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

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.

Inclusion Criteria:

• 1) Coming subjects to see patients in CMRR for a complaint mnésique 2) Introducing a score in Tiny Mental the upper Test (MMSE) in 28/30 without error in under score of the recall of the 3 words 3) Introducing a score of 10/10 in the test of the 5 words of B2C 4) Introducing a score in the ladder CDR (Clinical Dementia Rating) equal to 0 5) Having given a lit consent 6) Being affiliated member or beneficiary of the regime of French national health and pensions organization

Exclusion Criteria:

• Major, all the vulnerable persons under 18 under tutelage, under legal guardianship, deprived of freedom, hospitalized in a health Establishment or social for quite other reason that searches it
• Record of neurological or psychiatric pathology and inability for sensory reasons to perform a cognitive balance sheet