Antioxidants, Overstating the Case, Too Much of the Old School
There's nothing like a catchy headline: "Increased antioxidant capacity reverses some effects of aging". Reading the article shows that nothing of the sort is going on, of course. Antioxidants are indeed involved, but this is no more than the normal byplay of scientists attempting to figure out just a little more of mammalian biochemistry as it relates to aging:
The study is one of the first experiments to assess memory performance among aging mice genetically engineered with an abundance of an antioxidant enzyme called extra cellular superoxide dismutase. As this group of mice aged, they performed better on memory tasks and demonstrated cellular improvements in the hippocampus, a part of the brain required for memory.Conversely, the same experiments in younger mice showed that high levels of the antioxidant were detrimental to memory function.
Previous studies have concluded that oxidative stress contributes to aging and aging-related impairments in memory. Klann conjectures that high antioxidant levels, within reason, could promote longevity and reduce the risk of dementia associated with normal aging and neurodegenerative disorders such as Alzheimer's disease.
Oxidative stress shows up as a part of the biochemistry of a wide range of neurodegenerative conditions - it follows that damping down that stress should help slow the progression of symptoms by slowing the destruction of cells. Slow is not reverse, however. In addition, this sort of approach doesn't actually address underlying causes at all, as recent research into Alzheimer's illustrates:
Dr. Atamna believes that the combination of functional heme deficiency, which harms mitochondria needed to produce energy, together with the increase in oxidative damage caused by the peroxidase, is what eventually kills the cell.
Increased oxidative damage to neurons - through increased activity of reactive oxygen species, or increased vulnerability to the same - is quite far down the chain of damage, failures and consequences.
There's nothing wrong with promoting your research, research that usefully adds to our knowledge of neurodegenerative conditions and their biochemistry, but keep it responsible. There is little chance that this sort of work will lead to any more than "finger in the widening crack in the dam" approaches to treating age-related neurogeneration - the old school approach of pumping chemicals into our systems to try and address end results of underlying damage is not the way forward. The new approaches of metabolic tinkering and optimization to minimize ongoing damage are not much better.
We must put more effort into addressing the underlying biochemical damage of aging - not just slowing its accumulation by tweaking the processes that cause damage, but actually stepping in to repair damage. This is a much more plausibly efficient way forward, whatever the details of its implementation - strike at the root, not the branches.
Technorati tags: life extension, medical research, SENS