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Located at SFU鈥檚 medical imaging facility in Surrey Memorial Hospital, the MEG maps brain activity in real time, providing high-precision, non-invasive imaging for both research and surgical planning. It allows researchers to detect and study the magnetic fields produced by the brain鈥檚 electrical activity.

Wiesman鈥檚 recent study, , explores why dopamine replacement therapy (DRT) is more effective for some PD patients than others.

Dopamine deficiency plays a key role in the development of PD, contributing to motor and cognitive symptoms. While DRT is commonly used to relieve these symptoms, in some patients it may activate chemical pathways in the brain in ways that reduce its effectiveness.

By observing patients鈥� brain activity before and after medication, and mapping dopamine receptors and transporters in the cortex, Wiesman and his colleagues at Karolinska Institute in Sweden examined changes in brain rhythms in dopamine-rich regions. They found that DRT increased fast patterns of rhythmic activity in cortical areas with high dopamine density in some patients, but not others.

In certain PD patients, the medication appeared to over-activate cortical dopamine systems, disrupting normal brain rhythms and diminishing the benefits of treatment. The findings help explain why patients respond differently to DRT and may also inform research into individual variability in other brain disorders.

We spoke with Professor Wiesman about his research.

Can you walk us through what you observed when dopamine therapy worked鈥攁nd when it didn鈥檛?

For pretty much every person living with Parkinson鈥檚 disease, dopamine therapies work! In fact, whether someone benefits from these medications is even used in diagnosing the disease. The question is why it works less well for some folks compared to others. We found that in some people dopamine therapies can activate parts of the brain that are not meant to be treated with these medications, and this limited how helpful they were for treating symptoms.

What appears to be happening in patients who are less responsive to dopamine replacement therapy?

We think that these less-responsive patients are having more 鈥渙ff-target鈥� effects of dopamine therapies. This doesn鈥檛 mean that the medications aren鈥檛 activating the right dopamine pathways, but rather that they are also activating the wrong ones at the same time, masking what could otherwise be even better clinical effects.

After observing the affects of DRT in real time, do you have ideas for improving PD treatment?

We are hoping that this method for real-time measurement of brain responses to dopamine therapies could help guide prescribing. If a person is initially showing stronger 鈥渙ff-target鈥� brain activations from the medications, this could be used to change their dose or even consider additional medications to help personalize treatment and maximize the benefit that each patient gets from DRT. In the longer-term, we also think that this could be useful for developing new drugs that activate these 鈥渙ff-target鈥� pathways less.

How do these findings relate to other brain disorders?

It is really difficult to guide drugs into specific areas of the brain, and so there are lots of medications that have 鈥渙ff-target鈥� effects on brain signalling. Our approach isn鈥檛 limited to studying dopamine therapies in people living with PD, and could be adapted to other neurological disorders like Alzheimer鈥檚 disease to understand why some folks respond better to their medications than others.

How fascinating is it to look inside the human brain, learn how it works and then be able to treat problems?

It鈥檚 the coolest part of my job! The idea that we can sit someone in a funny-looking chair and measure how their brain signalling is orchestrating their thoughts, movements, and feelings never fails to amaze me. Being able to then apply this to clinical questions that affect so many people is a privilege that I don鈥檛 take lightly.

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