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Alzheimer's Disease Mechanisms and Emerging Roads to Novel Therapeutics
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Ten years of remarkable progress in understanding the fundamental biochemistry of Alzheimer's disease have been followed by ten years of remarkable and increasing clinical insight into the natural progression of the disorder. The concept of a long, intermediary, prodromal phase between the first appearance of amyloid plaques and tangles and the manifestation of dementia is now well established. The major challenge for the next decade is to chart the many cellular processes that underlie this phase and link the biochemical alterations to the clinical manifestation of Alzheimer's disease. We discuss here how genetics, new cell culture systems, and improved animal models will fuel this work. We anticipate that the resulting novel insights will provide a basis for further drug development for this terrible disease.
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“However, the side effects associated with targeting β- and γ-secretases arise because these enzymes have a wide range of substrates that are vital in other physiological processes.170”
From Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies. (2024) · cites this paper as [170]
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“When Aβ antibodies, such as bapineuzumab (31), did not yield significant therapeutic effects, research shifted towards inhibiting the formation of Aβ.109,170”
From Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies. (2024) · cites this paper as [170]
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“109,170 However, the side effects associated with targeting β - and γ -secretases arise because these enzymes have a wide range of substrates that are vital in other physiological processes.”
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Metadata
- Authors
- Sala Frigerio, C., & De Strooper, B.
- Affiliations
- VIB Center for the Biology of Disease, Vlaams Instituut voor Biotechnologie, Leuven 3000, Belgium;,
- Venue
- Annual Review of Neuroscience
- Publisher
- Annual Reviews
- Published
- 2016-07-08
- Volume
- 39
- Issue
- 1
- Pages
- 57-79
- ISSN
- 0147-006X (ISSN-L)
- 1545-4126
- OpenAlex
- W2219854607
- Cited by
- 116
- References
- 163
- Citations by year
- 2025: 10 · 2024: 9 · 2023: 10 · 2022: 10 · 2021: 11 · 2020: 22 · 2019: 14 · 2018: 16 · 2017: 14
- FWCI
- 1.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Lirias (submittedVersion)
- Funders
- Fonds Wetenschappelijk Onderzoek
- KU Leuven
- Vlaamse regering
- 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, prodromal symptoms, amyloid plaques, neurofibrillary tangles, disease progression, genetic risk factors, cell culture model, animal models, drug development
- MeSH terms
- Alzheimer Disease, Animals, Brain, Disease Models, Animal, Humans, Amyloid beta-Peptides, tau Proteins, Plaque, Amyloid
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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