NAA Services for Anti-GluR3 Antibody

It is well known that natural autoantibodies (NAAs) can be valuable markers of disease activity and severity, an effective aid for disease classification and a guide for therapy. Since anti-glutamate receptor 3 (GluR3) autoantibodies are highly specific for epilepsy, based on years of extensive experience in disease diagnosis and NAA research, Creative Biolabs now offers a full range of high-quality antibody services against GluR3 marker for epilepsy research.

Background of Anti-GluR3 Antibody

Glutamate receptors (GluR) are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. NAAs to the "B" peptide (372-395 aa) of GluR3 are found in serum and cerebrospinal fluid (CSF) of some patients with different types of epilepsy. Anti-GluR3B antibodies are produced primarily in the periphery due to specific/non-specific "irritation" of the immune system. Once they reach the brain via a leaky blood-brain barrier (BBB) they may cause neuronal/glial damage and facilitate the outburst of epilepsy and additional neurological abnormalities. Anti-GluR3 antibodies are “active” and potentially pathogenic molecules since they display a glutamate-like activity and thus induce glutamate receptor-mediated ion currents.

Model of GluR3 antibody-mediated in vitro cytotoxicity Fig.1 Model of GluR3 antibody-mediated in vitro cytotoxicity. (Whitney, 2000)

The Role of Anti-GluR3 Antibody in Epilepsy

Epilepsy is a major health problem, affecting almost 1-2% of the world population. Both the GluR-activating and the neuronal-killing potential of anti-GluR3 antibody suggest that they may contribute to epilepsy. Since such anti-GluR3B antibodies can activate and/or kill neurons in vitro and in vivo, they may contribute to epilepsy. Yet, more recent data clearly show that anti-GluR3 antibodies are neither specific nor restricted to Rasmussen’ s encephalitis (RE), as they are found in some patients with other types of epilepsy. Numerous cases proved that the presence of anti-GluR3 antibodies was highly specific for epilepsy compared to healthy controls.

Schematic presentation of three distinct subpopulations of epilepsy patients Fig.2 Schematic presentation of three distinct subpopulations of epilepsy patients. (Ganor, 2005)

What We Can Do about NAA?

Aided by our well-established platforms and experienced scientists, we can provide comprehensive NAA services, from NAA detection, NAA profiling, to NAA epitope mapping. Our customized services can cover every step of your project. In addition, a wide spectrum of NAA products is available for your choice.

Features of our Anti-GluR3 Services Including but Not Limited to

Detection and analysis of anti-GluR3 autoantibodies may have important diagnostic and therapeutic implications. With the help of our professional scientists, Creative Biolabs is confident in providing unique NAA services about GluR3 biomarker to meet every customer's requirements. If you are interested in the service we provide, please feel free to contact us for more detail and information.

References:

  1. Whitney, K.D.; McNamara, J.O. GluR3 autoantibodies destroy neural cells in a complement-dependent manner modulated by complement regulatory proteins. Journal of Neuroscience. 2000, 20(19): 7307-7316.
  2. Ganor, Y.; et al. Autoimmune epilepsy: distinct subpopulations of epilepsy patients harbor serum autoantibodies to either glutamate/AMPA receptor GluR3, glutamate/NMDA receptor subunit NR2A or double-stranded DNA. Epilepsy research. 2005, 65(1-2): 11-22.
For Research Use Only | Not For Clinical Use

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