[Compensatory function of transthyretin in Alzheimer's disease].

Alzheimer's disease (AD) is the most common form of age-related primary neurodegenerative diseases characterized by progressive memory loss, aphasia, and intellectual and mental breakdown. Pathogenesis of AD is based on the early synaptic dysfunction following neurodegeneration and neuronal death. According to modern concepts, the development of neuropathological processes is due to progressively deposited intermediates of amyloid fibrils that represent oligomers consisting of short peptide named amyloid beta protein (Abeta). In this context, it is reasonable to propose that one of the compensatory mechanisms of AD might be inhibition of Abeta oligomerization by sequestration or clearance of Abeta. Experiments with transgenic animals and epidemiological studies demonstrate that major protein of cerebrospinal fluid, transthyretin, is a natural neuroprotector that inhibits Abeta amyloid formation and restore cognitive functions. The study of Abeta-transthyretin complexes allowed to create peptides that are mimetics of transthyretin. These mimetics inhibit amyloid formation in vitro and, therefore, could be used in therapeutic treatment of AD.