Plasma levels of amyloid β-protein 42 are increased in women with mild cognitive impairment

Assini, Andrea; Cammarata, Sergio; Vitali, Antonella; Colucci, Monica; Giliberto, Luca; Borghi, Roberta; Inglese, Marianna; Volpe, Stefano; Ratto, S; Dagna-Bricarelli, Francesca; Baldo, Chiara; Argusti, Alessandra; Odetti, Patrizio; Piccini, Alessandra; Tabaton, Massimo

doi:10.1212/01.wnl.0000137040.64252.ed

Cited by 103 publications

(60 citation statements)

References 33 publications

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“…22,23 However, other studies revealed the occurrence of high plasma Aβ 42 , but not Aβ 40 , in the patients with mild cognitive impairment (MCI). 24,25 Still other studies showed an increase in Aβ 42 and/or Aβ 40 in plasma of AD patients. 26,27 Decrease in Aβ 42 and/or the ratio of Aβ 42 /Aβ 40 in plasma of AD patients compared with non-AD demented individuals and controls has also been reported.…”

Section: Introductionmentioning

confidence: 90%

Serum concentration of beta amyloid peptide and the activity of angiotensin converting enzyme in alzheimers disease patients: search for a potential biomarker

2016

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Section: Introductionmentioning

confidence: 90%

Serum concentration of beta amyloid peptide and the activity of angiotensin converting enzyme in alzheimers disease patients: search for a potential biomarker

2016

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“…Plasma total Aβ or Aβ-42 are increased in cases of familial AD (Kosaka et al, 1997;Scheuner et al, 1996) and in Downs syndrome with amyloid precursor protein (APP) triplication (Schupf et al, 2001) but the results were not consistent with the diagnosis of sporadic AD (Assini et al, 2004;Fukumoto et al, 2003;Mayeux et al, 1999;Schupf et al, 2001;Tamaoka et al, 1996;Vanderstichele et al, 2000). Peripheral Aβ is transported via receptor for advanced glycation end products (RAGE) across the BBB into the brain (Deane et al, 2004) and Aβ elimination from brain across the BBB by cell surface low-density lipoprotein receptor related protein-1 (LRP) (Sagare et al, 2007).…”

Section: Biomarkers In Plasmamentioning

confidence: 99%

Biomarkers for Alzheimer’s disease and other forms of dementia: Clinical needs, limitations and future aspects

Cedazo-Minguez

Winblad

2010

Experimental Gerontology

129

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To cite this version:Angel Cedazo-Minguez, Bengt Winblad. Biomarkers for Alzheimer's disease and other forms of dementia: clinical needs, limitations and future aspects. Experimental Gerontology, Elsevier, 2009, 45 (1), pp. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ACCEPTED MANUSCRIPT

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“…In addition, levels of CSF A␤42 are inversely related to brain amyloid load as imaged with Pittsburgh Compound B (17, 18). Based on these results, it has been proposed that plasma levels of A␤42 increase before the onset of AD and decline shortly after the onset of dementia and with progression of symptoms (10,13,(19)(20)(21), although decline in CSF A␤42 precedes cognitive decline associated with AD (17, 18). However, these observations are not consistent across studies, and the relation of A␤ peptides to AD has been attributed to the effects of age (22), high levels of A␤40 (23), or a low plasma A␤42/A␤40 ratio (24).…”

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confidence: 99%

“…Among nondemented elderly, plasma A␤42 has been found to be increased in women with mild cognitive impairment (10), in adults with Down syndrome who subsequently develop dementia (11,12), and in healthy elderly before late-onset AD (13,14). In nondemented elderly, plasma A␤42 levels were elevated and then declined over time, with a corresponding decline in a cognitive-screening test score (15).…”

mentioning

confidence: 99%

Peripheral Aβ subspecies as risk biomarkers of Alzheimer's disease

Schupf

Tang

Fukuyama

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

212

151

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Plasma A␤42 and A␤40 levels are putative biomarkers for Alzheimer's disease (AD), but their significance and predictive value have been inconclusive. In AD transgenic models, plasma and cerebrospinal fluid levels of A␤42 and A␤40 increase with age but subsequently decrease when A␤ begins to accumulate in brain and with the onset of cognitive impairment. To determine the predictive value of A␤ levels in elderly populations, we investigated how plasma A␤42, A␤40, and a protofibrillar subspecies of A␤42 changed over time and with the onset of cognitive impairment or AD. In a cohort of 1,125 elderly persons without dementia, 104 (9.2%) of the participants developed AD over 4.6 years of followup. Higher plasma A␤42 levels at the onset of the study were associated with a threefold increased risk of AD. However, conversion to AD was accompanied by a significant decline in plasma A␤42, a decreased A␤42/A␤40 ratio and, with the onset of cognitive impairment, decreased protofibrillar A␤42 levels. Our results suggest individuals with elevated plasma A␤42 are at increased risk of AD and that with the onset of disease, the decline in some forms of A␤ may reflect compartmentalization of A␤ peptides in the brain.plasma amyloid beta40 and beta42 ͉ protofibrillar Abeta A myloid ␤-peptides A␤40 and A␤42 are the two major species generated by sequential proteolytic cleavage by ␤-and ␦-secretases of the amyloid precursor protein (APP) (1). Subsequent deposition of A␤42 has been considered an initial and critical step in the pathogenesis of Alzheimer's disease (AD). Brain levels of A␤42 increase with the development of dementia and are correlated with cognitive decline (2). Mutations in the APP and presenilin (PSEN1 and 2) genes, which result in a dominantly inherited form of early-onset AD, are accompanied by an increase in plasma A␤42 and A␤40 levels in patients before disease onset and are elevated in their unaffected relatives as well (3-5). Furthermore, both A␤42 and A␤40 plasma levels are increased in cognitively normal first-degree relatives of cases with late-onset AD without known mutations (6).The relation between brain and plasma A␤ in health and disease is complex, but studies of AD transgenic mice have provided some insights. Within a few months of birth, APP transgenic mice secreted more A␤42 and A␤40 than their wild-type littermates (7,8), and A␤ secretion is increased throughout the life of APP transgenic mice. Both plasma and cerebrospinal fluid (CSF) levels of A␤42, and to a lesser extent A␤40, increase with age, but both precipitously decrease as A␤42 and A␤40 levels rise in the brain (7). By 1 year, there are frank A␤ plaques, and subsequently there are characteristic agerelated behavioral changes in memory. However, Lesne and colleagues (9) reported that the behavioral effects are not the result of the A␤ accumulation in brain, but the increase in the protofibrillar subspecies of A␤.These observations in mice represent a model for changes in plasma A␤ as a biomarker associated with AD in humans.Among nondemented...

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Plasma levels of amyloid β-protein 42 are increased in women with mild cognitive impairment

Abstract: The elevation of Abeta42 plasma levels in women with MCI may represent a biologic explanation for the sex-dependent increased incidence of late-onset AD in women identified by epidemiologic studies.

Cited by 103 publications

References 33 publications

Serum concentration of beta amyloid peptide and the activity of angiotensin converting enzyme in alzheimers disease patients: search for a potential biomarker

Serum concentration of beta amyloid peptide and the activity of angiotensin converting enzyme in alzheimers disease patients: search for a potential biomarker

Biomarkers for Alzheimer’s disease and other forms of dementia: Clinical needs, limitations and future aspects

Peripheral Aβ subspecies as risk biomarkers of Alzheimer's disease

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