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FEBRUARY 2019 ISSUE - Digital Edition

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BLOOD TEST FOR<br />

ALZHEIMER’S MARKER?<br />

Washington University scientists, in<br />

collaboration with C2N Diagnostics,<br />

showed that the protein tau increases in<br />

blood after peripheral administration of an<br />

anti-tau antibody.<br />

The study in mice found that the level<br />

of tau increase in blood correlated with the<br />

tau pathology in the brain.<br />

C2N Diagnostics, LLC based St Louis,<br />

Missouri has developed technology<br />

platforms like the Stable Isotope Spike<br />

Absolute Quantitation (SISAQ) and Stable<br />

Isotope Labeling Kinetic (SILK) that<br />

enable the measurement of the absolute<br />

concentration of peptides and specific<br />

proteins in both CSF and plasma.<br />

“We focus on a variety of assays<br />

– using the primary platform of mass<br />

spectrometry – to quantitate proteins<br />

and other biomolecules implicated<br />

in neurodegeneration,” said Joel B.<br />

Braunstein, MD, CEO, C2N Diagnostics.<br />

These assays are currently available<br />

for use in preclinical research and clinical<br />

research drug development settings. Some<br />

of these assays may be used in the future<br />

to serve as a clinical diagnostic aid in the<br />

detection and monitoring of pathways<br />

implicated in Alzheimer’s disease and<br />

other forms of neurodegeneration, he<br />

added.<br />

CASCADE<br />

how these proteins relate to each<br />

other.<br />

Impairments in cholesterol and<br />

glucose metabolism, inflammation,<br />

oxidative stress and dysfunctional<br />

‘garbage collection system of the<br />

brain’ are all supposed to help<br />

push the amyloid accumulation,<br />

which then probably causes<br />

damage to the synapses leading<br />

to tau aggregation.<br />

New findings show both<br />

Aβ and tau oligomers bind to<br />

amyloid-β protein precursor<br />

(AβPP). And the presence of this<br />

protein is required for both Aβ<br />

and tau to enter neurons and<br />

induce abnormal synaptic function<br />

and memory. It is also proposed<br />

that extracellular oligomers of<br />

Aβ and tau act in parallel and<br />

upstream of AβPP in Alzheimer’s<br />

pathogenesis.<br />

However, therapeutic<br />

approaches aimed at decreasing<br />

Aβ levels and tau-based clinical<br />

trials are yet to produce positive<br />

findings.<br />

<strong>FEBRUARY</strong> <strong>2019</strong> / FUTURE MEDICINE / 27

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