Proteomic Identification of Lower Apolipoprotein A-I in Alzheimer’s Disease

Liu, Hsing Cheng; Hu, Chaur Jong; Chang, Jui‐Hsing; Sung, Su Whan; Lee, Long Shyong; Yuan, Rey Yue; Leu, Sy Jye

doi:10.1159/000090676

Cited by 72 publications

(61 citation statements)

References 62 publications

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“…Besides the simultaneous use of high concentrations of total or phosphorylated tau combined with reduced concentrations of A ␤ 42 to predict conversion of patients with mild cognitive impairment (MCI) to AD [8] , several techniques including proteomics allowed us to identify other proteins involved in A ␤ metabolism and vascular physiology as biomarkers for AD [9] . Thus a decrease in apolipoprotein A-I (APOA1) levels in AD patients was consistently reported [7,[10][11][12] .…”

Section: Introductionmentioning

confidence: 78%

“…That is why extensive searches for peripheral biochemical markers for AD are still conducted. The results show alterations for multiple proteins in cerebrospinal fluid samples and in serum [7] . Besides the simultaneous use of high concentrations of total or phosphorylated tau combined with reduced concentrations of A ␤ 42 to predict conversion of patients with mild cognitive impairment (MCI) to AD [8] , several techniques including proteomics allowed us to identify other proteins involved in A ␤ metabolism and vascular physiology as biomarkers for AD [9] .…”

Section: Introductionmentioning

confidence: 88%

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An <i>Apolipoprotein A-I</i> Gene Promoter Polymorphism Associated with Cognitive Decline, but Not with Alzheimer’s Disease

Helbecque

Codron

Cottel

et al. 2007

Dement Geriatr Cogn Disord

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Background/Aims: Accumulating biological and epidemiological evidence suggests a close link between cholesterol metabolism and the pathophysiology of Alzheimer’s disease (AD). The observation that the use of statins reduces the risk of AD sustains this hypothesis. Apolipoprotein A-I (APOA1) is the major component of the high-density lipoproteins, particles involved in reverse cholesterol transport. Therefore, genetic polymorphisms in the gene encoding APOA1 might influence cholesterol metabolism and be a risk factor for AD. A previous study suggested an impact of a G→A polymorphism at position –75 bp in the APOA1 gene on the risk for early-onset AD and on the age at onset of the disease. We studied this polymorphism in 3 independent European population samples. Methods: Genotyping was conducted asdescribed in the previous study. Results: We were unable to show any impact of this polymorphism on the risk of AD. Conversely, subjects bearing the A allele of this polymorphism were at risk of cognitive decline. Conclusion: Our resultssuggest an impact of the G→A polymorphism at position –75 bp in the APOA1 gene on cognitive impairment, but not on the risk of AD.

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Section: Introductionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 88%

An <i>Apolipoprotein A-I</i> Gene Promoter Polymorphism Associated with Cognitive Decline, but Not with Alzheimer’s Disease

Helbecque

Codron

Cottel

et al. 2007

Dement Geriatr Cogn Disord

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show abstract

“…In sharp contrast to apoE, apoAI is not synthesized in the CNS and its presence in CSF indicates transit across the blood-brain barrier (124). Polymorphisms in the gene that encodes apoAI have been correlated with AD dementia or all-cause dementia (19, 20); plasma and serum apoAI levels are decreased in patients with AD dementia (22–24); and serum levels of apoAI have been associated inversely with risk of AD dementia (21). Furthermore, recent studies have shown the lack of apoAI increases cerebral amyloid angiopathy and memory deficits of AD dementia (125), and increasing plasma apoAI levels provides cognitive and neuropathological benefits in animal models of AD dementia (126).…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal Fluid Particles in Alzheimer Disease and Parkinson Disease

Yang

Keene

Peskind

et al. 2015

J Neuropathol Exp Neurol

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Human cerebrospinal fluid (CSF) contains diverse lipid particles, including lipoproteins that are distinct from their plasma counterparts and contain apolipoprotein (apo) E isoforms, apoJ, and apoAI, and extracellular vesicles, which can be detected by annexin V binding. The aim of this study was to develop a method to quantify CSF particles and evaluate their relationship to aging and neurodegenerative diseases. We used a flow cytometric assay to detect annexin V-, apoE-, apoAI-, apoJ- and amyloid (A) β42-positive particles in CSF from 131 research volunteers who were neurologically normal or had mild cognitive impairment (MCI), Alzheimer disease (AD) dementia, or Parkinson disease. APOE ε4/ε4 participants had CSF apoE-positive particles that were more frequently larger but at an 88% lower level vs. those in APOE ε3/ε3 or APOE ε3/ε4 patients; this finding was reproduced in conditioned medium from mouse primary glial cell cultures with targeted replacement of apoE. CSF apoE-positive and β-amyloid (Aβ42)-positive particle concentrations were persistently reduced one-third to one-half in middle and older age subjects; apoAI-positive particle concentration progressively increased approximately 2-fold with age. Both apoAI-positive and annexin V-positive CSF particle levels were reduced one-third to one-half in CSF of MCI and/or AD dementia patients vs. age-matched controls. Our approach provides new methods to investigate CNS lipid biology in relation to neurodegeneration and perhaps develop new biomarkers for diagnosis or treatment monitoring.

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“…Neurodegenerative diseases [36,37], blepharitis [38], Down syndrome [39], diabetic nephropathy [40] have also been investigated by means of 2Dgel analysis of sera Many potential serum markers were identified, but protein serum level seems to change dramatically only at an advanced disease stage.…”

Section: Two-dimensional Gel Electrophoresismentioning

confidence: 99%

Fractionation Techniques Improve the Proteomic Analysis of Human Serum

Mauri¹,

Petretto²,

Cuccabita³

et al. 2008

CPA

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Different fractionation steps have been developed to reduce the complexity of serum proteome and to allow the detection and the identification of single proteins. The nature of fractionation (performed either on denatured or native proteins), the efficiency of recovery, the capacity of directly identifying proteins or protein panels, the possibility of associating to other laboratory techniques influence the choice of the methods to be used in different experimental and clinical settings. In this review, the main fractionation techniques (such as electrophoresis, SELDI and liquid chromatography) are described for proteomic studies in clinical field, and their advantages and disadvantages are discussed on the basis of our experience. In particular, liquid-liquid fractionation performed by PF2D is discussed in detail because of its partial automation, its ability to improve mass spectrometry analysis of serum proteins and its potential application in clinical studies.

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Proteomic Identification of Lower Apolipoprotein A-I in Alzheimer’s Disease

Cited by 72 publications

References 62 publications

An <i>Apolipoprotein A-I</i> Gene Promoter Polymorphism Associated with Cognitive Decline, but Not with Alzheimer’s Disease

An <i>Apolipoprotein A-I</i> Gene Promoter Polymorphism Associated with Cognitive Decline, but Not with Alzheimer’s Disease

Cerebrospinal Fluid Particles in Alzheimer Disease and Parkinson Disease

Fractionation Techniques Improve the Proteomic Analysis of Human Serum

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