Aging Cellular

Aging of cells: they can be more efficient?

Our children and grandchildren continues to remind us of our youth, we could mental and physical feats with seemingly without effort or fatigue. So why the age-related loss of energy? And we can do something to stop or reduce its progression? Recent research suggests that the answer to the second question is "yes." But the first questions first.

More old, less energy
The grandchildren are fast, physically and mentally, because of its "super cell efficiency to convert food energy and maintenance of ample reserves of energy. But in the process of aging, health deteriorates important cellular components. Consequently, the ability to make our cells produce energy.

Perhaps the most important biochemical pathways affected by aging are associated with cellular structures, mitochondria. Mitochondria provide nearly all the energy of the cells in our body needs to stay healthy and active. And they have enough energy stored in the cell is like having enough fuel to heat your house during these cold winter days … that

can not survive without it!

There are things little by little, more people can take to support the production of energy in our mitochondria. (See journals Juvenon and longevity "> Mitochondria: Regulators of cell death and survival; alpha-lipoic under cellular stress, more energy "> Alpha lipoic acid: under cellular stress, more energy, title =" Carnitine Cousins "> Carnitine is first.) Month Journal This provides information indicating that there are also things we can do to help redirect limited cellular energy reserves in tissues of age, are accessible to a more vital cellular processes.

Energy consumption higher
The cells most affected by the decline related to age of energy production are of course those who have higher energy needs. The brain needs to produce more energy than any organ body, even during sleep. The nervous system requires a lot of this energy to synthesize signaling molecules (neurotransmitters) and cellular pumps to facilitate the transport of ions (salts) within and outside the cell (neuron) for the maintenance of electric charge.

Because of this strong demand for energy, central nervous system must have a constant supply enough energy to maintain optimal health. Lack of energy can lead to death of neurons, which leads to dysfunction of the nervous system.

Defense deficit
But what we do, especially as we age, for support the energy needs of the nervous system? Studies suggest a form of vitamin B3, nicotinamide, could help.

Nicotinamide is necessary for the synthesis of a molecule, nicotinamide adenine dinucleotide (NAD), which is essential for energy production in mitochondria. NAD is not only important for the production energy, but it is also necessary for the synthesis of the components of our genetic code, as well as the repair of DNA damage including code.

In the high intensity of stress NAD
What causes DNA damage?

Previous work have shown lately and what happens during ischemic stroke (stroke). At the biochemical level, increased oxidant production leads to damage cellular structures, much of the genetic material. Damage to DNA causes the activation of specific enzymes, PARP (poly A ribose polymerase) and SIRT1. These mobile machines use large amounts of high-energy molecules containing NAD to repair and protect DNA.

Other stress-producing events occur in the nervous system with increasing frequency with age. Are associated with high levels of toxic substances such as free radicals and other reactive oxygen species, in the cell. These substances have been shown to excite neurons in the supermarket that used to cause the release of the neurotransmitter, glutamate, beyond numbers.

Although glutamate is important for the transmission of nerve impulses, when produced in excess, can lead to a neuron electrically overdrive (commonly known as glutamate excitotoxicity). This results in the neuron excited state absorption substances charges, ions such as calcium and sodium in an attempt to restore normal ionic balance. Unfortunately for the neuron, the process requires much energy and if energy storage is compromised – for example, the low level NAD common in the elderly – the cell dies.

Register neurons
Vitamin B3 to the rescue? A series of articles reported on the effects of nicotinamide administration to animals or cell cultures, which were under the type of NAD-depleting stress as described above.

More Recently, a mouse model for stroke showed a decrease of NAD, coinciding with an increase of cerebral tissue damage. The damage was significantly lower in animals that received vitamin B3. Vitamin A precursor of NAD, was shown to stimulate the synthesis of this molecule in the high energy, and inhibit activation SIRT1 enzyme that consumes NAD. The net effect? An increase in the energy molecule and restoration of energy balance in neurons affected by stroke. (See "This update of research month.")

Other research has demonstrated the potential benefits of administration of nicotinamide to animals to develop symptoms of Alzheimer's disease. Fed with this form of vitamin B3 has significantly fewer symptoms of dementia than who received placebo. The mechanism, though not yet fully understood, seems to affect neither the PARP enzyme, the enzyme SIRT1, or both.

Another interesting hypothesis proposed that the excited neurons may cause some types of migraine. There is some evidence, though not yet convincingly that nicotinamide may be useful in this disease related to the central nervous system.

Potential health benefits
The work described above is encouraging. Other results of these and future studies may provide information to help reduce the vulnerability of the old times. It may even be the key to preventing the conditions that affect the nervous as Alzheimer's and Parkinson's.

Meanwhile, nicotinamide compound is relatively safe if taken in low doses (less than 500 mg per day), but can cause liver damage when taken in high doses in sensitive individuals. Consult your health care professional is recommended.

About the Author

Dr. Benjamin Treadwell, Ph.D. is an independent researcher in biochemistry with a life-long interest in metabolism and aging. He previously served as an Associate Professor of Biochemistry at Harvard Medical School and as Director of the Orthopedic Research Laboratory at Massachusetts General Hospital. He earned his Ph.D. in biochemistry at New York University and served as a Research Fellow at the Roche Institute of Molecular Biology in New Jersey.

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