Decreased serum amyloid β1–42 autoantibody levels in Alzheimer’s disease, determined by a newly developed immuno-precipitation assay with radiolabeled amyloid β1–42 peptide

Brettschneider, S.; Morgenthaler, Nils G.; Teipel, Stefan J.; Fischer-Schulz, Christina; Bürger, Katharina; Dodel, Richard; Du, Yansheng; Möller, Hans; Bergmann, Andreas; Hampel, Harald

doi:10.1016/j.biopsych.2004.12.008

Cited by 67 publications

(45 citation statements)

References 23 publications

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“…Several studies already evaluated anti-Abeta antibodies in cerebrospinal fluid and plasma of patients affected by AD 12,13 showing conflicting results. Some Authors did not find any variation between AD and controls, 14 others found reduced 12,13,15 or higher 16 levels of antibodies in AD patients. The discrepancies may be linked to sample size, to inclusion criteria or to different methods for the analyses, in particular Nath and colleagues 16 analyzed anti-Abeta antibodies levels to the aggregated form of Abeta, whereas other groups used only those against the soluble form.…”

Section: Discussionmentioning

confidence: 92%

“…Moreover, little is known about plasma levels of anti-Abeta 1-42 antibodies, which have been found decreased in cerebrospinal fluid 12 and showed conflicting results in plasma of patients with AD. [13][14][15][16] Considering that the majority of DS patients develop dementia around the age of 50 years, we report, in this study, the quantification of markers of APP metabolism, such as plasma sAPPa and Abeta 1-42 levels in young DS, analyzing the relationship with age, sex, and degree of mental retardation to define them as possible early biomarkers of Abeta accumulation. Currently, no data about anti-Abeta 1-42 antibodies plasma levels in DS are available; as therapeutic interventions, based on immunization to lower Abeta amounts are in progress for AD, we evaluated this parameter in plasma from DS subjects to evidence possible modification in subjects prone to develop Alzheimer's like dementia.…”

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confidence: 99%

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Increased Soluble APPα, Abeta 1-42, and Anti-Abeta 1-42 Antibodies in Plasma From Down Syndrome Patients

Conti

Galimberti

Piazza

et al. 2010

Alzheimer Disease &Amp; Associated Disorders

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Down syndrome (DS) is the most common genetic disorder characterized by an extra copy of chromosome 21. DS subjects show signs of progressive cognitive decline, and most of them develop Alzheimer's type dementia at the age of 50 to 55 years. The aim of this study was to evaluate amyloid precursor protein (APP) metabolites and anti-Abeta 1-42 antibodies plasma levels in DS as possible biomarkers of Abeta accumulation potentially leading to neurodegeneration. We investigated plasma levels of sAPPalpha, Abeta 1-42, and anti-Abeta 1-42 antibodies by enzyme-linked immunosorbent assay in 24 DS subjects, 10 non-DS mentally retarded subjects and 18 age-matched controls. We found that sAPPalpha levels were about 1.5-fold higher and Abeta 1-42 levels were about 6-fold higher in DS respect to mentally retarded patients and to controls. DS patients showed Abeta 1-42 antibodies levels 4-fold higher than non-DS mentally retarded group and 2-fold higher than controls. Moreover, anti-Abeta 1-42 antibodies levels were inversely correlated with age in DS subjects. Our results suggested sAPPalpha as a possible peripheral marker for the alteration in APP metabolism in DS and highlighted an alteration in anti-abeta antibodies, for the first time evaluated in plasma from DS subjects.

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Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 99%

Increased Soluble APPα, Abeta 1-42, and Anti-Abeta 1-42 Antibodies in Plasma From Down Syndrome Patients

Conti

Galimberti

Piazza

et al. 2010

Alzheimer Disease &Amp; Associated Disorders

View full text Add to dashboard Cite

show abstract

“…Several advocates for the therapeutic use of anti-Aβ monoclonal antibodies have suggested that similar antibodies play a critical role in delaying disease onset (Brettschneider et al, 2005; Henkel et al, 2007). However, given the amount of Aβ that is constitutively produced throughout life, the immunological resources required to maintain such a response over 60 or more years would be inordinate.…”

Section: Discussionmentioning

confidence: 99%

Aβ-specific Th2 cells provide cognitive and pathological benefits to Alzheimer's mice without infiltrating the CNS

Cao

Arendash

Dickson

et al. 2009

Neurobiology of Disease

108

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We have found that a small number of purified Th2-biased Aβ-specific T cells are sufficient to provide profound cognitive and pathological benefits in an APP+PS1 mouse model for Alzheimer’s disease. Six weeks after receiving T cell infusions, cognitively-impaired mice performed significantly better in working memory tasks, which correlated with higher plasma levels of soluble Aβ. Pathological analysis of the hippocampus revealed a 30% decrease of plaque- associated microglia and less vascular amyloidosis in T cell treated mice. The infusion of Aβ-specific Th2 cells also reduced plasma levels of IFN-γ, TNF-α, GM-CSF, IL-2 and IL-4, which are elevated in untreated APP+PS1 mice. No significant immune cell infiltration and no anti-Abeta antibody titers occurred in the T cell treated mice. These results demonstrate that Aβ-specific Th2 cells are sufficient to reverse cognitive impairment and provide multiple pathological benefits in an Alzheimer’s mouse model.

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“…The results of these studies have been inconsistent: some reported that Aβ auto-antibodies in AD were lower than in normal subjects [7, 8, 9, 10], some unaltered [11, 12, 13], and some increased [14, 15, 16]. The inconsistent results may have been caused by several factors including nonspecific bindings [17], serum Aβ interference [18], incorrect diagnosis [19, 20], structural conformation of Aβ1-42, and/or small sample size.…”

Section: Introductionmentioning

confidence: 99%

Beta-amyloid auto-antibodies are reduced in Alzheimer's disease

Gong

Moore

et al. 2014

Journal of Neuroimmunology

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Accumulation and cytotoxicity of amyloid beta (Aβ) are understood as the major cause of Alzheimer's disease (AD). There is evidence that naturally occurring antibodies against amyloid beta (Aβ) protein play a role in Aβ-clearance, and such a mechanism appears to be impaired in AD. In the present study, the anti-Aβ antibodies in the serum from individuals with and without late onset AD were measured using ELISA and dot-blot methods. Aβ auto-antibodies in serum were mainly targeted to Aβ1-15 epitope and its titer was significantly lower in AD patients than elderly non-AD controls (NC). The dot-blot analysis further demonstrated that auto-antibodies against fibrillar Aβ42, Aβ1-15 and Aβ16-30 epitopes were all in a lower level in AD than in NC. The isotypes of the auto-antibodies were mainly non-inflammatory IgG2 type. We also analyzed the relationship of auto-Aβ antibodies levels with the genotypes of Apolipoprotein E (ApoE) and ANKK1/DRD2 gene.

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Decreased serum amyloid β1–42 autoantibody levels in Alzheimer’s disease, determined by a newly developed immuno-precipitation assay with radiolabeled amyloid β1–42 peptide

Cited by 67 publications

References 23 publications

Increased Soluble APPα, Abeta 1-42, and Anti-Abeta 1-42 Antibodies in Plasma From Down Syndrome Patients

Increased Soluble APPα, Abeta 1-42, and Anti-Abeta 1-42 Antibodies in Plasma From Down Syndrome Patients

Aβ-specific Th2 cells provide cognitive and pathological benefits to Alzheimer's mice without infiltrating the CNS

Beta-amyloid auto-antibodies are reduced in Alzheimer's disease

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