The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
A death receptor 6-amyloid precursor protein pathway regulates synapse density in the mature CNS but does not contribute to Alzheimer’s disease-related pathophysiology in murine models.
Abstract
Recent studies implicate death receptor 6 (DR6) in an amyloid precursor protein (APP)-dependent pathway regulating developmental axon pruning, and in a pruning pathway operating during plastic rearrangements in adult brain. DR6 has also been suggested to mediate toxicity in vitro of Aβ peptides derived from APP. Given the link between APP, Aβ, and Alzheimer's disease (AD), these findings have raised the possibility that DR6 contributes to aspects of neurodegeneration in AD. To test this possibility, we have used mouse models to characterize potential function(s) of DR6 in the adult CNS and in AD-related pathophysiology. We show that DR6 is broadly expressed within the adult CNS and regulates the density of excitatory synaptic connections onto pyramidal neurons in a genetic pathway with APP.DR6 knock-out also gives rise to behavioral abnormalities, some of which are similar to those previously documented in APP knock-out animals. However, in two distinct APP transgenic models of AD, we did not observe any alteration in the formation of amyloid plaques, gliosis, synaptic loss, or cognitive behavioral deficits with genetic deletion of DR6, though we did observe a transient reduction in the degree of microglial activation in one model. Our results support the view that DR6 functions with APP to modulate synaptic density in the adult CNS, but do not provide evidence for a role of DR6 in the pathophysiology of AD.
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The involvement of DR6 in Alzheimer's neurodegeneration could not be proved in two transgenic mouse models of AD deficient for DR6.
“the involvement of DR6 in Alzheimer’s neurodegeneration could not be proved in two transgenic mouse models of AD deficient for DR6 (Kallop et al., 2014)”
From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Kallop et al., 2014
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“Quantification of CD68 or Iba1 staining and enlarged dark cluster areas was performed using morphometric-based methods as previously described (Le Pichon et al., 2013; Kallop et al., 2014).”
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Meilandt, W. J., Maloney, J. A., Imperio, J., Lalehzadeh, G., Earr, T., Crowell, S., Bainbridge, T. W., Lu, Y., Ernst, J. A., Fuji, R. N., et al. (2019) · Alzheimer's Research & Therapy · doi:10.1186/s13195-019-0553-5 · Cited by 45
Self-citationEtxeberria, A., Shen, Y.-A. A., Vito, S., Silverman, S. M., Imperio, J., Lalehzadeh, G., Soung, A. L., Du, C., Xie, L., Choy, M. K., et al. (2024) · The Journal of Neuroscience · doi:10.1523/jneurosci.2347-23.2024 · Cited by 34
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Metadata
- Authors
- Kallop, D. Y., Meilandt, W. J., Gogineni, A., Easley-Neal, C., Wu, T., Jubb, A. M., Yaylaoglu, M., Shamloo, M., Tessier-Lavigne, M., Scearce-Levie, K., & Weimer, R. M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2014-05-07
- Volume
- 34
- Issue
- 19
- Pages
- 6425-6437
- ISSN
- 0270-6474
- 1529-2401
- Cited by
- 54
- References
- 5
- Language
- en
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