The Biology of Ageing: Damage or Hyperfunction

Synopsis

The biological mechanisms at the heart of the ageing process are a long-standing mystery. An influential theory has it that ageing is the result of an accumulation of molecular damage, caused in particular by reactive oxygen species (ROS) produced by mitochondria. This theory also predicts that processes that protect against oxidative damage (involving detoxification, repair and turnover) protect against ageing and increase lifespan.

However, recent tests of the oxidative damage theory, many using the short-lived nematode worm Caernorhabditis elegans, have often failed to support the theory (1-3). This motivates consideration of alternative models. One new theory, conceived by M.V Blagosklonny, proposes that ageing is caused by hyperfunction, i.e over-activity during adulthood of processes (particularly hyperfunction can lead to hypertrophy associated pathologies, which cause the age increase in mortality.

This talk will assess whether the hyperfunction theory is at all consistent with what is known about C.elegans ageing, and conclude that it is (6). In pathology and/or hyperfunction, including high density packing of oocytes in the proximal gonad, oocyte hypertrophy to form tumour-like masses, massive yolk accumulation, cuticular hypertrophy and neurite outgrowth. Such changes appear to contribute to mortality in at least some cases (e.g. yolk accumulation). Gems’ assessment implies that the hyperfunction theory is a plausible alternative to the molecular damage theory to explain ageing in C.elegans.

1. Genes Develop 22, 3236 2008
2. Cell Metab 6, 280 2007
3. Proc Natl Acad Sci USA 109, 5785 2012
4. Cell Cycle 5, 2087 2006
5. Cell Cycle 7, 3344 2008
6. Antiox Redox Signal Sep 24. [Epub ahead of print] 2012

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Speaker

Professor David Gems
C.elegans Ageing Laboratory, Institute of Healthy Ageing, University College London