Insulin resistance, dyslipidemia, and apolipoprotein E interactions as mechanisms in cognitive impairment and Alzheimer's disease
Open accessAbstract
An increased risk for Alzheimer's disease is associated with dyslipidemia and insulin resistance. A separate literature shows the genetic risk for developing Alzheimer's disease is strongly correlated to the presence of the E4 isoform of the apolipoprotein E carrier protein. Understanding how apolipoprotein E carrier protein, lipids, amyloid β peptides, glucose, central nervous system insulin, and peripheral insulin interact with one another in Alzheimer's disease is an area of increasing interest. Here, we will review the evidence relating apolipoprotein E carrier protein, lipids, and insulin action to Alzheimer's disease and Aβ peptides and then propose mechanisms as to how these factors might interact with one another to impair cognition and promote Alzheimer's disease.
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In humans, ApoE genotype modifies the response to insulin treatment.
“In humans, ApoE genotype modifies the response to insulin treatment.”
From Apolipoprotein E metabolism and functions in brain and its role in Alzheimer's disease (2017) · cites this paper as [47]
The relationship between amyloid β and insulin resistance is modulated by ApoE genotype.
“The relationship between amyloid β and insulin resistance is also modulated by ApoE genotype [47].”
From Apolipoprotein E metabolism and functions in brain and its role in Alzheimer's disease (2017) · cites this paper as [47]
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The role of apolipoprotein E in Alzheimer's disease
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BackgroundGhrelin controls hippocampal spine synapse density and memory performance
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Self-citationapoE isoform–specific disruption of amyloid β peptide clearance from mouse brain
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- Authors
- Salameh, T. S., Rhea, E. M., Banks, W. A., & Hanson, A. J.
- Affiliations
- University of Washington (US)
- Corresponding author
- Banks, William A
- Venue
- Experimental Biology and Medicine
- Publisher
- Frontiers Media SA
- Published
- 2016-07-28
- Volume
- 241
- Issue
- 15
- Pages
- 1676-1683
- ISSN
- 0071-3384 (ISSN-L)
- 1535-3702
- 1535-3699
- PMC
- PMC4999626
- OpenAlex
- W2476631162
- Cited by
- 51
- References
- 12
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 4 · 2023: 1 · 2022: 5 · 2021: 10 · 2020: 5 · 2019: 6 · 2018: 3 · 2017: 4 · 2016: 1
- FWCI
- 3.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Experimental Biology and Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs
- National Institutes of Health
- National Institute on Aging (T32AG000057, R01AG046619, P01AG001751, K23AG047978)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- insulin resistance, dyslipidemia, apolipoprotein E, APOE ε4, Alzheimer's disease, cognitive impairment, amyloid-beta, lipids, glucose metabolism
- MeSH terms
- Alzheimer Disease, Apolipoproteins E, Humans, Insulin Resistance, Amyloid beta-Peptides, Dyslipidemias, Cognitive Dysfunction
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