LAUSR

To date, no disease-modifying treatment or cure is available for dementia. This disorder is becoming more common as the global population ages. There has been over several decades of extensive research focusing on how the pathology develops and progresses causing memory loss, brain damage, and eventually death – it provides the field with a deep understanding of what proteins, peptides, and signaling molecules contribute to neurodegeneration at the molecular, genetic, and cellular levels. The problem is, however, that there is a wide range of dementia types. A given disease can span heterogeneous clinical syndromes with diverse symptomatology, no matter whether it is “senile dementia” or an earlyonset form; moreover, it encompasses the mixed features of many syndromes in later stages of the disease. In confirmation of this, animal models, despite being purposely designed and widely used in dementia research, usually do not fully replicate neuropathological profiles that match pathological changes found in the human brain, much less in cognitive and intellectual decline as it occurs in patients. This made it hitherto insurmountable for scientists to conceptualize the basis underlying nerve cell dysfunctions in a range of dementias.