When neurons are out of shape failure to evolve cognition may signal age-related diseases
Early-onset age-related dementia can lead to impairment of thinking memory and other neurological processes. Now scientists at the CNIOs LOral Sexogerinaire (OLG) and INRAE (Instituting the Research Initiative in Science and Technology) France have demonstrated that a neuronal dysregulation known as a TREM-2 dysregulation is a crucial factor in the development of most forms of the disease. In a study using live-embeddable functional circuits implanted into mice the scientists observed neuronal outgrowth among the pathologies associated with Alzheimers disease Huntingtons disease stroke congenital heart disease and peripheral neuropathy: waschemic stroke (an affliction leading to blood clots swelling and tissue damage) and activated immune cells (cytotoxic shock) caused by infections such as strep throat.
Improvements in neuronal health promote immunity.
These neuronal changes can be attributed to the fact that an extensive protective enzyme (called NAPRTN) is expressed in glial cells (brain cells) in the hippocampal region of the brain. In accordance to this hypothesis it would be advantageous to our closest relatives to have NAPRTN in the brain: Older mice have an enhanced sense of smell and generate more odorant molecules which have a beneficial effect on the brain explains OLG researcher Frederic Daoust and member of the Institute of Neuroimaging and Cognition (INRAE) at LOral. This is the case of rodents that have lived for many years: These rodents were often used to study brain diseases in 184 mice. We therefore wanted to see in great detail if providing extensive NAPRTN activation in mice that have been exposed to diseases of the brain leads to a negative impact on brain activity.
In mice and humans the scientists demonstrate that the neurons which are affected by the dysregulation I described above by NAPRTN are degenerating and are incapable of renewing their biophysical and electrical properties. Deceleration of cognitive function and problems in memory and learning were observed between the age of two and 20 years and were significantly exacerbated by the age of 40 years. It is surprising that the effects we observed occur so soon after brain regenerative changes have taken place in human adults. And this is indeed the case says Daoust and the agents of the team including Chrissy Seney. In the short term this phenomenon may indicate persistent impairments of the development of cognitive function in the elderly.