Mitochondria size does matter in Alzheimer's

Treatment for Alzheimer's disease may lie in modifying the length of subcellular structures in the brain responsible for metabolising energy, mitochondria.


Research conducted by scientists at the Queensland Brain Institute (QBI) at The University of Queensland (UQ) and Harvard University found in cases where the mitochondria were abnormally long, they had a toxic effect inducing cell death.


Director, Centre for Ageing Dementia Research (CADR) at QBI and co-author of the paper, Professor Jürgen Götz, said, “Alzheimer's disease belongs to a group of neurodegenerative diseases termed ‘tauopathies', charaterised by clumps of the protein tau inside neurons.


“In instances where neurons express toxic levels of human tau, the mitochondria are elongated.


“All cells rely on mitochondria for energy metabolism, and neurons in particular, so controlling the length of these subcellular structures is very important for brain function.”


The research provides novel targets for therapeutic intervention.


“Treatments currently available for these diseases have at most modest effects, in part due to our limited understanding of how Alzheimer's disease starts and progresses,” Professor Götz said.


The good news is, genetic and drug interventions aimed at reducing mitochondrial length reverse the toxic effects of tau, and can now get underway.


“An aspect of mitochondrial regulation that is being increasingly appreciated are changes in size and shape of the organelle, through a process termed 'mitochondrial dynamics',” Professor Götz said.


Alzheimer's disease affects almost 280,000 Australians. This number grows by 1,600 each week and is expected to reach over 1 million people by 2050.


Dementia is currently the third leading cause of death in Australia, after heart disease and stroke, with one in four people over the age of 85 suffering from dementia.


Between 2000 and 2008, deaths attributed to Alzheimer's disease increased 66 per cent, while those attributed to the number one cause of death, heart disease, decreased 13 per cent (


From the paper ‘Tau promotes neurodegeneration via DRP1 mislocalization in vivo' for publication in Neuron, August 23, 2012 (print edition).


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22 August 2012.