Function and Comorbidities of Apolipoprotein E in Alzheimer's Disease
Identifieur interne : 000C41 ( Pmc/Curation ); précédent : 000C40; suivant : 000C42Function and Comorbidities of Apolipoprotein E in Alzheimer's Disease
Auteurs : Valérie Leduc ; Dorothée Domenger ; Louis De Beaumont ; Daphnée Lalonde ; Stéphanie Bélanger-Jasmin ; Judes PoirierSource :
- International Journal of Alzheimer's Disease [ 2090-0252 ] ; 2011.
Abstract
Alzheimer's disease (AD)—the most common type of dementia among the elderly—represents one of the most challenging and urgent medical mysteries affecting our aging population. Although dominant inherited mutation in genes involved in the amyloid metabolism can elicit familial AD, the overwhelming majority of AD cases, dubbed sporadic AD, do not display this Mendelian inheritance pattern. Apolipoprotein E (APOE), the main lipid carrier protein in the central nervous system, is the only gene that has been robustly and consistently associated with AD risk. The purpose of the current paper is thus to highlight the pleiotropic roles and the structure-function relationship of APOE to stimulate both the functional characterization and the identification of novel lipid homeostasis-related molecular targets involved in AD.
Url:
DOI: 10.4061/2011/974361
PubMed: 21559182
PubMed Central: 3089878
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PMC:3089878Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>Alzheimer's disease (AD)—the most common type of dementia among the elderly—represents one of the most challenging and urgent medical mysteries affecting our aging population. Although dominant inherited mutation in genes involved in the amyloid metabolism can elicit familial AD, the overwhelming majority of AD cases, dubbed sporadic AD, do not display this Mendelian inheritance pattern. Apolipoprotein E (APOE), the main lipid carrier protein in the central nervous system, is the only gene that has been robustly and consistently associated with AD risk. The purpose of the current paper is thus to highlight the pleiotropic roles and the structure-function relationship of APOE to stimulate both the functional characterization and the identification of novel lipid homeostasis-related molecular targets involved in AD.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Int J Alzheimers Dis</journal-id>
<journal-id journal-id-type="publisher-id">IJAD</journal-id>
<journal-title-group><journal-title>International Journal of Alzheimer's Disease</journal-title>
</journal-title-group>
<issn pub-type="epub">2090-0252</issn>
<publisher><publisher-name>SAGE-Hindawi Access to Research</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">21559182</article-id>
<article-id pub-id-type="pmc">3089878</article-id>
<article-id pub-id-type="doi">10.4061/2011/974361</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Function and Comorbidities of Apolipoprotein E in Alzheimer's Disease</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Leduc</surname>
<given-names>Valérie</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1, 2</sup>
</xref>
<xref ref-type="aff" rid="I2"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Domenger</surname>
<given-names>Dorothée</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1, 2</sup>
</xref>
<xref ref-type="aff" rid="I2"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>De Beaumont</surname>
<given-names>Louis</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1, 2</sup>
</xref>
<xref ref-type="aff" rid="I2"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lalonde</surname>
<given-names>Daphnée</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1, 2</sup>
</xref>
<xref ref-type="aff" rid="I2"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bélanger-Jasmin</surname>
<given-names>Stéphanie</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1, 2</sup>
</xref>
<xref ref-type="aff" rid="I2"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Poirier</surname>
<given-names>Judes</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1, 2, 3</sup>
</xref>
<xref ref-type="aff" rid="I2"></xref>
<xref ref-type="aff" rid="I3"></xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
</contrib-group>
<aff id="I1"><sup>1</sup>
Department of Psychiatry, Douglas Mental Health University Institute, Perry Pavilion, E-3207.1, 6875 Lasalle Boulevard, Verdun, QC, Canada H4H1R3</aff>
<aff id="I2"><sup>2</sup>
Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada H3A2B4</aff>
<aff id="I3"><sup>3</sup>
McGill Centre for Studies in Aging, Verdun, QC, Canada H4H1R3</aff>
<author-notes><corresp id="cor1">*Judes Poirier: <email>judes.poirier@mcgill.ca</email>
</corresp>
<fn fn-type="other"><p>Academic Editor: Mikko Hiltunen</p>
</fn>
</author-notes>
<pub-date pub-type="collection"><year>2011</year>
</pub-date>
<pub-date pub-type="epub"><day>5</day>
<month>4</month>
<year>2011</year>
</pub-date>
<volume>2011</volume>
<elocation-id>974361</elocation-id>
<history><date date-type="received"><day>30</day>
<month>11</month>
<year>2010</year>
</date>
<date date-type="accepted"><day>9</day>
<month>2</month>
<year>2011</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2011 Valérie Leduc et al.</copyright-statement>
<copyright-year>2011</copyright-year>
<license license-type="open-access"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p>
</license>
</permissions>
<abstract><p>Alzheimer's disease (AD)—the most common type of dementia among the elderly—represents one of the most challenging and urgent medical mysteries affecting our aging population. Although dominant inherited mutation in genes involved in the amyloid metabolism can elicit familial AD, the overwhelming majority of AD cases, dubbed sporadic AD, do not display this Mendelian inheritance pattern. Apolipoprotein E (APOE), the main lipid carrier protein in the central nervous system, is the only gene that has been robustly and consistently associated with AD risk. The purpose of the current paper is thus to highlight the pleiotropic roles and the structure-function relationship of APOE to stimulate both the functional characterization and the identification of novel lipid homeostasis-related molecular targets involved in AD.</p>
</abstract>
</article-meta>
</front>
<floats-group><fig id="fig1" position="float"><label>Figure 1</label>
<caption><p>Illustration of the lipid-free (a) and DPPC-bound (b) conformational states of APOE isoforms. (a) In a lipid-free state, the NT and CT domains of APOE interact with each other. (b) The tridimensional conformation of APOE significantly changes when bound to lipid and adopts the shape of a horseshoe, with the CT domain oriented toward the lipoprotein surface. APOE or E: apolipoprotein E; the red dots line represents salt bridges; C: cysteine; R: arginine; E: glutamate; DPPC: dipalmitoylphosphatidylcholine; NT: N-terminal domain containing the low-density lipoprotein binding sites; CT: C-terminal domain comprising the lipoprotein binding and APOE self-association sites.</p>
</caption>
<graphic xlink:href="IJAD2011-974361.001"></graphic>
</fig>
<fig id="fig2" position="float"><label>Figure 2</label>
<caption><p>Cholesterol transport in the CNS. APOE is synthesized by astrocytes and assembles free cholesterol (FC) and phospholipids (PLs) to form HDL-like particles. (1) Lipidation of these lipoparticles is facilitated via the mobilization and distribution of lipids to the cell surface by ABCA1/G1. Once secreted in the extracellular space, these HDL-like particles are directed either toward the circulation through the BBB and/or to neurons requiring lipids. (2) These APOE-HDL-like particles are recognized and endocytosed by members of the cell surface LDLR family (LDLR, LRP, APOER2, VLDLR), and (3) the FC is released within neurons and can be used for neurite elongation and/or synaptogenesis (4). As a result of lipid internalization, the endogenous synthesis of cholesterol within neurons (via the HMGCR pathway) is repressed (5). Excess cholesterol will be removed from neurons through its conversion into 24S-hydroxycholesterol (24S-OH) which is mediated by cholesterol 24S-hydroxylase (CYP46) (6). This sterol can now freely cross lipophilic membranes of the BBB and exit the brain for elimination (7). APOE or E: apolipoprotein E; BBB: blood-brain barrier; RER: rough endoplasmic reticulum; HMGCR: 3-hydroxy-3-methylglutaryl coenzyme A reductase; HDL: high-density lipoprotein; LDLR: low-density lipoprotein receptor.</p>
</caption>
<graphic xlink:href="IJAD2011-974361.002"></graphic>
</fig>
<table-wrap id="tab1" position="float"><label>Table 1</label>
<caption><p>Key structural and functional differences between the three main human APOE isoforms.</p>
</caption>
<table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="1" colspan="1">Description</th>
<th align="center" rowspan="1" colspan="1">E2</th>
<th align="center" rowspan="1" colspan="1">E3</th>
<th align="center" rowspan="1" colspan="1">E4</th>
</tr>
</thead>
<tbody><tr><td align="left" rowspan="2" colspan="1">Primary sequence difference</td>
<td align="center" rowspan="1" colspan="1">C112</td>
<td align="center" rowspan="1" colspan="1">C112</td>
<td align="center" rowspan="1" colspan="1"><bold>R112</bold>
</td>
</tr>
<tr><td align="center" rowspan="1" colspan="1"><bold>C158</bold>
</td>
<td align="center" rowspan="1" colspan="1">R158</td>
<td align="center" rowspan="1" colspan="1">R158</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">Structure particularity</td>
<td align="center" rowspan="1" colspan="1">Disruption of salt bridge network in the NT domain</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1">Domain interaction (creation of salt bridges R112-E109 and <bold>R61-E255</bold>
)</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">LDLR binding</td>
<td align="center" rowspan="1" colspan="1"><2% normal receptor binding activity</td>
<td align="center" rowspan="1" colspan="1">High</td>
<td align="center" rowspan="1" colspan="1">High</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">Lipoprotein binding</td>
<td align="center" rowspan="1" colspan="1">HDL</td>
<td align="center" rowspan="1" colspan="1">HDL</td>
<td align="center" rowspan="1" colspan="1">VLDL/LDL</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">Protein stability</td>
<td align="center" rowspan="1" colspan="1">+++</td>
<td align="center" rowspan="1" colspan="1">++</td>
<td align="center" rowspan="1" colspan="1">+</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">Molten-like-globule propensity</td>
<td align="center" rowspan="1" colspan="1">+</td>
<td align="center" rowspan="1" colspan="1">++</td>
<td align="center" rowspan="1" colspan="1">+++</td>
</tr>
</tbody>
</table>
<table-wrap-foot><fn><p>E: glutamate; C: cysteine; R: arginine; LDLR: low-density lipoprotein receptor; HDL: high-density lipoprotein; VLDL: very-low-density lipoprotein; +/++/+++, respectively, low/medium/high.</p>
</fn>
</table-wrap-foot>
</table-wrap>
<table-wrap id="tab2" position="float"><label>Table 2</label>
<caption><p>APOE polymorphisms in humans and species differences.</p>
</caption>
<table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="1" colspan="1">ApoE residue <break></break>
(+signal peptide)</th>
<th align="center" rowspan="1" colspan="1">Population prevalence <break></break>
(%)</th>
<th align="center" rowspan="1" colspan="1">112 <break></break>
(130)</th>
<th align="center" rowspan="1" colspan="1">158 <break></break>
(176)</th>
</tr>
</thead>
<tbody><tr><td align="left" rowspan="1" colspan="1">Human</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
</tr>
<tr><td align="left" rowspan="1" colspan="1"> APOE2</td>
<td align="center" rowspan="1" colspan="1">8</td>
<td align="center" rowspan="1" colspan="1">C</td>
<td align="center" rowspan="1" colspan="1">C</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1"> APOE3</td>
<td align="center" rowspan="1" colspan="1">77</td>
<td align="center" rowspan="1" colspan="1">C</td>
<td align="center" rowspan="1" colspan="1">R</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1"> <bold>APOE4</bold>
</td>
<td align="center" rowspan="1" colspan="1"><bold>15</bold>
</td>
<td align="center" rowspan="1" colspan="1"><bold>R</bold>
</td>
<td align="center" rowspan="1" colspan="1"><bold>R</bold>
</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">Chimp</td>
<td align="center" rowspan="1" colspan="1">100</td>
<td align="center" rowspan="1" colspan="1">R</td>
<td align="center" rowspan="1" colspan="1">R</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">Gorilla</td>
<td align="center" rowspan="1" colspan="1">100</td>
<td align="center" rowspan="1" colspan="1">R</td>
<td align="center" rowspan="1" colspan="1">R</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">Orangutan</td>
<td align="center" rowspan="1" colspan="1">100</td>
<td align="center" rowspan="1" colspan="1">R</td>
<td align="center" rowspan="1" colspan="1">R</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">Mice</td>
<td align="center" rowspan="1" colspan="1">100</td>
<td align="center" rowspan="1" colspan="1">R</td>
<td align="center" rowspan="1" colspan="1">R</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">Rats</td>
<td align="center" rowspan="1" colspan="1">100</td>
<td align="center" rowspan="1" colspan="1">R</td>
<td align="center" rowspan="1" colspan="1">R</td>
</tr>
</tbody>
</table>
<table-wrap-foot><fn><p>APOE: apolipoprotein E; C: cysteine; R: arginine.</p>
</fn>
</table-wrap-foot>
</table-wrap>
<table-wrap id="tab3" position="float"><label>Table 3</label>
<caption><p>Summary of the most common neurodegenerative diseases of the CNS, some distinctive features, and their associations with the human APOE isoforms.</p>
</caption>
<table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="2" colspan="1">Neurodegenerative disease</th>
<th align="center" colspan="3" rowspan="1">Pathological and clinical characteristics</th>
<th align="center" colspan="3" rowspan="1">APOE isoform association</th>
</tr>
<tr><th align="center" rowspan="1" colspan="1">Protein deposition</th>
<th align="center" rowspan="1" colspan="1">Dementia</th>
<th align="center" rowspan="1" colspan="1">Risk<sup>1</sup>
</th>
<th align="center" rowspan="1" colspan="1">Age at onset<sup>1</sup>
</th>
<th align="center" rowspan="1" colspan="1">Dementia</th>
<th align="center" rowspan="1" colspan="1">Severity/progression rate</th>
</tr>
</thead>
<tbody><tr><td align="left" rowspan="1" colspan="1">AD</td>
<td align="center" rowspan="1" colspan="1">Extracellular amyloid-<italic>β</italic>
(“SP”) NCI tau (“NFT”)</td>
<td align="center" rowspan="1" colspan="1">++</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↗ (dose effect)</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↘<italic>ε</italic>
2↗ (dose effect)</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">PiD</td>
<td align="center" rowspan="1" colspan="1">NCI tau (“Pick Body”)</td>
<td align="center" rowspan="1" colspan="1">++</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↗(4/4<, 2/2>/-AD)</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↘ (dose effect)</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">CBD</td>
<td align="center" rowspan="1" colspan="1">GCI (+NCI) tau (“doughnut”)</td>
<td align="center" rowspan="1" colspan="1">++</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↗</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">PSP</td>
<td align="center" rowspan="1" colspan="1">GCI (+NCI) tau (“tuft”)</td>
<td align="center" rowspan="1" colspan="1">+</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
2↗</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">LBD</td>
<td align="center" rowspan="1" colspan="1">NCI <italic>α</italic>
-synuclein (“non- classical LB”) (+ SP, + NFT)</td>
<td align="center" rowspan="1" colspan="1">++</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↗(4/4<, 2/2>/-AD)</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↘ survival</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">MSA</td>
<td align="center" rowspan="1" colspan="1">GCI (+NCI) <italic>α</italic>
-synuclein (“Papp-Lantos Body”) (GCI + NCI tau)</td>
<td align="center" rowspan="1" colspan="1">(+)</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↗</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">PD</td>
<td align="center" rowspan="1" colspan="1">NCI <italic>α</italic>
-synuclein (classical LB)</td>
<td align="center" rowspan="1" colspan="1">+</td>
<td align="center" rowspan="1" colspan="1">(<italic>ε</italic>
4↗) <italic>ε</italic>
2↗</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↘ (><italic>ε</italic>
3><italic>ε</italic>
2)</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↗</td>
<td align="center" rowspan="1" colspan="1"></td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">HD</td>
<td align="center" rowspan="1" colspan="1">Neuronal intranuclear huntingtin</td>
<td align="center" rowspan="1" colspan="1">+</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↗</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">ALS</td>
<td align="center" rowspan="1" colspan="1">(NCI TDP-43)</td>
<td align="center" rowspan="1" colspan="1">5% FTD</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↗</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↘<italic>ε</italic>
2↗</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">MS</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1">4/4↗</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↗ severity</td>
</tr>
<tr><td align="left" rowspan="1" colspan="1">ARMD</td>
<td align="center" rowspan="1" colspan="1">Extracellular amyloid-<italic>β</italic>
(“drusen”)</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↘<italic>ε</italic>
2↗</td>
<td align="center" rowspan="1" colspan="1"><italic>ε</italic>
4↗<italic>ε</italic>
2↘</td>
<td align="center" rowspan="1" colspan="1"></td>
<td align="center" rowspan="1" colspan="1"></td>
</tr>
</tbody>
</table>
<table-wrap-foot><fn><p> AD: Alzheimer's disease; PiD: Pick's disease; CBD: Corticobasal dementia; PSP: Progressive supranuclear palsy; LBD: Lewy body dementia; MSA, multiple system atrophy; PD: Parkinson's disease; HD: Huntington's disease; ALS: Amyotrophic lateral sclerosis; MS: Multiple sclerosis; ARMD: Age-related macular degeneration; NCI: neuronal cytoplasmic inclusion; GCI: glial cytoplasmic inclusion; SP: senile plaque; NFT: neurofibrillary tangle; LB: Lewy body; ++ indicates very present, + moderately present, (+) present in a subset; <sup>1</sup>
the parentheses indicate that the association is less consistently found.</p>
</fn>
</table-wrap-foot>
</table-wrap>
</floats-group>
</pmc>
</record>
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