A Gentle Introduction to the Dreaded Mitochondrial-Lysosomal Axis

Is it really right that you know more about the workings of your car than your body? You can always buy another car if you fail to take good care of the one you have. If you want to live a longer, healthier life, however, it is a very good idea to become more educated about what is actually going on inside that aging body of yours. A great deal more is known about the biochemistry of aging than present day medical technologies allow us to manipulate safely, but this state of affairs is changing rapidly. Getting yourself up to speed is the first step towards deciding how you should help to shape your future health and longevity.

With that in mind, here's a little about the mitochondrial-lysosomal axis theory of aging and its relationship to your aging process. Like much of modern biochemistry, a summary of the science is actually nowhere near as complex as the name makes it sound. The following paper describes a relationship between cellular processes, damage and failure modes that take place in the mitochondria and the lysosomes, components within the cell known as organelles.

The lysosomal-mitochondrial axis theory of postmitotic aging and cell death:

Aging (senescence) is characterized by a progressive accumulation of macromolecular damage, supposedly due to a continuous minor oxidative stress associated with mitochondrial respiration. Aging mainly affects long-lived postmitotic cells, such as neurons and cardiac myocytes, which neither divide and dilute damaged structures, nor are replaced by newly differentiated cells. Because of inherent imperfect lysosomal degradation (autophagy) and other self-repair mechanisms, damaged structures (biological "garbage") progressively accumulate within such cells, both extra- and intralysosomally. Defective mitochondria and aggregated proteins are the most typical forms of extralysosomal "garbage", while [lipofuscin] represents intralysosomal "garbage".

Based on findings that autophagy is diminished in lipofuscin-loaded cells and that cellular lipofuscin content positively correlates with oxidative stress and mitochondrial damage, we have proposed the mitochondrial-lysosomal axis theory of aging, according to which mitochondrial turnover progressively declines with age, resulting in decreased ATP production and increased oxidative damage.

The inherited Batten disease shows what happens when lipofuscin buildup truly runs amok - a very early death. As the above paper shows, scientists are building an ever greater understanding of exactly how it is that our cells run down with age. Some groups - such as those funded by donations to the Methuselah Foundation, or those aiming at specific age-related conditions resulting from this damage - are working towards fixing these problems.

If we want to see more rapid progress towards therapies capable of repairing this sort of age-related cellular damage, more funding and more researchers are needed in these areas. This is something that you can help to bring about; so take a moment to think about your priorities!

Technorati tags: ,

Comments

Post a comment; thoughtful, considered opinions are valued. Comments incorporating ad hominem attacks, advertising, and other forms of inappropriate behavior are likely to be deleted.

Note that there is a comment feed for those who like to keep up with conversations.