2011 NEUROSCIENCE, WASHINGTON, DC
J.D. Randall,1 H. Zetterberg,3 E. Mortberg,2 S. Rubertsson,2 G. Provuncher,1 P. Patel,1 E. Ferrell,1 D. Fournier,1 C. Kan,1 T. Campbell,1 A. Rivnak,1 B. Pink,1 K. Minnehan,1 T. Piech,1 D. Duffy,1K. Blennow,3D. Wilson1
1Quanterix Corporation, Cambridge, MA; 2Department of Surgical Sciences, Anaesthesia and Intensive Care, Uppsala University, Uppsala, Sweden; 3Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at the University of Gothenburg, Molndal, Sweden.
Background: Tau, a microtubule associated protein, plays an important role in the assembly of tubulin monomers into microtubules and maintaining the cytoskeleton and axonal transport. The presence of tau in cerebrospinal fluid (CSF), serum or plasma is thought to represent neuronal damage from physical trauma or apoptotic death of neurons. During ischemic injury from cardiac arrest, cell death could occur from the initial hypoxic insult as well as an apoptotic cascade resulting in delayed neuronal death. The measurement of tau in CSF has been well documented, but the presence and measurement of tau in human blood components has been difficult due to inadequate sensitivity of current assay methods. A direct link between acute oxygen deprivation and the appearance of tau in human periphery has not been previously studied. We employed a new technology (Single Molecule Arrays, SiMoA) capable of ultrasensitive protein measurements to look for changes in serum tau in patients following cardiac arrest and resuscitation, and to correlate these changes to 6-month cognitive outcome.
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