Tag Archives: mitochondrial dysfunction

Deficit accumulation as an explanation for ageing and frailty – from the subcellular to the substantial

Prof Kenneth Rockwood is Director of Geriatric Medicine Research at Dalhousie University, Canada and serves on the International Advisory Panel of Age and Ageing journal.

Prof Susan Howlett is  also at Dalhousie, University, Canada in the Department of Pharmacology.d

A lot happens at the molecular and cellular levels as we age. A recent review in Cell  identified nine hallmarks of ageing, including genomic instability, mitochondrial dysfunction, cellular senescence and stem cell exhaustion.  These, of course, are intrinsically inter-related; the DNA damage that underlies the hallmark genomic instability accelerates with telomere shortening (another hallmark) and is associated with altered protein homeostasis (another hallmark still). This molecular and cellular deficit accumulation is now widely understood as the basis of how we age. Continue reading

Sarcopenia (Part 2)

The inaugural UK conference on sarcopenia was held in central London on 9th July 2013.

Sarcopenia

Sarcopenia

Delegates included clinicians, therapists, nutritionists and scientists, with representatives from Spain, Belgium, the Netherlands, Poland, the Ukraine, the United States and Japan.

Mitochondrial dysfunction

Professor Doug Turnbull, Professor of Neurology at Newcastle University and Director of the LLHW Centre for Ageing and Vitality and of the Wellcome Trust Centre for Mitochondrial Research, outlined the role of mitochondrial dysfunction in the development of sarcopenia. He explained that two types of mitochondria are found in muscle, subsarcolemma and intermyofibrillar: the latter are the majority and are heavily networked. Numerous studies have shown a decline in mitochondrial oxidative metabolism with age, and specifically that segments of muscle have severe deficiency. The mechanism for this involves high levels of mutations within the mitochondrial genome, with evidence that this leads to muscle fibre splitting and breakage. There is also increasing evidence that mitochondria are implicated in motor neurone loss, typically reduced by 34 per cent in people aged 80-90 years compared to those aged 30-40 years. Professor Turnbull concluded by commenting that exercise has been demonstrated to increase mitochondrial density and function, highlighting a possible mechanism for the treatment of sarcopenia. Continue reading