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Emerging diagnostics and therapeutics for Alzheimer disease
Abstract
Alzheimer disease (AD) is the most common contributor to dementia in the world, but strategies that slow or prevent its clinical progression have largely remained elusive, until recently. This Review highlights the latest advances in biomarker technologies and therapeutic development to improve AD diagnosis and treatment. We review recent results that enable pathological staging of AD with neuroimaging and fluid-based biomarkers, with a particular emphasis on the role of amyloid, tau and neuroinflammation in disease pathogenesis. We discuss the lessons learned from randomized controlled trials, including some supporting the proposal that certain anti-amyloid antibodies slow cognitive decline during the mildly symptomatic phase of AD. In addition, we highlight evidence for newly identified therapeutic targets that may be able to modify AD pathogenesis and progression. Collectively, these recent discoveries-and the research directions that they open-have the potential to move AD clinical care toward disease-modifying treatment strategies with maximal benefits for patients.
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“While recent anti-Aβ antibody therapies targeting plaques have been shown to be effective in slowing the clinical course of AD”
From Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer’s disease (2024) · cites this paper as [53]
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“they can lead to blood vessel damage, detected as amyloid-related imaging abnormalities (ARIA) on MRI [53].”
From Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer’s disease (2024) · cites this paper as [53]
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Cavalcanti, F. L. D., Coutinho, L. B. C., Silveira, M. E. P. L. S., Lima, M. M., Gadelha, Y. M. D. F., & Coutinho, G. B. C. (2024) · International Journal of Health Science · doi:10.22533/at.ed.1594252411038
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蒋, 禹. (2025) · Advances in Clinical Medicine · doi:10.12677/acm.2025.151016
Metadata
- Authors
- Self, W. K., & Holtzman, D. M.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Holtzman, David M.
- Venue
- Nature Medicine
- Published
- 2023-09
- Volume
- 29
- Issue
- 9
- Pages
- 2187-2199
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W4386437808
- Cited by
- 381
- References
- 159
- Citations by year
- 2026: 91 · 2025: 140 · 2024: 134 · 2023: 15
- FWCI
- 14.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (RF1NS090934, RF1AG047644)
- U.S. Department of Health & Human Services | NIH | National Institute on Aging (U19AG069701)
- Cure Alzheimer’s Fund
- JPB Foundation
- 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, biomarkers, amyloid, tau protein, neuroinflammation, anti-amyloid antibodies, disease-modifying therapy, neuroimaging, fluid biomarkers, pathological staging, cognitive decline, therapeutic target, dementia
- MeSH terms
- Alzheimer Disease, Humans, Technology, Neuroimaging, Cognitive Dysfunction
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