

Scientists might just have discovered a groundbreaking new form of treatment for Parkinson's disease and potentially other cognitive health issues too, allowing the brain to be 'brought back to life' thanks to the drug.
As it is our body's central hub, any illnesses or diseases that affect are brain are always going to cause worry, yet they appear to prove the most challenging for scientists and doctors to combat despite advances in medical science.
Certain studies have reached 'eureka moments' where aspirin can be used to treat certain forms of brain cancer, and many are aware of the strange yet legitimate connections between certain daily behaviors and issues later in life.
However, this new research might not only help treat Parkinson's disease, but it signs have shown its capacity to reverse the effects and hypothetically rejuvenate the brain to an earlier and healthier state.
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As reported by ScienceDaily, a new study published in the academic journal Science Signaling has proposed that a drug designed the limit the spread of a certain key enzyme inside the brain could help fight against the effects of Parkinson's disease.
Using a drug named MLi-2, the aim is to target and inhibit the production of the enzyme LRRK2 inside the brain, which is heavily linked to the deteriorating long term effects of Parkinson's.
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The study so far has been conducted on mice who have been genetically modified with over active LRRK2 enzymes, which are then treated with this new inhibitor to test whether it can work.
Over the course of three months not only did the negative effects produced by the LRRK2 enzyme stop, but the mice's brains also showed signs of regenerating the already damaged areas, effectively reversing the effects of the disease and bringing the brain back to life.
"These findings suggest that it might be possible to improve, not just stabilize, the condition of patients with Parkinson's disease," outlined Suzanne Pfeffer, one of the study's co-authors and the Emma Pfeiffer Merner Profesor in Medical Sciences at Stanford University.
"We're so excited about these findings," Pfeffer added. "They suggest this approach has great promise to help patients in terms of restoring neuronal activity in this brain circuit. There are multiple LRRK2 inhibitor clinical trials underway, and our hope is that these findings in mice will hold true for patients in the future."
In terms of the drug itself, MLi-2, as mentioned, inhibits the brain's overproduction of the leucine-rich repeat kinase 2 (LRRK2) enzyme, which is the primary cause behind at least 25% of Parkinson's disease cases.
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When interacting with your brain, LRRK2 causes the cells to lose their primary cilia, which is effectively their 'antenna' that they use to communicate with other parts of the brain.
This is worrying enough on its own, but is especially destructive in the event when dopamine neurons become stressed and release a signal called a 'sonic hedgehog'.
Healthy brains produce neuroprotective factor proteins, which shield your cells and prevent them from dying, but this is prevented from happening when certain striatal cells have been affected by overactive LRRK2 enzymes and have lost their primary cilia, causing increasing amounts of brain cells to die over time.
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What the drug also showed the capacity to do was to regrow previously damaged primary cilia in cells, effectively restoring communication throughout the brain and mitigating the effect and risk of sonic hedgehog signals throughout the brain.
While the signs of Parkinson's can be spotted as early as 15 years before patients develop the tremor that many associate with the disease, this provides a promising sign for cases that doctors can't quite catch that early on, and could be life saving if it is as effective in humans as it has been in mice.