The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Alzheimer's Disease: Exploring the Landscape of Cognitive Decline
Open accessPreprint — published as 10.1021/acschemneuro.4c00339 · Paper page
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and impaired daily functioning. The pathology of AD is marked by the accumulation of amyloid-beta plaques and tau protein tangles in brain, along with neuroinflammation and synaptic dysfunction. Genetic factors, such as mutations in APP, PSEN1, and PSEN2 genes, as well as APOE ε4 allele, contribute to increased risk of acquiring AD. Currently available treatments provide symptomatic relief but do not halt disease progression. Research efforts are focused on developing disease-modifying therapies that target the underlying pathological mechanisms of AD. Advances in identification and validation of reliable biomarkers for AD hold great promise for enhancing early diagnosis, monitoring disease progression, and assessing treatment response in clinical practice, in effort to alleviate the burden of this devastating disease. In this paper, we analyze data from the CAS Content Collection to summarize the research progress in Alzheimer’s disease. We examine the publication landscape in effort to provide insights into current knowledge advances and developments. We also review the most discussed and emerging concepts and assess the strategies to combat the disease. We explore the genetic risk factors, pharmacological targets, and comorbid diseases. Finally, we inspect clinical applications of products against AD with their development pipelines and efforts for drug repurposing. The objective of this review is to provide a broad overview of the evolving landscape of current knowledge regarding AD, to outline challenges, and evaluate growth opportunities to further efforts in combating the disease.
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Cites
The central role of DNA damage in the ageing process
Schumacher, B., Pothof, J., Vijg, J., & Hoeijmakers, J. H. J. (2021) · Nature · doi:10.1038/s41586-021-03307-7 · Cited by 907
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Metadata
- Authors
- Tenchov, R., Sasso, J., & Zhou, Q. A.
- Affiliations
- American Chemical Society (US)
- Corresponding author
- Zhou, Qiongqiong Angela
- Venue
- ACS Chemical Neuroscience
- Publisher
- American Chemical Society (ACS)
- Published
- 2024-04-25
- Volume
- 15
- Issue
- 21
- Pages
- 3800-3827
- ISSN
- 1948-7193 (ISSN-L)
- PMC
- PMC11587518
- OpenAlex
- W4403334326
- Cited by
- 170
- References
- 1
- Citations by year
- 2026: 115 · 2025: 53 · 2024: 2
- FWCI
- 9.70
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- ACS Chemical Neuroscience (publishedVersion, cc-by)
- ChemRxiv (acceptedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- 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, cognitive decline, amyloid plaques, neuroinflammation, synaptic dysfunction, genetic risk factors, APP mutations, presenilin 1, presenilin 2, APOE ε4, disease-modifying therapy, biomarkers, early diagnosis, drug repurposing, comorbid diseases, therapeutic target, drug development pipeline
- MeSH terms
- Alzheimer Disease, Animals, Humans, Cognitive Dysfunction
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