Hirano bodies may block Alzheimer's-related cell death
In the fight against Alzheimer's disease, abnormal protein structures known as Hirano bodies may help reduce cell death, researchers believe.
Scientists at the University of Georgia, using cell cultures, determined that cells with Hirano bodies appear to play some sort of protective role as Alzheimer's disease progresses. By observing cell cultures with or without the tau protein, they concluded in their NIH-funded study that cells with Hirano bodies experienced significantly reduced cell death compared with those without the Hirano bodies.
Also, they determined that mixtures of amyloid precursor protein, C31 and tau; or of AICD (amyloid precursor protein intracellular domain) and tau, (all believed to be factors in Alzheimer's progression in the brain) caused higher levels of synergistic cell death than any of the elements did on their own. Hirano bodies are believed to play a role in cell death induced by AICD, or c31, (a part of AICD), which are released inside cells as amyloid precursor protein and amyloid-beta plaque begins to build up.
"This synergistic cell death is very exciting," lead study author Matthew Furgerson said in a statement. "Other groups have shown synergy between extracellular amyloid-beta or amyloid precursor protein with tau, but these new results show that there may be an important interaction that occurs inside the cells."
This is early research that is a long way from definitively establishing whether Hirano bodies are the key to stopping Alzheimer's advance. But they are becoming a new focus in Alzheimer's research, and the scientists are attempting to flesh out their role in Alzheimer's well beyond the better known amyloid-beta plaques, tau protein and neurofibrillary tangles that have drawn longer, and greater attention. The team plans to continue its focus with an Alzheimer's mouse model that allows it to study Hirano bodies in greater detail, well beyond post-mortem brain tissue studies that have previously been the only way to do this.
Read about their research in detail in PLoS One.