Characterisation of two antibodies to oligomeric Aβ and their use in ELISAs on human brain tissue homogenates

Helmond, Zoë Van; Heesom, Kate J; Love, Seth

doi:10.1016/j.jneumeth.2008.09.002

Cited by 38 publications

(34 citation statements)

References 32 publications

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“…In these investigations, oligomerspecific capture antibodies were used (Lee et al, 2006;van Helmond et al, 2009). The results from the study by Lee et al (2006) were similar to ours; although the ELISA was found to measure primarily oligomeric A␤, it was not oligomer-specific, and its relative sensitivity for detecting crosslinked vs. monomeric A␤ was 5:1.…”

Section: Discussionsupporting

confidence: 60%

“…The results from the study by Lee et al (2006) were similar to ours; although the ELISA was found to measure primarily oligomeric A␤, it was not oligomer-specific, and its relative sensitivity for detecting crosslinked vs. monomeric A␤ was 5:1. In the study by van Helmond et al (2009), a standard curve was generated for A␤ oligomers but not for A␤ monomer, so no conclusions could be reached as to the specificity of the ELISA for oligomers.…”

Section: Discussionmentioning

confidence: 99%

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Specificity and sensitivity of the Abeta oligomer ELISA

Klaver

Patrias

Finke

et al. 2011

Journal of Neuroscience Methods

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Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Specificity and sensitivity of the Abeta oligomer ELISA

Klaver

Patrias

Finke

et al. 2011

Journal of Neuroscience Methods

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“…Previous studies by our group found no effect of simulated post-mortem delay of up to 72 h on Aβ measurements [39]. Braak tangle stage was not significantly different between groups used for pairwise comparisons; however the normotensive group tended to include more cases with lower Braak tangle pathology (including 3 cases with Braak tangle stage III) (Supplementary Figure 1).…”

Section: Measurement Of Aβ Plaque Loadmentioning

confidence: 59%

Effects of Hypertension and Anti-Hypertensive Treatment on Amyloid-β (Aβ) Plaque Load and Aβ-Synthesizing and Aβ-Degrading Enzymes in Frontal Cortex

Ashby

Miners

Kehoe

et al. 2016

JAD

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Epidemiological data associate hypertension with a predisposition to Alzheimer's disease (AD) and a number of post-mortem and in vivo studies also demonstrate that hypertension increases amyloid-beta (Aβ) pathology. In contrast anti-hypertensive medications reportedly improve cognition and decrease the risk of AD, while certain classes of anti-hypertensive drugs are associated with decreased AD-related pathology. We investigated the effects of hypertension and anti-hypertensive treatment on Aβ plaque load in post-mortem frontal cortex in AD. Aβ load was significantly increased in hypertensive (N = 20) relative to normotensive cases (N = 62) and was also significantly higher in treated (N = 9) than untreated hypertensives (N = 11). We then looked into mechanisms by which hypertension and treatment might increase Aβ load, focusing on Aβ-synthesising enzymes, β-and γ-secretase, and Aβ-degrading enzymes, angiotensin-converting enzyme (ACE), insulin-2 degrading enzyme (IDE) and neprilysin. ACE and IDE protein levels were significantly lower in hypertensive (N = 21) than normotensive cases (N = 64), perhaps translating to decreased Aβ catabolism in hypertensives. ACE level was significantly higher in treated (N = 9) than untreated hypertensives (N = 12), possibly reflecting feedback upregulation of the reninangiotensin system. Prospective studies in larger cohorts stratified according to antihypertensive drug class are needed to confirm these initial findings and to elucidate the interactions between hypertension, anti-hypertensive treatments and Aβ metabolism.Keywords: Alzheimer's disease, amyloid β protein, anti-hypertensive, hypertension, β-secretase, BACE, γ-secretase, angiotensin-converting enzyme, insulin-degrading enzyme Abbreviations: Aβ = amyloid-beta; AβPP = amyloid-beta precursor protein; ACE = angiotensin-converting enzyme; ACEI = angiotensin-converting enzyme inhibitor; AD = Alzheimer's disease; AngII = angiotensin II; ARB = angiotensin receptor blocker; BBB = blood brain barrier; CCB = calcium channel blocker; IDE = insulin-degrading enzyme; NEP = neprilysin; NFT = neurofibrillary tangle

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“…A wide panel of antibodies is now available 44,[69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86][87] that react more specifically with oligomeric Aβ than with monomeric Aβ, and some do not react with Aβ fibrils (Supplementary Table 1), indicating that Aβ oligomers do indeed have different structural epitopes. We are, however, still far from being able to use those antibodies to distinguish specific toxic conformations.…”

Section: An Alternative Interpretation Of Ab Oligomer Toxicitymentioning

confidence: 99%

The toxic Aβ oligomer and Alzheimer's disease: an emperor in need of clothes

2012

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The 'toxic Aβ oligomer' hypothesis has attracted considerable attention among Alzheimer's disease researchers as a way of resolving the lack of correlation between deposited amyloid-β (Aβ) in amyloid plaques-in terms of both amount and location-and cognitive impairment or neurodegeneration. However, the lack of a common, agreed-upon experimental description of the toxic Aβ oligomer makes interpretation and direct comparison of data between different research groups impossible. Here we critically review the evidence supporting toxic Aβ oligomers as drivers of neurodegeneration and make some suggestions that might facilitate progress in this complex field.

show abstract

Characterisation of two antibodies to oligomeric Aβ and their use in ELISAs on human brain tissue homogenates

Cited by 38 publications

References 32 publications

Specificity and sensitivity of the Abeta oligomer ELISA

Specificity and sensitivity of the Abeta oligomer ELISA

Effects of Hypertension and Anti-Hypertensive Treatment on Amyloid-β (Aβ) Plaque Load and Aβ-Synthesizing and Aβ-Degrading Enzymes in Frontal Cortex

The toxic Aβ oligomer and Alzheimer's disease: an emperor in need of clothes

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