The clinical promise of biomarkers of synapse damage or loss in Alzheimer’s disease
Open accessAbstract
BACKGROUND: Synapse damage and loss are fundamental to the pathophysiology of Alzheimer's disease (AD) and lead to reduced cognitive function. The goal of this review is to address the challenges of forging new clinical development approaches for AD therapeutics that can demonstrate reduction of synapse damage or loss. The key points of this review include the following: Synapse loss is a downstream effect of amyloidosis, tauopathy, inflammation, and other mechanisms occurring in AD.Synapse loss correlates most strongly with cognitive decline in AD because synaptic function underlies cognitive performance.Compounds that halt or reduce synapse damage or loss have a strong rationale as treatments of AD.Biomarkers that measure synapse degeneration or loss in patients will facilitate clinical development of such drugs.The ability of methods to sensitively measure synapse density in the brain of a living patient through synaptic vesicle glycoprotein 2A (SV2A) positron emission tomography (PET) imaging, concentrations of synaptic proteins (e.g., neurogranin or synaptotagmin) in the cerebrospinal fluid (CSF), or functional imaging techniques such as quantitative electroencephalography (qEEG) provides a compelling case to use these types of measurements as biomarkers that quantify synapse damage or loss in clinical trials in AD. CONCLUSION: A number of emerging biomarkers are able to measure synapse injury and loss in the brain and may correlate with cognitive function in AD. These biomarkers hold promise both for use in diagnostics and in the measurement of therapeutic successes.
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An EEG study with transgenic mice demonstrated a close correlation between neuronal accumulation of α-synuclein and slowing of brain oscillations and changes in network excitability.
“An EEG study with transgenic mice demonstrated a close correlation between neuronal accumulation of α-synuclein and slowing of brain oscillations and changes in network excitability [22, 41].”
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Synaptic loss is one of the strongest correlates of cognitive decline in AD, even more so than Aβ plaques and tau tangles.
“It is well-known that synaptic loss is one of the strongest correlates of cognitive decline in AD, even more so than Aβ plaques and tau tangles [139].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [139]
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Tau Oligomer–Containing Synapse Elimination by Microglia and Astrocytes in Alzheimer Disease
Taddei, R. N., Perbet, R., Mate de Gerando, A., Wiedmer, A. E., Sanchez-Mico, M., Connors Stewart, T., Gaona, A., Melloni, A., Amaral, A. C., Duff, K., et al. (2023) · JAMA Neurology · doi:10.1001/jamaneurol.2023.3530 · Cited by 110 · see citing works
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Oligodendrocyte progenitor cells in Alzheimer's disease: from physiology to pathology
Zou, P., Wu, C., Liu, T. C.-Y., Duan, R., & Yang, L. (2023) · Translational Neurodegeneration · doi:10.1186/s40035-023-00385-7 · Cited by 97 · see citing works
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Imaging Synaptic Density: The Next Holy Grail of Neuroscience?
Serrano, M. E., Kim, E., Petrinovic, M. M., Turkheimer, F., & Cash, D. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.796129 · Cited by 67 · see citing works
LILRB2-mediated TREM2 signaling inhibition suppresses microglia functions
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Advanced Overview of Biomarkers and Techniques for Early Diagnosis of Alzheimer’s Disease
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Current therapeutics for Alzheimer’s disease and clinical trials
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- Authors
- the Synaptic Health Endpoints Working Group, Colom-Cadena, M., Spires-Jones, T., Zetterberg, H., Blennow, K., Caggiano, A., DeKosky, S. T., Fillit, H., Harrison, J. E., Schneider, L. S., Scheltens, P., de Haan, W., Grundman, M., van Dyck, C. H., Izzo, N. J., & Catalano, S. M.
- Affiliations
- UK Dementia Research Institute (GB)
- Sahlgrenska University Hospital (SE)
- University of Florida (US)
- Alzheimer's Drug Discovery Foundation (US)
- University of Southern California (US)
- Yale University (US)
- Cognition Therapeutics (United States) (US)
- Corresponding author
- Catalano, Susan M.
- ORCID
- Venue
- Alzheimer's Research & Therapy
- Published
- 2020-03-02
- Volume
- 12
- Issue
- 1
- Pages
- 21-21
- ISSN
- 1758-9193 (ISSN-L)
- PMC
- PMC7053087
- OpenAlex
- W3011252852
- Cited by
- 328
- References
- 154
- Citations by year
- 2026: 24 · 2025: 47 · 2024: 56 · 2023: 57 · 2022: 73 · 2021: 45 · 2020: 26
- FWCI
- 6.43
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Alzheimer s Research & Therapy (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UCL Discovery (University College London) (submittedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (submittedVersion, other-oa)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- Amgen
- Biogen
- National Institutes of Health (UL1TR001863)
- Genentech
- Medical Research Council (MR/V00610X/1)
- National Institute on Aging (R01AG062276, P30AG066508, P30AG066530)
- National Center for Advancing Translational Sciences
- 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 › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Alzheimer's disease, synaptic loss, synaptic damage, biomarkers, SV2A, neurogranin, synaptotagmin, cerebrospinal fluid, quantitative EEG, amyloidosis, tauopathy, neuroinflammation, cognitive decline, clinical trial endpoints, drug development
- MeSH terms
- Alzheimer Disease, Electroencephalography, Humans, Synapses, Biomarkers, Positron-Emission Tomography, Functional Neuroimaging
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