Deficiency in LRP6-mediated Wnt signaling contributes to synaptic abnormalities and amyloid pathology in Alzheimer’s disease
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Alzheimer's disease (AD) is an age-related neurological disorder characterized by synaptic loss and dementia. The low-density lipoprotein receptor-related protein 6 (LRP6) is an essential coreceptor for Wnt signaling, and its genetic variants have been linked to AD risk. Here we report that neuronal LRP6-mediated Wnt signaling is critical for synaptic function and cognition. Conditional deletion of Lrp6 gene in mouse forebrain neurons leads to age-dependent deficits in synaptic integrity and memory. Neuronal LRP6 deficiency in an amyloid mouse model also leads to exacerbated amyloid pathology due to increased APP processing to amyloid-β. In humans, LRP6 and Wnt signaling are significantly downregulated in AD brains, likely by a mechanism that depends on amyloid-β. Our results define a critical pathway in which decreased LRP6-mediated Wnt signaling, synaptic dysfunction, and elevated Aβ synergistically accelerate AD progression and suggest that restoring LRP6-mediated Wnt signaling can be explored as a viable strategy for AD therapy.
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Pathways neuroprotective in Alzheimer's disease appeared more cohesive in AD resistant neurons than in vulnerable neurons, namely the transforming growth factor beta receptor signaling pathway (in DG) and the canonical Wnt signaling pathway (in DG, S1 and V1).
“We found that pathways neuroprotective in AD (Caraci et al., 2008; Liu et al., 2014; Tesseur et al., 2006)appeared more cohesive in AD resistant neurons than in vulnerable neurons, namely the transforming growth factor beta receptor signaling pathway (in DG) and the canonical Wnt signaling pathway (in DG, S1 and V1).”
From Selective Neuronal Vulnerability in Alzheimer’s Disease: A Network-Based Analysis (2020) · cites this paper as Liu et al., 2014
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- Authors
- Liu, C.-C., Tsai, C.-W., Deak, F., Rogers, J., Penuliar, M., Sung, Y. M., Maher, J. N., Fu, Y., Li, X., Xu, H., Estus, S., Hoe, H.-S., Fryer, J. D., Kanekiyo, T., & Bu, G.
- Affiliations
- Mayo Clinic (US)
- Georgetown University (US)
- Xiamen University (CN)
- University of Kentucky (US)
- Corresponding author
- Bu, Guojun
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2014-10
- Volume
- 84
- Issue
- 1
- Pages
- 63-77
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC4199382
- OpenAlex
- W2050543389
- Cited by
- 222
- References
- 74
- Citations by year
- 2026: 15 · 2025: 22 · 2024: 15 · 2023: 21 · 2022: 23 · 2021: 22 · 2020: 17 · 2019: 23 · 2018: 20 · 2017: 19 · 2016: 12 · 2015: 12 · 2014: 1
- FWCI
- 9.75
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- National Institute on Aging (P01AG030128, R01AG044420, P30AG028383, R01AG027924, R01AG021173, R01AG031784, RF1AG046205, R01AG046205, R01AG035355, P50AG016574)
- National Institute of Neurological Disorders and Stroke (R01NS046673, P01NS074969)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, LRP6, Wnt signaling, synaptic dysfunction, amyloid-beta, amyloid pathology, APP processing, memory impairment, cognitive impairment
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Animals, Female, Hippocampus, Humans, Male, Mice, Transgenic, Organ Culture Techniques, Synapses, Amyloid beta-Peptides, Mice, Knockout, Cell Line, Tumor, Mice, HEK293 Cells, Wnt Signaling Pathway, Low Density Lipoprotein Receptor-Related Protein-6
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