compaction in Alzheimer’s disease (2024) · cites this paper as [2]
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Metadata
- Authors
- Gandy, S., & DeKosky, S. T.
- Affiliations
- James J. Peters VA Medical Center (US)
- University of Virginia (US)
- Venue
- Annual Review of Medicine
- Publisher
- Annual Reviews
- Published
- 2013-01-14
- Volume
- 64
- Issue
- 1
- Pages
- 367-383
- ISSN
- 0066-4219 (ISSN-L)
- 1545-326X
- PMC
- PMC3625402
- OpenAlex
- W2135220503
- Cited by
- 110
- References
- 100
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 5 · 2023: 4 · 2022: 7 · 2021: 4 · 2020: 10 · 2019: 2 · 2018: 5 · 2017: 12 · 2016: 9 · 2015: 17 · 2014: 17 · 2013: 13
- FWCI
- 2.09
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Annual Review of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX000348)
- GlaxoSmithKline
- National Institute on Aging (AG 05-133, P50 AG 05138, P01AG025204, P50AG005133, P50AG005138, AG025204, U19AG010483)
- National Institute of Neurological Disorders and Stroke (R01NS075685)
- 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
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, presenilin mutations, amyloid-beta, gamma-secretase, amyloid precursor protein, familial Alzheimer's disease, anti-amyloid antibodies, prion-like seeding, neurofibrillary tangles, amyloid metabolism
- MeSH terms
- Alzheimer Disease, Brain, DNA, Humans, Immunologic Factors, Mutation, Global Health, Incidence, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Practice Guidelines as Topic
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