Looking for an Alzheimer’s cure
It is well established that the build-up of beta-amyloid plaques in the brain is associated with Alzheimer’s disease. Beta-amyloid peptides interfere with the proper function of brain cells; specifically, with the function of mitochondria (the “battery” of a cell). MITOABETA (Investigation of beta-amyloid peptide effects on mitochondria protein homeostasis: From pathogenesis to therapy of Alzheimer Disease) is an EU-funded project that investigated how beta-amyloid peptides interact with cellular components and influence their function. The ultimate goal was to develop a treatment from the project’s findings. Researchers found that although the beta-amyloid peptides are not taken up by mitochondria, they completely inhibit the uptake of precursor proteins that are necessary for mitochondrial function. In contrast, the amyloid precursor protein (APP) did not show this inhibitory effect. These results indicate a novel mechanism why mitochondrial defects accumulate in Alzheimer’s disease. The scientists investigated how other cellular components affect the mitochondrial interaction with beta-amyloid peptide and APP. They found that these components affect the negative effects of the beta-amyloid peptides. This research revealed important aspects of beta-amyloid peptide biochemistry. Understanding the effect of these peptides on the brain is an important step in working towards a suitable treatment for Alzheimer’s disease.
Keywords
Alzheimer’s disease, dementia, beta-amyloid plaques, mitochondria, amyloid precursor protein (APP)
