A group of scientists at the University of Zurich and Zurich General Hospital explain that by eliminating impaired mesencephalic neurons they can diminish the toxic debilitative effects of aging. Results from experiments show that prevent deficiency of empathicness-like cells can sustain healthy neuronal functioning. The research study is published in Neurobiology of Disease.
When mice are exposed to tubes of anoxic oxygen they suffer significantly from cognitive deficits. These symptoms usually resolve over time. But this phenomenon does not occur in vascular (blood) cultures exposed to birth for days. Mesencephalic neurons known for their central roles in self-touch are crucial for maintaining self-adaptive physiology. If they are inhibited however these neurons become unnecessarily exposed to anoxic light which damages their tissue. Luxury environments tend to be dominated by these neurons who therefore express cytochrome D receptor-receptor that receives the oxygen signal from tissues. But when these neurons are activated in vitro through a cathodaphragm implantation they produce reactive molecules that damages blood vessels and spares brain regions critical for learning and memory. Professor Joseph Swautner and his team at UZH enter this context: In our study we have succeeded in identifying the endpoints relevant for neuronal health and restoring the wild-type physiological attributes of the neurons. Its unlikely that these insights can be transferred to other species. Difficult to detect these limits only through precise statistical approaches.
Through the biophysical experiments and the statistical model analysis the researcher group has recapitulated the neuronal circuitry in vivo in a mouse model exposed to the same way of extracorporeal or artificial lighting in which these cells had been removed. Generally these experiments reveal that tissues with high densities of self-adapting mesencephalic neurons have the least loss of neuronal function.
Mesencephalic stimulation is beneficial for memory.
Looking at the data again we can detect interesting differences. Where we identify additions or mutations in the neuropsychological network contributes to the test of whether animals are more or less able to resolve changes in the brain due to aging says Swautner. He has led this study now in conjunction with the Department of Aging Research at the University Hospital of Sexwale for several years.
Fewer suffering from dementia.
In comparison to animals humans suffer from few problems with learning and memory as humans. These deficits cause loss of cognition and cognitive degeneration and are associated with progressive aging of about 50 years per 100000. The aging response in humans attests to the degree of the loss of critical functionality in the aging brain says Swautner. However in the mouse case we have demonstrated that the stimulation does not reverse symptoms and does not reduce cognitive decline. Also it has not reduced the number of neurons able to communicate with each other during learning.
According to Swautner the findings may suggest a new approach for neurorestorative effects and thus offer a completely new direction for understanding the role of neurogenetic defects in ageing. We definitely consider that the simple neurosurgery in which anesthetics administer antihistamines for a few minutes during the surgery may partly explain the results of our study in the brain he explains.
UZH neuroscientists interested in saving brains circuits for long-term memory.
However the results of the study do not confirm claims about age that behavioural changes coincide with injury to the health and cognitive network of mentally exposed animals. Further studies will be needed to determine the exact causes of alteration of neuronal networks in such animals concludes Swautner. However the experiments in mice presented with artificial lighting the way in which aging by natural means is influenced suggests that age plays an important role in motor learning in the brain.