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In the past 20 years, it has been recognized that soluble oligomers of amyloid β (Aβ) protein can cause synapse and neuronal damage and microglial hyperplasia
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Soluble Aβ levels in the brains of Alzheimer's disease (AD) patients are associated with synaptic changes and cognitive impairment, which has inspired extensive research on the state of water-soluble Aβ oligomers (oAβ)
In the past 20 years, it has been recognized that soluble oligomers of amyloid β (Aβ) protein can cause synapse and neuronal damage and microglial hyperplasia
More and more evidences show that oAβ (1) mainly causes defects in synaptic transmission in electrically active neurons, (2) can reduce long-term electric potential in the hippocampus of mice and induce long-term depression, and (3) when the brain oAβ level When compared with the level of amyloid plaques, it can distinguish between people with Alzheimer's and non-Alzheimer's
Aβ has a dynamic balance among various monomers, oligomers, and highly ordered filaments, all of which have different synaptic toxicity characteristics
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The complex balance between Aβ oligomers/polymers of various sizes poses an inherent challenge to the separation and study of naturally occurring oAβ species
Aβ has a dynamic balance among various monomers, oligomers, and highly ordered filaments, all of which have different synaptic toxicity characteristics
Previously, researchers reported a sensitive sandwich immunoassay that uses a conformation-specific antibody (1C22) for capture and an N-terminal antibody (3D6) as a detector to quantitatively detect low levels of oAβ in human CSF
Although there is more and more evidence that soluble oAβ plays a central role in the pathogenesis of early AD , there are still great challenges in using a sensitive and specific method to detect and quantify oAβ in human plasma
Development of a specific 71A1/3D6 immunoassay for amyloid beta oligomers
Development of a specific 71A1/3D6 immunoassay for amyloid β oligomers Development of a specific 71A1/3D6 immunoassay for amyloid β oligomersRecently, researchers have developed an ultra-sensitive oAβ immunoassay that uses a new capture antibody (71A1) and N-terminal antibody 3D6 for detection, which can specifically and quantitatively detect human brain, cerebrospinal fluid (CSF) and plasma In the soluble oAβ
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It uses a new capture antibody (71A1) and N-terminal antibody 3D6 for detection, which can specifically and quantitatively detect soluble oAβ in human brain, cerebrospinal fluid (CSF) and plasma.
Experimental data shows that two new antibodies (71A1; 1G5) have oAβ selectivity, can mark Aβ plaques in non-fixed AD brain slices, and can effectively neutralize the synaptic toxicity of AD brain-derived oAβ
Therefore, researchers have created a sensitive, high-throughput, and cost-effective method to quantify synaptic toxicity oAβ in human plasma, which is promising for high-throughput analysis of elderly and AD subjects to evaluate this The dynamics of key pathogenic species and their response to treatment
Original source:
Original source: Original source:Lei Liu et al.
Lei Liu et al.
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