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Diabetes-Associated SorCS1 Regulates Alzheimer's Amyloid-β Metabolism: Evidence for Involvement of SorL1 and the Retromer Complex
Abstract
SorCS1 and SorL1/SorLA/LR11 belong to the sortilin family of vacuolar protein sorting-10 (Vps10) domain-containing proteins. Both are genetically associated with Alzheimer's disease (AD), and SORL1 expression is decreased in the brains of patients suffering from AD.SORCS1 is also genetically associated with types 1 and 2 diabetes mellitus (T1DM, T2DM). We have undertaken a study of the possible role(s) for SorCS1 in metabolism of the Alzheimer's amyloid-β peptide (Aβ) and the Aβ precursor protein (APP), to test the hypothesis that Sorcs1 deficiency might be a common genetic risk factor underlying the predisposition to AD that is associated with T2DM. Overexpression of SorCS1cβ-myc in cultured cells caused a reduction (p= 0.002) in Aβ generation. Conversely, endogenous murine Aβ 40 and Aβ 42 levels were increased (Aβ 40,p= 0.044; Aβ 42,p= 0.007) in the brains of female Sorcs1 hypomorphic mice, possibly paralleling the sexual dimorphism that is characteristic of the genetic associations of SORCS1 with AD and DM. Since SorL1 directly interacts with Vps35 to modulate APP metabolism, we investigated the possibility that SorCS1cβ-myc interacts with APP, SorL1, and/or Vps35. We readily recovered SorCS1:APP, SorCS1:SorL1, and SorCS1:Vps35 complexes from nontransgenic mouse brain. Notably, total Vps35 protein levels were decreased by 49% (p= 0.009) and total SorL1 protein levels were decreased by 29% (p= 0.003) in the brains of female Sorcs1 hypomorphic mice. From these data, we propose that dysfunction of SorCS1 may contribute to both the APP/Aβ disturbance underlying AD and the insulin/glucose disturbance underlying DM.
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SorL1 interacts with APP and VPS35, and interaction of SorL1 with VPS35 is necessary for SorL1 to control APP metabolism.
“SorL1 is a Vps10 family member in the retromer complex that interacts with APP and VPS35, and the interaction of SorL1 with VPS35 is necessary for SorL1 to control APP metabolism (Lane et al., 2010).”
From VPS35 haploinsufficiency increases Alzheimer’s disease neuropathology (2011) · cites this paper as Lane et al., 2010
Loss of function of SorCS1 leads to an increase of Aβ and a decrease of VPS35 levels.
“loss of function of SorCS1, a SorL1 family protein and a risk factor for type 2 diabetes, also leads to an increase of Aβ and a decrease of VPS35 levels (Lane et al., 2010)”
From VPS35 haploinsufficiency increases Alzheimer’s disease neuropathology (2011) · cites this paper as Lane et al., 2010
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VPS35 haploinsufficiency increases Alzheimer’s disease neuropathology
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Sex specific molecular networks and key drivers of Alzheimer’s disease
Guo, L., Cao, J., Hou, J., Li, Y., Huang, M., Zhu, L., Zhang, L., Lee, Y., Duarte, M. L., Zhou, X., et al. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00624-5 · Cited by 49
“analysis Snap-frozen mouse hemi-brains were harvested in lysis buffer [36] and processed via step-wise solubilization [36, 37], followed by SDS-PAGE to determine levels of LRP10, CD34, NBR1, ACBD3, LRP1, LRP3, LRP6, LDLR, pTau, total tau and β-actin.”
Method
Metadata
- Authors
- Lane, R. F., Raines, S. M., Steele, J. W., Ehrlich, M. E., Lah, J. A., Small, S. A., Tanzi, R. E., Attie, A. D., & Gandy, S.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2010-09-29
- Volume
- 30
- Issue
- 39
- Pages
- 13110-13115
- ISSN
- 0270-6474
- 1529-2401
- PMC
- PMC3274732
- Cited by
- 143
- References
- 4
- Language
- en
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