Neuroscience, it’s a-progressing. While you were going about your business the scientists found out how space can mess with your brain, hinted at a mechanism to slow down aging and identified a new target for antidepressants
Last year, we all were impressed by “The Martian”’s Mark Watney's quick wit and impressive problem-solving abilities (if you have no idea what I’m talking about then go to Netflix asap). Yet new research voices concern about the phenomenon called “space brain”, chronic dementia risk caused by galactic cosmic ray exposure -- something that Mark Watney would apparently suffered from if his journey to Mars was real. Researchers from University of California, Irvine, found that not only does space wreck your bone density and muscle volume, after longer period of time outside of our Earth’s protective magnetosphere (comparable to a 2-3 years roundtrip to Mars) it also could promote permanent cognitive deficits and even dementia.
For this study mice were exposed to radiation equivalent to the one experienced in space. Six month after exposure their brains still showed alarm-raising levels of inflammation and neuron damage which went along with poor performance on behavioral tests measuring learning and memory. Another alarming side-effect of being exposed to the cosmic radiation for too long is the loss of “fear extinction” -- a tool the brain uses to suppress traumatic events, such as to learn to enjoy driving again after a scary car accident. This inability to unlearn stressful associations and the subsequent risk of developing anxiety might pose a big problem for astronauts who need to solve a lot of problems under pressure. This space dementia sure is a barrier in our plans to colonize Mars, however, it is not a problem we cannot solve: preventive measures (such as medication protecting neurotransmission), spacecraft shielding, better helmets and other solutions are being explored the very same moment you’re reading this. To boldly go where no man has gone before and so on and so forth.
Much better news are reserved for everyone who is not that keen on aging (and wants to live forever): Copenhagen researchers found that a body's own substance called NAD+ postpones the aging process and extends the lifespan. It does so by working against two aging mechanisms: less effective DNA repair and poor functioning mitochondria (cell power plants). However, the study was performed on mice and roundworms suffering from a neurodegenerative disease, so hold your horses, transhumanists! Here’s what went down: the poor creatures were genetically modified to have a disease which makes the part of the brain responsible for coordination degenerate at a fast rate and prevents normal DNA repair (which was supposed to simulate early aging). Then, they were injected with NAD+ and interesting things started to happen: the severity of the disease was reduced, muscular function -- normalized, memory loss -- delayed, lifespan -- extended. This all seems to have happened due to wondrous ability of NAD+ to repair DNA and to maintain mitochondria happy and healthy. Considering the fact that NAD+ level substantially decreases as we age this holds a potential to slow down aging process with a simple replenishment of this coenzyme. Another pleasant side-effect of keeping our cells young is the potentially much later onset of such neurodegenerative diseases as Alzehimer’s and Parkinson’s. (”Live Forever” by Oasis starts playing in the distance)
(If you want to become dazzled about human race’s progress in life sciences and to start pondering about living forever I also recommend reading this not really neuroscience but still fascinating piece of news).
Another good piece of news comes for people suffering from a treatment-resistant depression. So far these patients are in a quite distressing situation as there are not many alternatives to resort to once the commonly used pills like Prozac failed. A new study from the Northwestern University discovered a promising new target in the brain which can be manipulated to ease even the stubbornly clingy depression which doesn’t respond to medication. The researchers found that the common antidepressant types, such as SSRIs and tricyclic antidepressants, block BMP pathway in hippocampus, our memory making center. The blockage of this pathway, in turn, leads to an increased neurogenesis, the birth of new cells (which is generally a very good thing for learning and memory). However, they weren’t sure whether blocking this pathway was deciding for the antidepressants' effect as this medication acts on a variety of multiple mechanisms in the brain. To investigate that, the scientists gave the ever-suffering mice a protein called noggin which is known to specifically block this exact BMP pathway. The results did not disappoint them: not only did noggin target BMP much more precisely and effectively than Prozac and tricyclics, the mice also showed significantly less anxious and depressed behaviour (which in mice terms means they didn’t hang hopelessly when held by the tail but rather energetically tried to get upright). This whole thing is quite promising as discovering a new biochemical target to aim our weapons at can bring us closer to developing new therapies for people whose brains are not big fans of Prozac.