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Truncated and Extended Forms of Amyloid Beta Peptides in Alzheimer's Disease: Genesis, Toxicity and Identification as Biological Markers

2014-08-27 03:13:28 | BioPortfolio

Summary

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.

Study Design

Control: Active Control, Endpoint Classification: Pharmacokinetics Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Basic Science

Conditions

Alzheimer Disease

Intervention

Alzhamyd

Location

Robert
Nice
Alpes-Maritimes
France
06001

Status

Not yet recruiting

Source

Centre Hospitalier Universitaire de Nice

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:13:28-0400

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