As another birthday has passed I thought this week’s entry
should be on an associated theme- the biology of ageing. This is another huge
topic that I will be indulging in only the most superficial of levels. But the
process of ageing in cells is fascinating in terms of both the mechanism and
possible future research.
Telomeres are regions of DNA with repeat, non coding information
which protect the ends of the chromosome from deterioration during replication.
As chromosome ends shorten with each replication, eventually the DNA that keeps
everything ticking over nicely will be lost. Instead, telomeres are shortened
during each cell division and while they exist, new cells can maintain their
structural and functional integrity. In regular cells the shortening of
telomeres leads to apoptosis (programmed cell death) but in abnormal cells,
continued cell division once the telomere is depleted may lead to chromosome
instability with associated consequences-from ageing to cancer.
The mechanism for ageing even at a cellular level is not
fully understood (no matter what the latest wonder cream advertisement suggests).
One of the ways in which scientists study this mechanism is by analysing
disorders that cause premature ageing, such as Hutchinson-Gilford Progeria
Syndrome (HGPS). The disease is caused by mutations in the gene LMNA and its symptoms represent areas of
ageing manifesting so rapidly, that suffers live to a mean age of only 12.6
years. Studies have shown that the average length of telomeres in HGPS patients
is much shorter than people of the same age. However, the method by which the
mutation in the LMNA gene causes
telomere shortening is not fully understood.
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| An example of cluster telomeres (purple areas) in 'boquet' proteins in yeast during meiosis. |
A recent study compared telomere length with physical
performance in advanced age. Telomere size data was collected from adults aged
between 53-80 years of age and their performance in tasks (ranging from walking
to chair rise speed) was measured. Perhaps unsurprisingly, there was no
correlation between age deteriorating-physical performance and telomere length.
Therefore, the importance of telomeres in the process of ageing remains at a
cellular level only.
On a more positive note, scientists are looking at the
potential use of rejuvenating senescent cells (cells that can no longer divide
and replicate) as a method for postponing the ageing process. While still only a
scientific pipe dream, it may be possible to reprogram cells by induced
pluripotent stem cells (iPSCs) or by modifying the senescent cell signalling
pathways with pharmacological or natural agents. It should be noted that senescent
cells do have important roles in keeping the body functioning properly,
including regulating the wound healing mechanism and mobilizing the immune system
to clear cancer cells. Therefore, any attempts at the rejuvenation of senescent
cells would have to weigh the risks to these important processes against the
benefits of halted ageing.
The biological ageing process is so complex that the
scientific community is only piercing the surface of potential understanding in
order to replicate the mechanisms involved. While it may never be possible to
eliminate ageing (nor perhaps should we aim for it), the goal of prolonging a
healthy life span is worthy at a time when an ageing population is seen as an increasing
economical and social worry. How far research can take us towards that goal
remains to be seen.
Further reading:
Basu, N. et al. (2013). ‘Telomeres and Telomere Dynamics:
Relevance to Cancers of the GI Tract’, Expert
Review of Gastroenterology and Hepatology, 7 (8), pp. 733-748.
Decker, M.L., Chavez, E., Vulto, I. and Lansdorp, P.M.
(2009). ‘Telomere Length in Hutchinson-Gilford Progeria Syndrome’, Mechanisms of Aging and Development, 130
(6), pp. 377-383.
Gardner, M.P. et al. (2013). ‘Telomere Length and Physical
Performance at Older Ages: An Individual Participant Meta-Analysis’, PloS One, 8 (7), e.69526.
Sikora, E. (2013). ‘Rejuvination of Senescent Cells- The
Road to Postponing Human Aging and Age-Related Disease?’ Experimental Gerontology, 48 (7), pp. 661-666.
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