RemeGenix' Novel Models of Alzheimer’s and Dementia are specifically designed animal models that will
serve as a drug development platform for not only RemeGenix' internal needs, but will also serve as a
catalyst for a number of different partnership opportunities.
The Company’s co-founder has recently published several manuscripts discussing the most recent and compelling data,
and the Company will continue to work diligently to ensure that this model will become one of the preferred animal
models used in the development of drugs to treat Alzheimer’s and/or dementia today.
We are hopeful that the industry in general will realize, from the recent failures in this space, that the existing models are
not appropriate, and that they lack biological relevance to the human disease.
Our models are biologically relevant to existing human dementia and have been shown to have significant cognitive decline independently of
plaque formation. Dr. D'Adamio developed this model by mimicking the genetics of human disease, instead of developing
a model with a specific pathological readout. By creating genetically faithful models, we will be able to
rapidly and accurately translate our drug development efforts to the clinic, and significantly reduce our risk of failure.
Problems with Current Models: As discussed above, the existing models of AD are faulty,
and have been built on a preconceived idea that plaques are the key
to the cause of the disease. Unfortunately, in order to generate Amyloid plaques in mice,
researchers have discovered that gross over-expression (thus making the model irrelevant to human biology) of many human
mutations in mice is necessary. This has resulted in the generation of models that are genetically
irrelevant to human disease.
The fact that numerous therapeutic approaches that have showed promise in mice but have failed in humans
is a strong indication that these mice do not model the true pathogenic mechanisms of human AD.