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Non-Fibrillar Oligomeric Amyloid-β within Synapses
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The biophysical assessment in postmortem Alzheimer's disease brain corroborates in vitro and in vivo evidence of displacement of amyloid-β oligomers, representing a potential mechanism of action underlying protection against amyloid-β oligomer-induced synaptic degradation observed with S2R modulators.
“This interaction assessed biophysically, in the postmortem brain from individuals with Alzheimer’s disease, corroborates in vitro and in vivo evidence of displacement of amyloid-β oligomers [64], representing a potential mechanism of action underlying the protection against amyloid-β oligomer-induced synaptic degradation [153,154,155,156,157] observed with S2R modulators [64].”
From Sigma-2 Receptors—From Basic Biology to Therapeutic Target: A Focus on Age-Related Degenerative Diseases (2023) · cites this paper as [155]
Other suggested Aβ binding partners at synapses include the α7-nicotinic receptor, Ephrin A4, PSD95 and LilrB2.
“Other suggested Aβ binding partners at synapses include the α7-nicotinic receptor [49], Ephrin A4 [73], PSD95 [35, 50, 52] and LilrB2 [32].”
From Transmembrane protein 97 is a potential synaptic amyloid beta receptor in human Alzheimer’s disease (2024) · cites this paper as [52]
Oligomeric Aβ accumulates within synapses.
“We and others have observed that oligomeric amyloid beta (Aβ) peptide causes synaptic dysfunction, accumulates within in synapses, and is associated with synapse loss around plaques [34, 41, 52, 60, 64].”
From Transmembrane protein 97 is a potential synaptic amyloid beta receptor in human Alzheimer’s disease (2024) · cites this paper as [52]
Oligomeric amyloid beta (Aβ) peptide causes synaptic dysfunction.
“We and others have observed that oligomeric amyloid beta (Aβ) peptide causes synaptic dysfunction, accumulates within in synapses, and is associated with synapse loss around plaques [34, 41, 52, 60, 64].”
From Transmembrane protein 97 is a potential synaptic amyloid beta receptor in human Alzheimer’s disease (2024) · cites this paper as [52]
Oligomeric Aβ is associated with synapse loss around plaques.
“We and others have observed that oligomeric amyloid beta (Aβ) peptide causes synaptic dysfunction, accumulates within in synapses, and is associated with synapse loss around plaques [34, 41, 52, 60, 64].”
From Transmembrane protein 97 is a potential synaptic amyloid beta receptor in human Alzheimer’s disease (2024) · cites this paper as [52]
The combination of array tomography with FRET enhances the lateral resolution to ~10 nm in the selected single synaptic terminals allowing us to determine whether proteins are close enough to be interacting.
“The combination of array tomography with FRET enhances the lateral resolution to ~ 10 nm in the selected single synaptic terminals allowing us to determine whether proteins are close enough to be interacting [23, 52].”
From Transmembrane protein 97 is a potential synaptic amyloid beta receptor in human Alzheimer’s disease (2024) · cites this paper as [52]
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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., et al. (2020) · Alzheimer's Research & Therapy · doi:10.1186/s13195-020-00588-4 · Cited by 328
Self-citationSynaptic dysfunction in Alzheimer's disease: Mechanisms and therapeutic strategies
Chen, Y., Fu, A. K. Y., & Ip, N. Y. (2019) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2018.11.006 · Cited by 258
Proteomic differences in amyloid plaques in rapidly progressive and sporadic Alzheimer’s disease
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Metadata
- Authors
- Pickett, E. K., Koffie, R. M., Wegmann, S., Henstridge, C. M., Herrmann, A. G., Colom-Cadena, M., Lleo, A., Kay, K. R., Vaught, M., Soberman, R., Walsh, D. M., Hyman, B. T., & Spires-Jones, T. L.
- Affiliations
- The University of Edinburgh Centre for Cognitive and Neural Systems, Centre for Dementia Prevention and the Euan MacDonald Centre for Motor Neurone Disease Research, Edinburgh, UK
- Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA
- Department of Neurology, Institut d’Investigacions Biomèdiques Sant Pau - Hospital de Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red en Enfermedades Neurodegenerativas, CIBERNED, Spain
- Laboratory for Neurodegenerative Research, Center for Neurologic Diseases, Brigham and Women’s Hospital and Harvard Medical School, Harvard Institutes of Medicine, Boston, MA, USA
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2016-08-03
- Volume
- 53
- Issue
- 3
- Pages
- 787-800
- ISSN
- 1387-2877
- 1875-8908
- Cited by
- 90
- References
- 15
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