Understanding the cause of sporadic Alzheimer’s disease
Abstract
The increasing prevalence of Alzheimer's disease (AD) and a lack of effective prevention or disease-modifying therapies are global challenges with devastating personal, social and economic consequences. The amyloid β (Aβ) hypothesis posits that cerebral β-amyloidosis is a critical early event in AD pathogenesis. However, failed clinical trials of Aβ-centric drug candidates have called this hypothesis into question. Whereas we acknowledge that the Aβ hypothesis is far from disproven, we here re-visit the links between Aβ, tau and neurodegeneration. We review the genetics, epidemiology and pathology of sporadic AD and give an updated account of what is currently known about the molecular pathogenesis of the disease.
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Modeling these pathological hallmarks has largely relied on transgenic cellular and animal models harboring genetic mutations linked to ADAD.
“Modeling these pathological hallmarks has largely relied on transgenic cellular and animal models harboring genetic mutations linked to ADAD (3–5).”
From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [5]
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- Authors
- Zetterberg, H., & Mattsson, N.
- Affiliations
- National Hospital for Neurology and Neurosurgery (GB)
- San Francisco VA Medical Center (US)
- Corresponding author
- Zetterberg, Henrik
- Venue
- Expert Review of Neurotherapeutics
- Publisher
- Informa UK Limited
- Published
- 2014-05-23
- Volume
- 14
- Issue
- 6
- Pages
- 621-630
- ISSN
- 1473-7175 (ISSN-L)
- 1744-8360
- OpenAlex
- W2153645950
- Cited by
- 73
- References
- 133
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 13 · 2023: 5 · 2022: 7 · 2021: 10 · 2020: 3 · 2019: 6 · 2018: 4 · 2017: 5 · 2016: 2 · 2015: 2 · 2014: 6
- FWCI
- 0.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Expert Review of Neurotherapeutics (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- 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
- sporadic Alzheimer's disease, beta-amyloidosis, tau protein, neurodegeneration, pathogenesis, genetic risk factors, clinical trial failure, disease-modifying therapy
- MeSH terms
- Aging, Alzheimer Disease, Brain, Humans, Amyloid beta-Peptides, tau Proteins
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