Current methods to diagnose Alzheimer´s Disease (AD) comprise computer tomography (CT), magnet resonance imaging (MRI) or positron emission tomography (PET) visualizing abnormalities in the brain. Other approaches concerns to the determination of biomarkers such as tau/ phospho-tau or beta Amyloid in body fluids (blood, liquor). However, CSF level of tau is a general marker for neuronal dysfunction and not specific for AD alone (also increased in Creutzfeldt Jacob). In AD patients, decreased levels of Abeta42 could be shown, however the values of concentrations in various AD patients differ dramatically so that Abeta42 alone is not a sufficient reliable marker. Furthermore Abeta42 seems to be decreased only in patients who already have clinical symptoms of AD. It is a strong medical need for diagnostic markers which are able to predict AD at a very early stage before clinical symptoms occur. This would allow earlier treatments before neuronal damage starts. <br><br> <strong>Technology</strong><br> We offer a novel approach for the early recognition of pre-symptomatic stages of AD even 20-30 years before clinical changes/ symptoms like mild cognitive impairment (MCI) or AD occur. The assay is based on the detection of the Aß38:Aß42 concentration ratio. A decrease of the Aß38:Aß42 ratio (value <1,5) in a phenotypically healthy, pre-symptomatic person is hypothized to be indicative that this person will develop MCI and AD later in life. This statement is based on findings in the human neuroblastoma cell line SHSY5Y stably expressing APP by investigating the expression and procession of AAP and is further based on postulating a gamma-secretase cleavage mechanism of APP-TMS (TM: transmembrane).<br><br>
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