Alzheimer’s disease is caused by a buildup of amyloid beta in the brain, which causes plaques that disrupt nerve cells. Now, research conducted by scientists at the University of Bergen is improving our understanding of exactly why this happens, identifying both a section of a cell and a protein that are central to the process.

Our understanding of Alzheimer’s disease is always evolving, with new discoveries being made every month. Just recently we’ve learned that mimicking movements could help patients relearn lost abilities, and we’ve even gained insights into how the disease impairs perception.

For the new research, the team studied patients with major physical and psychological problems, all of whom had a particular gene defect that causes a reduction in the amount of a particular protein in their systems, known as PITRM1.

Scanning the subjects’ brains revealed the telltale amyloid beta buildup in their brains. Further testing with laboratory mice exhibiting the same loss of PITRM1 backed up the finding, revealing a similar protein deposition in the brain.

Not only is the knowledge that the protein plays a central role in such neurological diseases likely to prove useful in developing new treatments, but the location of PITRM1 – found in mitochondria – confirms that these cell powerhouses play an important part as well.

“The results conclude a long discussion about the relationship between mitochondria and accumulation of amyloid in the brain” said research Janniche Torsvik. “We have found that mitochondria play a crucial role in the process of protein deposition.”

Full details of the research are published online in the journal EMBO Molecular Medicine.

Source: University of Bergen


Henry Sapiecha