ApoE Cascade Hypothesis in the pathogenesis of Alzheimer’s disease and related dementias

The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer’s disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). The three APOE alleles encode protein isoforms that differ from one another only at amino acid positions...

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Published inNeuron (Cambridge, Mass.) Vol. 110; no. 8; pp. 1304 - 1317
Main Authors Martens, Yuka A., Zhao, Na, Liu, Chia-Chen, Kanekiyo, Takahisa, Yang, Austin J., Goate, Alison M., Holtzman, David M., Bu, Guojun
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 20.04.2022
Subjects
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Amino Acids
Apolipoprotein E2 - genetics
Apolipoprotein E4 - genetics
Apolipoprotein E4 - metabolism
Apolipoproteins E - metabolism
Humans
Protein Isoforms - metabolism
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Abstract The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer’s disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). The three APOE alleles encode protein isoforms that differ from one another only at amino acid positions 112 and 158: apoE2 (C112, C158), apoE3 (C112, R158), and apoE4 (R112, R158). Despite progress, it remains unclear how these small amino acid differences in apoE sequence among the three isoforms lead to profound effects on aging and disease-related pathways. Here, we propose a novel “ApoE Cascade Hypothesis” in AD and age-related cognitive decline, which states that the biochemical and biophysical properties of apoE impact a cascade of events at the cellular and systems levels, ultimately impacting aging-related pathogenic conditions including AD. As such, apoE-targeted therapeutic interventions are predicted to be more effective by addressing the biochemical phase of the cascade. In this review, Martens et al. propose a novel “ApoE Cascade Hypothesis,” which states that the biochemical and biophysical properties of apoE impact a cascade of events at the cellular and systems levels, ultimately leading to Alzheimer’s disease and age-related cognitive decline.
AbstractList The ε4 allele of the apolipoprotein E gene ( APOE4 ) is a strong genetic risk factor for Alzheimer’s disease (AD) and several other neurodegenerative conditions including Lewy body dementia (LBD). The three APOE alleles encode protein isoforms which differ from one another only at amino acid positions 112 and 158; apoE2 (C112, C158), apoE3 (C112, R158), and apoE4 (R112, R158). Despite progress, it remains unclear how these small amino acid differences in apoE sequence among the three isoforms lead to profound effects on aging and disease-related pathways. Here, we propose a novel “ApoE Cascade Hypothesis” in AD and age-related cognitive decline that the biochemical and biophysical properties of apoE impact a cascade of events at the cellular and systems levels ultimately impacting aging-related pathogenic conditions including AD. As such, apoE-targeted therapeutic interventions are predicted to be more effective by addressing the biochemical phase of the cascade. In this review, Martens et al. propose a novel “ApoE Cascade Hypothesis” that the biochemical and biophysical properties of apoE impact a cascade of events at the cellular and systems levels ultimately leading to Alzheimer’s disease and age-related cognitive decline.
The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer’s disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). The three APOE alleles encode protein isoforms that differ from one another only at amino acid positions 112 and 158: apoE2 (C112, C158), apoE3 (C112, R158), and apoE4 (R112, R158). Despite progress, it remains unclear how these small amino acid differences in apoE sequence among the three isoforms lead to profound effects on aging and disease-related pathways. Here, we propose a novel “ApoE Cascade Hypothesis” in AD and age-related cognitive decline, which states that the biochemical and biophysical properties of apoE impact a cascade of events at the cellular and systems levels, ultimately impacting aging-related pathogenic conditions including AD. As such, apoE-targeted therapeutic interventions are predicted to be more effective by addressing the biochemical phase of the cascade. In this review, Martens et al. propose a novel “ApoE Cascade Hypothesis,” which states that the biochemical and biophysical properties of apoE impact a cascade of events at the cellular and systems levels, ultimately leading to Alzheimer’s disease and age-related cognitive decline.
The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). The three APOE alleles encode protein isoforms that differ from one another only at amino acid positions 112 and 158: apoE2 (C112, C158), apoE3 (C112, R158), and apoE4 (R112, R158). Despite progress, it remains unclear how these small amino acid differences in apoE sequence among the three isoforms lead to profound effects on aging and disease-related pathways. Here, we propose a novel "ApoE Cascade Hypothesis" in AD and age-related cognitive decline, which states that the biochemical and biophysical properties of apoE impact a cascade of events at the cellular and systems levels, ultimately impacting aging-related pathogenic conditions including AD. As such, apoE-targeted therapeutic interventions are predicted to be more effective by addressing the biochemical phase of the cascade.
The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). The three APOE alleles encode protein isoforms that differ from one another only at amino acid positions 112 and 158: apoE2 (C112, C158), apoE3 (C112, R158), and apoE4 (R112, R158). Despite progress, it remains unclear how these small amino acid differences in apoE sequence among the three isoforms lead to profound effects on aging and disease-related pathways. Here, we propose a novel "ApoE Cascade Hypothesis" in AD and age-related cognitive decline, which states that the biochemical and biophysical properties of apoE impact a cascade of events at the cellular and systems levels, ultimately impacting aging-related pathogenic conditions including AD. As such, apoE-targeted therapeutic interventions are predicted to be more effective by addressing the biochemical phase of the cascade.The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). The three APOE alleles encode protein isoforms that differ from one another only at amino acid positions 112 and 158: apoE2 (C112, C158), apoE3 (C112, R158), and apoE4 (R112, R158). Despite progress, it remains unclear how these small amino acid differences in apoE sequence among the three isoforms lead to profound effects on aging and disease-related pathways. Here, we propose a novel "ApoE Cascade Hypothesis" in AD and age-related cognitive decline, which states that the biochemical and biophysical properties of apoE impact a cascade of events at the cellular and systems levels, ultimately impacting aging-related pathogenic conditions including AD. As such, apoE-targeted therapeutic interventions are predicted to be more effective by addressing the biochemical phase of the cascade.
Author Holtzman, David M.
Kanekiyo, Takahisa
Yang, Austin J.
Goate, Alison M.
Bu, Guojun
Liu, Chia-Chen
Martens, Yuka A.
Zhao, Na
AuthorAffiliation 2 Division of Neuroscience, National Institute on Aging, Bethesda, MD, USA
3 Ronald M. Loeb Center for Alzheimer’s Disease, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA
1 Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
4 Department of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO, USA
AuthorAffiliation_xml – name: 1 Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
– name: 2 Division of Neuroscience, National Institute on Aging, Bethesda, MD, USA
– name: 3 Ronald M. Loeb Center for Alzheimer’s Disease, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA
– name: 4 Department of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO, USA
Author_xml – sequence: 1
  givenname: Yuka A.
  surname: Martens
  fullname: Martens, Yuka A.
  organization: Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
– sequence: 2
  givenname: Na
  surname: Zhao
  fullname: Zhao, Na
  organization: Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
– sequence: 3
  givenname: Chia-Chen
  surname: Liu
  fullname: Liu, Chia-Chen
  organization: Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
– sequence: 4
  givenname: Takahisa
  surname: Kanekiyo
  fullname: Kanekiyo, Takahisa
  organization: Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
– sequence: 5
  givenname: Austin J.
  surname: Yang
  fullname: Yang, Austin J.
  organization: Division of Neuroscience, National Institute on Aging, Bethesda, MD, USA
– sequence: 6
  givenname: Alison M.
  surname: Goate
  fullname: Goate, Alison M.
  organization: Ronald M. Loeb Center for Alzheimer’s Disease, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA
– sequence: 7
  givenname: David M.
  surname: Holtzman
  fullname: Holtzman, David M.
  organization: Department of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer’s Disease Research Center, Washington University in St. Louis, St. Louis, MO, USA
– sequence: 8
  givenname: Guojun
  surname: Bu
  fullname: Bu, Guojun
  email: bu.guojun@mayo.edu
  organization: Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35298921$$D View this record in MEDLINE/PubMed
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Y.A.M. and T.K. led the initial drafting of the manuscript, figures and edited the manuscript. N.Z., C-C.L., A.J.Y., A.M.G., and D.M.H co-edited the manuscript. GB supervised the writing and edited the manuscript. All authors have read and agreed on the final manuscript.
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Snippet The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer’s disease (AD) and several other neurodegenerative conditions,...
The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions,...
The ε4 allele of the apolipoprotein E gene ( APOE4 ) is a strong genetic risk factor for Alzheimer’s disease (AD) and several other neurodegenerative...
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SubjectTerms Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Amino Acids
Apolipoprotein E2 - genetics
Apolipoprotein E4 - genetics
Apolipoprotein E4 - metabolism
Apolipoproteins E - metabolism
Humans
Protein Isoforms - metabolism
Title ApoE Cascade Hypothesis in the pathogenesis of Alzheimer’s disease and related dementias
URI https://dx.doi.org/10.1016/j.neuron.2022.03.004
https://www.ncbi.nlm.nih.gov/pubmed/35298921
https://www.proquest.com/docview/2641001000
https://pubmed.ncbi.nlm.nih.gov/PMC9035117
Volume 110
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