A Hundred Years of Alzheimer's Disease Research
Open accessAbstract
On the 100th anniversary of Alzheimer's lecture describing the clinicopathological entity which bears his eponym, this article reviews the major areas of progress in our understanding of the disease and outlines the many gaps still remaining. The progress toward effective mechanistic therapy is reviewed.
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The amyloid hypothesis states that Aβ peptides lie upstream of all the pathological events occurring in AD, including NFT formation, synaptic dysfunction, and neuronal death.
“The amyloid hypothesis states that Aβ peptides lie upstream of all the pathological events occurring in AD, including NFT formation, synaptic dysfunction, and neuronal death (Oddo et al., 2003b; Hardy, 2006).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Hardy, 2006
The passage labeled Abstract (page unavailable) describes amyloid deposition as central to the amyloid hypothesis and discusses Aβ toxicity and electrophysiological effects. It does not state that Aβ lies upstream of all AD pathology, specifically NFT formation, synaptic dysfunction, and neuronal death. (LLM, conf=0.82)
Experimental — accuracy not yet measuredMitochondrial dysfunction and oxidative stress may encourage the development of amyloid plaques and NFTs.
“mitochondrial dysfunction and oxidative stress may encourage the development of amyloid plaques and NFTs”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Hardy, 2006
The passages on amyloid deposition and neurofibrillary tangles (labeled Abstract; no page supplied) discuss APP, presenilin, and MAPT mutations, but do not link mitochondrial dysfunction or oxidative stress to the development of either lesion. Searches for “mitochondrial,” “oxidative stress,” and “reactive oxygen species” found no passage addressing that proposed link. (LLM, conf=0.74)
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1 retracted
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- Authors
- Hardy, J.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Hardy, John
- ORCID
- Hardy, John
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2006-10
- Volume
- 52
- Issue
- 1
- Pages
- 3-13
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2166625407
- Cited by
- 467
- References
- 26
- Citations by year
- 2026: 11 · 2025: 11 · 2024: 14 · 2023: 18 · 2022: 17 · 2021: 22 · 2020: 21 · 2019: 16 · 2018: 29 · 2017: 14 · 2016: 26 · 2015: 29 · 2014: 24 · 2013: 33 · 2012: 34
- FWCI
- 3.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging
- 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, clinicopathological diagnosis, pathogenesis, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Humans, Research, Research Design, History, 20th Century, History, 21st Century
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