Plasma amyloid beta peptides: an Alzheimer’s conundrum or a more accessible Alzheimer’s biomarker?

Poljak, Anne; Sachdev, Perminder S.

doi:10.1080/14737175.2016.1217156

Cited by 8 publications

(9 citation statements)

References 25 publications

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“…The need to find alternative body fluids for biomarker identification in AD has recently led investigators to analyze currently known CSF biomarkers for AD in plasma [45][46][47][48][49][50][51][52][53][54][55][56][57] . Studies in this area have shown conflicting results with (i) no difference between AD and control patients 47,49,50 51,55 .…”

Section: Early Stage Of Ad: Csf and Plasma Biomarkersmentioning

confidence: 99%

Correlation between cognition and plasma noradrenaline level in Alzheimer’s disease: a potential new blood marker of disease evolution

et al. 2020

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Recent evidence showing degeneration of the noradrenergic system in the locus coeruleus (LC) in Alzheimer's disease (AD) has motivated great interest in noradrenaline (NA) as a potential brain hallmark of the disease. Despite the current exploration of blood markers for AD, the deregulation of the plasma NA concentration ([NA] plasma) in AD is currently not well understood. This retrospective study includes a cohort of 71 patients (32 AD patients, 22 with other dementia and 17 without dementia) who were given consultations for memory complaints in the Cognitive Neurology Center of Lariboisière (Paris) between 2009 and 2014. As previously described in brain tissue, we show for the first time a linear correlation between [NA] plasma and Mini Mental State Examination (MMSE) score in AD patients. We observed that high [NA] plasma in AD patients was associated with higher [Aβ 1-42 ] CSF than in other AD patients with [NA] plasma similar to NC patients. In parallel, we observed a lower (p-Tau/Tau) CSF in AD patients with low [NA] plasma than in non-AD patients with [NA] plasma similar to [NA] plasma in NC patients. Our data suggest that [NA] plasma could be a potential biomarker of disease evolution in the context of AD and could possibly improve early diagnosis.

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Section: Early Stage Of Ad: Csf and Plasma Biomarkersmentioning

confidence: 99%

Correlation between cognition and plasma noradrenaline level in Alzheimer’s disease: a potential new blood marker of disease evolution

et al. 2020

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“…Study in animal models also shown increased LPO precedes amyloid plaque formation in a mice model of Alzheimer amyloidosis [46]. Some studies also shown abnormal and increased plasma Aβ levels seen in patients associated with cognitive decline and dementia [9], [10], [47], [48].…”

Section: Discussionmentioning

confidence: 94%

“…The increased Aβ levels in blood may in turn result in a stronger Aβ accumulation in cerebral region, which reinforces neuronal degeneration [8]. Plasma is the liquid portion of blood that suspends cells such as red blood cells, white blood cells, and platelets and studies demonstrated that quantification of plasma Aβ is considered as an emerging diagnostic tool for cognitive dysfunction and dementia [9], [10] and it has received strong interest as a reliable biomarker of neurodegenerative diseases, since blood sampling is much less invasive as lumbar puncturing that is currently required for CSF Aβ measurement [8], [11]. Study shown increased plasma Aβ42 peptide levels are associated with earlier onset of AD and increased threat of death [12].…”

Section: Introductionmentioning

confidence: 99%

Abnormal amyloid β 42 expression and increased oxidative stress in plasma of CKD patients with cognitive dysfunction: A small scale case control study comparison with Alzheimer's disease

et al. 2017

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BackgroundCognitive dysfunction has been increasingly recognized in chronic kidney disease (CKD) patients. Senile plaques are important pathophysiological characteristic of cognitive dysfunction. The major component of plaques is the amyloid β (Aβ) peptide released from proteolytic cleavage of amyloid precursor protein (APP). Plasma Aβ has been a focus of the growing literature on blood based biomarkers for cognitive dysfunction. Oxidative stress is prevalent in CKD and it plays an important role in cognitive dysfunction. Increased oxidative stress leads to cause cleavage of APP and Aβ production. The aim of this study is to assess the antioxidant status and Aβ42 levels in plasma of CKD patients with cognitive dysfunction compared to CKD without cognitive dysfunction.MethodsA total of 60 subjects divided into 30 CKD without cognitive dysfunction and 30 CKD with cognitive dysfunction based on neuropsychological assessment tests. To compare antioxidant status and Aβ42 levels in plasma, the following groups such as healthy subjects (n = 30), normocytic normochromic anemia (n = 30) and Alzheimer's disease (AD, n = 10) patients were also maintained. Plasma Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GPx), Reduced glutathione (GSH) and lipid peroxidation (LPO) were determined by spectrophotometrically. Aβ level was determined by immunoblotting method. The parameters were statistically compared with healthy, normocytic normochromic anemia and AD subjects.ResultsLike AD subjects, significantly increased Aβ and LPO level while decreased SOD, CAT, GPx and GSH levels were observed in plasma of CKD patients with cognitive dysfunction when compared to healthy, CKD without cognitive dysfunction and normocytic normochromic anemic subjects.ConclusionResults suggest that elevated plasma oxidative stress and Aβ were seen in CKD patients with cognitive dysfunction may be attributed to pathological changes within the brain.

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“…Deciphering the dynamic genetic architecture of plasma aβ concentrations could simultaneously implicate pathophysiological processes, pathways, and mechanisms contributing to aβ plaque accumulation in the asymptomatic preclinical and progressive phases of AD [29, 30] while suggesting novel health conditions that alter the association between plasma aβ and AD in epidemiological studies. This vital information may clarify the inconsistencies in reported associations between plasma aβ and AD across studies, as well as provide insight into the role (if any) of plasma aβ in AD pathogenesis and the utility of plasma aβ concentrations as AD biomarkers.…”

Section: Introductionmentioning

confidence: 99%

Whole exome sequence-based association analyses of plasma amyloid-β in African and European Americans; the Atherosclerosis Risk in Communities-Neurocognitive Study

et al. 2017

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ObjectiveWe performed single-variant and gene-based association analyses of plasma amyloid-β (aβ) concentrations using whole exome sequence from 1,414 African and European Americans. Our goal was to identify genes that influence plasma aβ42 concentrations and aβ42:aβ40 ratios in late middle age (mean = 59 years), old age (mean = 77 years), or change over time (mean = 18 years).MethodsPlasma aβ measures were linearly regressed onto age, gender, APOE ε4 carrier status, and time elapsed between visits (fold-changes only) separately by race. Following inverse normal transformation of the residuals, seqMeta was used to conduct race-specific single-variant and gene-based association tests while adjusting for population structure. Linear regression models were fit on autosomal variants with minor allele frequencies (MAF)≥1%. T5 burden and Sequence Kernel Association (SKAT) gene-based tests assessed functional variants with MAF≤5%. Cross-race fixed effects meta-analyses were Bonferroni-corrected for the number of variants or genes tested.ResultsSeven genes were associated with aβ in late middle age or change over time; no associations were identified in old age. Single variants in KLKB1 (rs3733402; p = 4.33x10-10) and F12 (rs1801020; p = 3.89x10-8) were significantly associated with midlife aβ42 levels through cross-race meta-analysis; the KLKB1 variant replicated internally using 1,014 additional participants with exome chip. ITPRIP, PLIN2, and TSPAN18 were associated with the midlife aβ42:aβ40 ratio via the T5 test; TSPAN18 was significant via the cross-race meta-analysis, whereas ITPRIP and PLIN2 were European American-specific. NCOA1 and NT5C3B were associated with the midlife aβ42:aβ40 ratio and the fold-change in aβ42, respectively, via SKAT in African Americans. No associations replicated externally (N = 725).ConclusionWe discovered age-dependent genetic effects, established associations between vascular-related genes (KLKB1, F12, PLIN2) and midlife plasma aβ levels, and identified a plausible Alzheimer’s Disease candidate gene (ITPRIP) influencing cell death. Plasma aβ concentrations may have dynamic biological determinants across the lifespan; plasma aβ study designs or analyses must consider age.

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Plasma amyloid beta peptides: an Alzheimer’s conundrum or a more accessible Alzheimer’s biomarker?

Cited by 8 publications

References 25 publications

Correlation between cognition and plasma noradrenaline level in Alzheimer’s disease: a potential new blood marker of disease evolution

Correlation between cognition and plasma noradrenaline level in Alzheimer’s disease: a potential new blood marker of disease evolution

Abnormal amyloid β 42 expression and increased oxidative stress in plasma of CKD patients with cognitive dysfunction: A small scale case control study comparison with Alzheimer's disease

Whole exome sequence-based association analyses of plasma amyloid-β in African and European Americans; the Atherosclerosis Risk in Communities-Neurocognitive Study

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