Goldilocks was on to something when she preferred everything "just right." Harvard Medical School researchers have found that when it comes to the length of mitochondria, the power-producing organelles, applying the fairy tale's mantra is crucial to the health of a cell. More specifically, abnormalities in mitochondrial length promote the development of neurodegenerative diseases such as Alzheimer's.
"There had been a fair amount of interest in mitochondria in Alzheimer's and tau-related diseases, but causality was unknown," said Brian DuBoff, first author of the study and a post-doctoral research fellow at Massachusetts General Hospital.
"Ultimately, a deeper understanding of the relationship between mitochondrial function and Alzheimer's may guide us to develop more targeted therapies in the future," said Mel Feany, HMS professor of pathology at Brigham and Women's Hospital and senior author of the paper.
The findings will be published online in the August 23 issue of Neuron.
Tau-related diseases are caused when tau, a protein most commonly found in neurons, malfunctions. Tau binds to microtubules in cells, a process known as stabilization. This binding is necessary so the microtubules can help maintain cell structure and aid in intracellular processes such as transporting molecules. When tau is defective, most often due to changes introduced during protein synthesis, it can accumulate in neurofibrillary tangles, one of the primary markers of Alzheimer's.
In this particular study, conducted in fruit flies with defective tau protein, DuBoff found that the mitochondria in the brain cells of these flies were elongated compared with the mitochondria in flies with normal tau. The elongation, he observed, adversely affected mitochondrial function.
"Normally, one mitochondrion will split into two, two mitochondria will join into one, and that's a critical process for the health and stability of the mi
|Contact: David Cameron|
Harvard Medical School