Our strategy

Therapeutic treatment based on amyloid hypothesis has now shown its limits. Alzprotect proposes an alternative strategy based on the fact that the cause of neurodegeneration is a loss of function of APP rather than a gain of toxic function (amyloid cascade hypothesis). Our target is AICD (APP intracellular domain), a neurotrophic factor/transcription factor lacking in the Alzheimer brain which loss or inactivation following PS1 mutations could be a cause of neurodegeneration. Alzprotect therapeutic strategy is to stimulate the good pathway of APP which increases AICD rather than inhibiting the pathway of APP that leads to amyloid plaques. This strategy has a double effect: restoring the loss of function of APP and activating neprilysin to decrease the amount of Abeta. We have found that specific molecules acting on the life span of APP metabolites can increase dramatically the production of AICD. Alzprotect develops some of these molecules as drug candidates for Alzheimer treatment.

Competitive advantages

AlzProtect compounds have the following advantages:

• They target an original mechanism of action
• Preclinical pharmacology is done on physiological animal models (rather than on transgenic animals which introduce biological bias)
• They are potential disease modifier drugs (not symptomatic drugs)
• They are small molecules with pharmaceutical potential
• They are proprietary