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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