How to protect neurons from degeneration?
Reducing calorie intake slows down the loss of neurons
To slow down the onset of neuron degeneration, the mice were either fed so that their body received fewer calories, or they were given a substance that activates SIRT1 – SRT. Both prevented memory deterioration and contributed to the maintenance of synaptic plasticity.
Alexander Shuster, sci-lib based on ScienceDaily: Reducing Caloric Intake Delays Nerve Cell LossActivation of the enzyme, which is known to play a role in the beneficial effects that prevent aging by reducing the amount of calories consumed, slows down the loss of brain neurons and supports cognitive function in mice, reports The Journal of Neuroscience (Graff et al., A Dietary Regimen of Caloric Restriction or Pharmacological Activation of SIRT1 to Delay the Onset of Neurodegeneration – VM).
The results of the study in the future may form the basis for the creation of new drugs that slow down the development of brain damage associated with aging.
The results of previous studies show that reducing the amount of calories consumed prolongs the life expectancy of various species and prevents the development of changes in the brain that are often associated with aging and neurodegenerative diseases, such as Alzheimer's disease. There is also evidence that reducing the amount of calories consumed activates the enzyme sirtuin-1 (SIRT1). As the results of various studies show, this enzyme prevents the development of brain damage associated with aging of the body.
As part of the current scientific work, the staff of the Picower Institute for Learning and Memory at the Massachusetts Institute of Technology and the Howard Hughes Medical Institute have checked whether reducing the amount of calories consumed can actually slow down the loss of nerve cells – a common phenomenon in the development of neurodegenerative diseases, and, if it can, whether activation is the basis for this SIRT1. Scientists were able not only to confirm that reducing the amount of calories consumed slows down the loss of neurons, but also to show that drugs that activate SIRT1 cause the same effect.
"There is a great interest in identifying chemical compounds that reproduce the effects observed when reducing the amount of calories consumed, which can slow down the development of problems associated with aging and/or diseases. If they turn out to be safe for humans, then, as the study shows, these compounds could be used as a preventive measure to slow down the onset of neurodegeneration associated with several diseases that affect the aging brain," says Luigi Puglielli, a specialist in gerontology, an employee of the University of Wisconsin at Madison.
In the work, the authors used a special line of laboratory mice, in whose brain changes associated with neuron degeneration were rapidly developing. Scientists have reduced the normal diet of animals by 30%. After three months of such a diet, the mice were tested for their ability to learn and for memory work. "We observed not only a slowdown in the onset of neurodegeneration in mice that consumed fewer calories, but also the absence of memory deficits and learning abilities detected in mice that were fed in the usual way, and not in accordance with diets," says Li–Huei Tsai (Li-Huei Tsai, head of the study).
Scientists gave different groups of mice a drug – activator SIRT1. Animals receiving this activator were characterized by less loss of neurons and better interneuronal connections (compared to mice that did not receive the drug). Also, laboratory mice that were given the SIRT1 activator were tested for memory and learning ability with the same success as healthy mice.
According to Dr. Tsai, now it is necessary to clarify a number of important details. For example, whether it is safe to use the studied approach for a long time, whether it will be effective in the case of other animals, whether it temporarily slows down the progression of neurodegeneration or allows you to stop it completely.
Portal "Eternal youth" http://vechnayamolodost.ru23.05.2013