Alzheimer's Research

First test worldwide for auto-antibodies against Amyloid peptides

The first test worldwide for the determination of serum auto-antibodies against Amyloid peptides is presented by DRG for the World Alzheimer´s Day 2011.
This test is part of a new product family, which supports the research in Alzheimer's disease.
The second test in this new product family is the Abeta-40 ELISA, for the detection of Amyloid β 1-40 peptides in serum, plasma and liquor:

Amyloid beta (1-40) (Human), EIA-5231

Amyloid beta Auto-Ab (Human) Serum, EIA-5099

Background information Alzheimer's disease:

Alzheimer's disease (AD) is characterized by the deposition of amyloid plaques, degeneration and loss of neurons, accumulation of fibrillary tangles in neurons, and a progressive loss of cognitive function.

Amyloid plaques are mainly composed of amyloid-beta (Aβ) 40 and 42 peptides derived from the proteolytic cleavage of amyloid precursor protein (APP).The concentration of Aβ peptides in serum and liquor depends on age and disease severity, and is further modulated by production of Aβ peptides in large peripheral organs, movement from brain interstitial fluid into blood stream, peripheral uptake and clearance of Aβ peptides in the liver and by naturally occurring auto-antibodies against Aβ peptides. This may explain why much of the plasma Aβ peptide data in cross-sectional studies does not show significant differences between sporadic AD and controls. In this respect, longitudinal studies seem more promising, showing initially elevated Aβ42 levels in those that eventually develop AD in the future.

Recent studies further indicate that the tendency of Aβ peptides to aggregate is greatly enhanced by the formation of reactive oxygen species by monoamine oxidase and the direct influence of nitric oxide synthase (NOS2).

As Aβ peptides are considered to play an early and pivotal role in AD pathogenesis, they may be a useful tool in diagnosing AD in the preclinical/early stages, as well as for monitoring potential Aβ peptide modifying therapies, since clearance of Aβ from the brain represents an important therapeutic strategy for prevention and treatment of AD.

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