The human population is grow one-time , and unless we maturate healthily , the elderly can be a huge societal and public wellness var. . Many scientist are therefore hunt for way to reduce some of the problem that do with aged bodies , in particular cognitive impairments or neurodegenerative disease , and scientist may have just stumbled upon a very promising candidate : an asthma drug .
You might be thinking that this is a middling bizarre connection , a respiratory disease and brain occasion , but there is method behind the madness . While cause versus result is n’t entirely clear , a common hallmark linked with long time - associate cognitive decline is lighting of the brainpower , driven by demurrer cells called microglia . Asthma is an instigative disease of the airways , so scientists therefore conclude that it might be potential to repurpose the powerful anti - incitive drugs used for this condition in gild to slow or overthrow genius ageing .
research worker from Paracelsus Medical University , Austria , resolve to test this hypothesis out , and focused on a market drug called montelukast . This works by blocking receptors for molecules telephone leukotrienes which mediate inflammatory responses , and while their role in the brain is undecipherable , heightened levels have been observed in the elderly brainiac .
For their probe , published inNature Communications , the scientists administer both young and of age bum montelukast for six weeks and compared their functioning on a test of acquisition and retentivity where the rats had to remember the location of a obscure platform in a water tank . Aged animals normally have deficit in this undertaking , taking longer than their young counterparts to learn , but remarkably montelukast treatment was plant to conclude the interruption between the two mathematical group , with the old git performing just as well as young informer . No improvement on the performance of the young rats , however , was observed .
To regain out what could be going on at the cellular level , the scientists examined the animals ’ mind and , sure enough , discovered a reduction in neuroinflammation in those belonging to the ripened animals . Not only that , but they also ascertain that cells in the hippocampus – crucial for acquisition and memory – went on a growth spurt , create young functional neuron . And when the scientists tested out the drug on wit cell in a dish , they observed the same encouragement in proliferation , but not in cells in which a particular leukotriene sensory receptor , called GPR17 , was deleted by the researcher .
But why are we only see these effects in sure-enough brain ? “ Good question ! ” jumper lead researcher Ludwig Aigner articulate to IFLScience . “ There are several potential reasons , but the point we want to make is that although leukotrienes are found in the young wit , they are present at much higher levels in cured brains and those of individuals with neurodegenerative diseases . So it ’s possible that blockade their receptors in young Einstein has no core because the leukotriene signaling mechanisms are not yet activated . ”
Perhaps the most supporting part of this study is the fact that the drug is already on the market place , meaning progress towards human trial should n’t take as grotesquely retentive as with a young compound . And Aigner sound out the squad has already apply for funding to do so , looking at the drug ’s efficacy in one character of dementia . But the drug ’s newfound usefulness may not end there : Aigner ’s team has also gathered some very preliminary information on beast models of Parkinson ’s disease which once again showed a restoration of cognitive function . “ But we do n’t acknowledge the underlying mechanism yet , ” he says .
