Toward the Treatment and Prevention of Alzheimer's Disease: Rational Strategies and Recent Progress

Gandy, Sam; DeKosky, Steven T.

doi:10.1146/annurev-med-092611-084441

Cited by 111Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Toward the Treatment and Prevention of Alzheimer's Disease: Rational Strategies and Recent Progress

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Gandy, Sam, DeKosky, Steven T.·2013·Annual Review of Medicine

DOI 10.1146/annurev-med-092611-084441PMC PMC3625402

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Abstract

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-tau.
“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]
The treatment-trials section links amyloidosis and tau pathology to Alzheimer’s disease and says tau pathology correlates with cognition. The biomarker-diagnosis section identifies amyloid plaques and neurofibrillary tangles as AD pathology. Our copy does not specify that the deposits are extracellular or the tangles intracellular and composed of phosphorylated tau. (LLM, conf=0.78)
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P3‐381: Three‐year follow‐up on the IVIg for Alzheimer's phase II study
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P2‐145: Development of an induced pluripotent stem cell (iPSC) Alzheimer's disease model using PSEN1 mutant fibroblasts
Sproul, A. A., Jacob, S., Nestor, M. W., Keilani, S., Jean, Y., Kahler, D., Santa‐María, I., Steele, J., Crary, J. F., Troy, C. M., et al. (2012) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2012.05.850 · Cited by 2 · see citing works
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Retracted
Environmental Exposures and the Risk for Alzheimer Disease
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Authors: Gandy, S., & DeKosky, S. T.
Affiliations: James J. Peters VA Medical Center (US)
University of Virginia (US)
ORCID: Gandy, Sam
DeKosky, Steven T.
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
DOI: 10.1146/annurev-med-092611-084441
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: Health Sciences › Medicine › Physiology › 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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Toward the Treatment and Prevention of Alzheimer's Disease: Rational Strategies and Recent Progress

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