Human apoE4-targeted replacement mice display synaptic deficits in the absence of neuropathology.
Open accessAbstract
The human APOE*4 allele is associated with an early age of onset and increased risk of Alzheimer's disease (AD). Long before the onset of AD, cognitive deficits can be identified in APOE*4 carriers. We examined neurons in the lateral amygdala of young apolipoprotein (apo) E3 and apoE4 targeted replacement (TR) mice for changes in synaptic integrity. ApoE4 mice displayed significantly reduced excitatory synaptic transmission and dendritic arborization. Despite these changes there were no signs of gliosis, amyloid deposition or neurofibrillary tangles in these mice. To our knowledge, this is the first study to suggest that cognitive deficits in APOE*4 carriers are due to inherent defects in synaptic function that appear prior to any age-dependent markers of neuropathology.
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ApoE4 knock-in mice showed significantly reduced excitatory synaptic transmission and dendritic arborization in the absence of noticeable neuropathological changes.
“apoE4 knock-in mice showed significantly reduced excitatory synaptic transmission and dendritic arborization in the absence of noticeable neuropathological changes (Wang et al., 2005).”
From Apolipoprotein E in Synaptic Plasticity and Alzheimer’s Disease: Potential Cellular and Molecular Mechanisms (2014) · cites this paper as Wang et al., 2005
A specific variant of the gene encoding apolipoprotein E is one of the best established risk factors for late onset/sporadic Alzheimer's disease.
“A specific variant of the gene encoding for apolipoprotein E, which transports cholesterol in the brain, is one of the best established risk factors for late onset/sporadic AD [43].”
From Loss of Mevalonate/Cholesterol Homeostasis in the Brain: A Focus on Autism Spectrum Disorder and Rett Syndrome (2019) · cites this paper as [43]
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References 61 · Cited by 138
- Authors
- Wang, C., Wilson, W. A., Moore, S. D., Mace, B. E., Maeda, N., Schmechel, D. E., & Sullivan, P. M.
- Affiliations
- Duke Medical Center (US)
- Duke University (US)
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Sullivan, Patrick M.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2005-03
- Volume
- 18
- Issue
- 2
- Pages
- 390-398
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2014248408
- Cited by
- 138
- References
- 61
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 4 · 2023: 3 · 2022: 10 · 2021: 11 · 2020: 9 · 2019: 6 · 2018: 6 · 2017: 5 · 2016: 10 · 2015: 4 · 2014: 10 · 2013: 9 · 2012: 5
- FWCI
- 3.00
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Department of Veterans Affairs
- National Institute on Aging (P50AG005128, P50 AG05128-18)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- APOE ε4, apolipoprotein E, Alzheimer's disease, targeted replacement mice, synaptic transmission, excitatory synapses, dendritic branching, lateral amygdala, cognitive impairment, preclinical Alzheimer's disease, synaptic dysfunction
- MeSH terms
- Affective Symptoms, Alzheimer Disease, Amygdala, Animals, Apolipoproteins E, Cognition Disorders, Dendrites, Disease Models, Animal, Humans, Male, Memory Disorders, Mice, Transgenic, Synaptic Transmission, Synapses, Gene Targeting, Excitatory Postsynaptic Potentials, Mice, Apolipoprotein E3, Apolipoprotein E4
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