The DOI matches its Crossref record; 163 of the 163 references it cites were found in a registry or an index.
Alzheimer's Disease Mechanisms and Emerging Roads to Novel Therapeutics
Open accessAbstract
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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Cited by
Sorted by citations
Zhang, J., Zhang, Y., Wang, J., Xia, Y., Zhang, J., & Chen, L. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01911-3 · Cited by 1,138
“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.”
BackgroundInflammasomes in neuroinflammatory and neurodegenerative diseases
Voet, S., Srinivasan, S., Lamkanfi, M., & van Loo, G. (2019) · EMBO Molecular Medicine · doi:10.15252/emmm.201810248 · Cited by 761
Synaptic dysfunction in Alzheimer's disease: Mechanisms and therapeutic strategies
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CSF1R inhibitor JNJ-40346527 attenuates microglial proliferation and neurodegeneration in P301S mice
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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
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