Researchers led by the ESRF, the European Synchrotron, have found that amyloid oligomers play a role in speeding up mitochondrial energetics during the early stages of Alzheimer’s, in contrast to what has been previously found in more advanced Alzheimer’s brain tissues.
The origin of Alzheimer’s disease, which affects 30 million people worldwide, is still not clear despite an international research effort and significant progress in research. And yet, identifying the factors driving this incurable neurodegenerative disease is essential to find better ways to diagnose Alzheimer, delay its onset and prevent progression. “Before understanding the pathology, we need to understand the biology”, explains Montse Soler López, head of the Structural Biology group at the ESRF and co-corresponding author of the study.
Alzheimer’s is an incurable disease that normally appears after the age of 65. However, changes in the brain begin 20 years before the disease appears. “We believe that malfunctioning of the mitochondria can take place 20 years before the person shows symptoms of the disease”, explains Soler López. For a long time, researchers have focused on the amyloid plaques in the brain as the potential cause of the disease. However, this hypothesis is currently being reconsidered.
Now Soler López’s team, together with scientist Irina Gutsche at the Institut de Biologie Structurale (CNRS, CEA, Université Grenoble Alpes) and researchers at the EMBL, conduct a new line of research focusing on aging factors, such as mitochondrial dysfunction. Mitochondria are often referred to as the “powerhouse of cell” because of their essential role in energy production. Over time, mitochondria suffer oxidative stress and this leads to their malfunction. A recent finding indicates that individuals with Alzheimer’s may exhibit an accumulation of amyloids within mitochondria, challenging the previously belief that amyloids were solely present outside neurons.
Read more on the ESRF website