Alzheimer Disease Clinical Trial
Beta amyloid immunoreactivity is probably due to a significant number of Ab catabolites
corresponding to N-terminally truncated and Cterminally truncated or extended forms which
display distinct propensity to aggregation. Very few things are known concerning the
mechanisms and proteases by which they are generated. Furthermore, the link between
truncation and toxicity has not been delineated.
Finally, little is known concerning Ab fragments in biological fluids and whether they could
be seen as early biomarkers and thereby, as putative targets for AD diagnostic. The present
project will allow to examine the human biological samples and to identify various cohorts
after complete clinical evaluation.
n/a
Endpoint Classification: Pharmacokinetics Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Basic Science
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