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Novel beta sheet breakers as candidates for Alzheimer's disease Approximately 15 percent of people who live to the age of 65 will develop some form of dementia; by age 85, that proportion increases to at least 35 percent. The most common of all the dementias is Alzheimer's disease. Existing in two forms, early onset familial disease (FAD) and late onset disease. Four million Americans currently suffer from the condition, and experts estimate that 22 million people around the world will be so afflicted by 2025. The peptide, 42 amino acid beta-amyloid, which is found in the plaques characteristic of Alzheimer's are now generally accepted markers and possibly etiological factors of Alzheimer's disease. This form of beta-amyloid readily forms toxic fibrils that are thought to cause neuronal damage by altering calcium regulation, mitochondrial damage and/or immune stimulation. In a recent dossier (click here for access) we report on progress that has been made by Mayo researchers leading to the identification of molecules able to prevent the build up of beta-amyloid 42. We now report on advances made by Hungarian researchers who have approached the problem of Alzheimer's through the development of molecules that prevent the fibrillation of beta-amyloid 42 once it has accumulated in the extracellular space rather than preventing its release per se. Specifically, this group has used a rational approach to design novel beta sheet breakers based on molecular modeling of the C-terminal sequence of the amyloid peptide as a template. These pentapeptide amides demonstrated efficacy in both in vitro and in vivo models of Alzheimer's and thus represent an exciting licensing opportunity for all companies involved in the development of improved treatments of this disease. Link to journal abstract:
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