New method found to inhibit Parkinson’s disease

Contrary to earlier discovery that a chemical found in a synthetic opioid, MPTP, induced a form of Parkinson's disease, a new study has found that it is an enzyme in the body that can metabolise compounds formed in the brain from alkaloids causing a neurodegenerative condition in mice.

The study  suggested that the enzyme, mitochondrial CYP2D6, presents a potentially powerful new target for Parkinson's treatment. "Over the past two or three decades, researchers have tried inhibiting the process by they believed MPTP was metabolised, with mixed success," he said.

"We believe that mitochondrial CYP2D6 is the more direct drug target, which might prove better in treating idiopathic Parkinson's disease," added one of the researchers. The study investigated the mechanism of Parkinson's disease when a specific cause cannot be pinpointed.

Previous studies have shown that MPTP and similar toxic compounds induce Parkinson's disease in rodents and primates. The mechanism of action, as scientists understood it, involved the compounds being oxidised to form MPP+, a toxic metabolite.

The enzyme that was believed to be responsible is called monoamine oxidase B (MAO-B), present in the nervous system's glial cells. In that conception of the mechanism, MPP+ was thought to then be transferred to dopamine neurons by dopamine transporter proteins, and, indeed, Parkinson's is characterised by unusually low dopamine levels in the brain.

Researchers have tried to stem the effects of Parkinson's by targeting two players in this presumed pathway, both MAO-B and the dopamine transporter protein, with only mixed success. In earlier work, Avadhani and colleagues had shown that the enzyme CYP2D6, localised to the body's energy factories, the mitochondria, could play a role in metabolising MPTP to MPP+.

In the new investigation, they took a closer look at beta-carbolines and isoquinolines, toxins that resemble MPTP which the body produces from substances found in tobacco smoke, alcohol, and some foods.

They found that, instead of MAO-B, it was mitochondrial CYP2D6 that activate the beta-carbolines and isoquinolines inside the dopamine-producing neurons, rather than the glial cells. This route of activation, in a mouse model, results in neuronal damage and oxidative stress, symptoms akin to Parkinson's. "CYP2D6 is known to play a role in influencing the activity of a number of drugs," said a researcher.

In an attempt to target this pathway, the researchers showed that mice lacking CYP2D6 did not exhibit severe symptoms than mice with the protein did. In addition, an inhibitor of CYP2D6 prevented neuronal damage in the mice.

"The CYP2D6 inhibitor ajmalicine is a member of the reserpine family of alkaloids, found in the plant Rauwolfia serpentine and was long used in India for treating mental illness, such as paranoia and schizophrenia," he said. "Mitochondrial targeting of such compounds is likely to be effective in treating Parkinson's patients, and pursuing that is our future strategy," said the researcher.

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Train your brain to form good habits through repetition

The researchers have created a model which shows that forming good (and bad) habits depends more on how often you perform an action than on how much satisfaction you get from it.

"Psychologists have been trying to understand what drives our habits for over a century, and one of the recurring questions is how much habits are a product of what we want versus what we do," said an Assistant Prof.

"Our model helps to answer that by suggesting that habits themselves are a product of our previous actions, but in certain situations those habits can be supplanted by our desire to get the best outcome," she  added.

For the study, the researchers developed a computer simulation, in which digital rodents were given a choice of two levers, one of which was associated with the chance of getting a reward.

The lever with the reward was the 'correct' one, and the lever without was the 'wrong' one.

The chance of getting a reward was swapped between the two levers, and the simulated rodents were trained to choose the 'correct' one.

When the digital rodents were trained for a short time, they managed to choose the new, 'correct' lever when the chance of a reward was swapped. However, when they were trained extensively on one lever, the digital rats stuck to the 'wrong' lever stubbornly, even when it no longer had the chance for a reward.

The rodents preferred to stick to the repeated action that they were used to, rather than have the chance for a reward.

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Treatment with marijuana compound can reverse memory loss

With increasing age, the quantity of the cannabinoids naturally formed in the brain reduces. When the activity of the cannabinoid system declines, we find rapid ageing in the brain.

 Prolonged low-dose treatment with a marijuana compound may help reverse memory loss and improve cognitive skills, a finding that could pave the way for slowing brain ageing or treating dementia in humans, researchers say. 

 According to the study, the brain ages much faster when mice do not possess any functional receptors for tetrahydrocannabinol, or THC — the chemical responsible for most of marijuana’s psychological effects.

 However, treatment with THC imitates the effect of cannabinoids produced naturally in the body, which fulfill important functions in the brain. 

 “With increasing age, the quantity of the cannabinoids naturally formed in the brain reduces. When the activity of the cannabinoid system declines, we find rapid ageing in the brain,” said Andreas Zimmer, professor at the University of Bonn in Germany. 

 In the study, the researchers administered a small quantity of THC to mice aged two, 12 and 18 months over a period of four weeks.

The results revealed that the cognitive functions of the older mice were just as good as the two-month-old mice.

 “The treatment completely reversed the loss of performance in the old animals. It looked as though the THC treatment turned back the molecular clock,” Zimmer said. 

 As a next step, the researchers want to conduct a clinical trial to investigate whether THC also reverses ageing processes in the brain in humans and can increase cognitive ability. 

Why do people lose memory?

The reasons behind memory loss can be many. Age is one of the major factors. Then there is depression, or other mental problems. Even certain medication can have a side-effect, resulting in memory loss. Stress and anxiety are also factors that can lead to memory loss.

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