Parkinson's disease

At present there is no cure for Parkinson’s disease, but researchers and scientists at Brain Research New Zealand and throughout the world are steadily making advancements in understanding the condition, its causes, and how to best treat it. Over four people million in the world have Parkinson's - more than those affected by multiple sclerosis, muscular dystrophy and Motor Neuron combined. The average age of diagnosis is 59, but it can also occur in younger people in their 20's, 30's and 40's. Read on to discover some of our current research into Parkinson's disease.  


What are the warning signs of dementia in Parkinson's disease?


In a cruel double-blow, most patients with Parkinson's disease also develop dementia over time.

What remains a mystery is the speed at which this happens.

Because the process is highly variable, making accurate predictions has been a tricky challenge for researchers.

For one team of Kiwi scientists, trying to get answers involved following the cases of 121 Parkinson's sufferers and crunching four years of longitudinal data.

Ultimately, they were able to pinpoint a specific criterion for mild cognitive impairment - a pre-dementia state - that yielded the highest risk of developing dementia within the period.

The team - Professor Tim Anderson, Dr Tracy Melzer, John Dalrymple-Alford and PhD student Kyla-Louise Horne - assessed the patients using 24 separate tests, searching for problems in the five different categories of cognitive impairment: memory, attention, decision-making, language, and awareness of space.

They discovered the best pointer to a patient with Parkinson's developing dementia in the following four years was that person failing two or more tests in any of the five categories. 

The team believes their findings will help improve patient management and prognosis - and even lead to new therapeutic interventions targeted for patients at imminent risk of dementia.

Originally published in the NZ Herald 'Brain Detectives: 10 Amazing Kiwi Insights'


Different PD-MCI criteria and risk of dementia in Parkinson’s disease: 4-year longitudinal study. Kyla-Louise Wood,Daniel J Myall, Leslie Livingston, Tracy R Melzer, Toni L Pitcher, Michael R MacAskill, Gert J Geurtsen, Tim J Anderson, & John C Dalrymple-Alford


BRNZ_Alzheimers Parkinsons

Alzheimer's, Parkinson's and the inner ear


Balance-related organs in our inner ear, called the "vestibular system", have been associated with higher cognitive functions like learning and memory.

Discovering more about these intriguing links has proved tough, however, simply because it has been difficult for scientists to navigate through the inner ear's bony labyrinth.

A new rat-based study focused on a surgical approach that effectively activates the individual sensors and nerves located in the inner ear could pave the way for an incredible new type of prostheses.

Such tiny devices - similar to cochlear implants to treat hearing loss - could potentially enhance memory and improve balance for Alzheimer's and Parkinson's disease patients and ageing populations.

Professor Paul Smith, who has been researching the concept with fellow Brain Research New Zealand principal investigator Dr Yiwen Zheng as part of a global collaboration, says the first "artificial vestibular systems" had been implanted in the past few years.

They worked by sensing head movement and electrically stimulating the nerves that normally supply nerves to the vestibular sensory receptors to provide the brain with the self-motion information it needed.

Over the past decade, it had become apparent this information - the result of a sensory system more than 500 million years old - was important for the "spatial memory" that tells us where we've been.

"We use vision and other sensory information as well, but the vestibular system is much older in evolutionary terms and therefore is a pivotal source of information for orientation in the world," Smith says.

Previously it was impossible to electrically stimulate specific parts of the system in small research animals like rats but Smith and his colleagues overcame the hurdle.

"We developed a surgical approach to selectively electrically stimulate all of the different receptor groups of the vestibular system in the rat - making it possible to investigate the effects of artificial vestibular stimulation on the brain and better understand the full consequences of vestibular implants for human patients."

Originally published in the NZ Herald 'Brain Detectives: 10 Amazing Kiwi Insights'


Anatomy and surgical approach of rat's vestibular sensors and nerves. Hitier M1, Sato G2, Zhang YF3, Zheng Y3, Besnard S4, Smith PF3, Curthoys IS5. J Neurosci Methods. 2016 Sep 1;270:1-8. doi: 10.1016/j.jneumeth.2016.05.013. Epub 2016 May 19.








Why genetics could mean individualised treatment for people with Parkinson's disease


Brain Research New Zealand Principal Investigators Professor John Dalrymple-Alford, Professor Tim Anderson and Daniel Myall are part of an international group of scientists exploring the curious connection between the processes that cause Parkinson's disease and a gene known as SNCA.

The SNCA gene codes for a protein normally associated with healthy brain function.

Unfortunately, this protein sometimes misbehaves, forms unwanted aggregates and causes brain cells to fail and eventually die.

The result is Parkinson's disease.

The spread of the malformed protein across the brain also leads to progressive loss of many brain functions and even to dementia.

A global collaboration has already found subtle variations within the molecular structure of the SNCA gene were linked with dementia in patients with Parkinson's.

Other variations were also linked, but more commonly in patients without additional cognitive impairment.

These insights came from looking at the fine detail of the entire SNCA gene and how it varied across people with Parkinson's disease.

Professor John Dalrymple-Alford and Professor Tim Anderson are part of a global study and an international effort to learn whether these genetic analyses can be combined with other clinical data.

Their new aim is to develop something that could provide accurate and individualised "risk scores" for future problems for those diagnosed with Parkinson's.

This could give doctors more information to discuss with patients when looking at treatment options, along with a better selection of participants for new drug trials.

Originally published in the NZ Herald 'Brain Detectives: 10 Amazing Kiwi Insights'


α-synuclein genetic variability: A biomarker for dementia in Parkinson disease.

Guella I, Evans DM, Szu-Tu C, Nosova E, Bortnick SF; SNCA Cognition Study Group, Goldman JG, Dalrymple-Alford JC, Geurtsen GJ, Litvan I, Ross OA, Middleton LT, Parkkinen L, Farrer MJ.  Ann Neurol. 2016 Jun;79(6):991-9. doi: 10.1002/ana.24664. Epub 2016 May 5.

Optogenetics lights the way forward for Parkinson’s patients

Dr Parr-Brownlie is a Neurophysiologist and lecturer working for Brain Research New Zealand (BRNZ). She’s one of small group of researchers in the world dedicated to researching optogenetics – which uses light to control cells in living tissue, typically neurons, that have been genetically modified to express light-sensitive ion channels. Essentially living tissues are controlled on a molecular level using light – something unfathomable yet amazing.

In collaboration with BRNZ colleague Dr Stephanie Hughes, Dr Parr-Brownlie’s research focuses on the neural mechanisms that underlie voluntary movements and the movement deficits of Parkinson’s disease.

“It’s great to bounce ideas off each other. We have such different backgrounds and that makes us a strong team” she says.

Ultimately, Louise hopes that one day the activation or silencing of cells with the use of optogenetics could restore movement or settle down involuntary movement in patients with Parkinson’s disease.

 “What we’ve found already is that there are probably better ways to stimulate the brain compared to the deep brain stimulation that’s currently used for patients,” Dr Parr-Brownlie explains. “The stimulation currently used is electrical stimulation that’s applied in a very regular pattern, so it’s almost like a clock ticking.

“Brain cells don’t work like that, they often have little patterns of activity, so what we did is we replayed patterns of activity in the brain and used optogenetic stimulation.

The technology is very specific, you can choose to stimulate one type of brain cell and not the other. We hope that we have fewer side effects as a result of using optogenetic stimulation. We hope in the future to do further studies to consolidate our findings and to take this technology to the human brain and for Parkinson’s patients,” she says.

With leaders of neuroscience in their midst like Dr Parr-Brownlie, Brain Research New Zealand is poised and ready to make significant contributions to the global fight against neurodegenerative diseases.

Targeting Drug Delivery within the brain - Building a system for human application

Associate Professor John Reynolds, a Brain Research New Zealand Principal Investigator located at the University of Otago has gained a 2016 research grant worth $4,859,256 over four years. 

“This programme will stimulate a high-profit, technology-based medical device and consumables industry in New Zealand for the treatment of brain disorders.

The technology will incorporate a delivery system for brain chemicals together with a controller that will manage timing and dose. Drug delivery will mimic natural release of neurochemicals in the brain, reducing side effects and improving treatment efficacy.

The new technology will enable smart, non-invasive drug delivery that will revolutionise the treatment of disorders with underlying neurochemical imbalances.

The team wish to expand their device concept into a drug delivery platform that will first be applied to better treat Parkinson’s disease (PD), preventing, and in theory reversing, current treatment-induced side effects in humans. The technology could also target chemotherapy to brain cancers and arrest epileptic seizures at the site of origin.”


What is Parkinson's disease?  

Parkinson’s disease is a neuro-degenerative condition which occurs when the brain produces insufficient quantities of the chemical dopamine. This causes motor symptoms such as stiffness, slowness of movement and tremor, and non-motor symptoms such as depression, anxiety, lack of smell, fatigue and trouble swallowing. Each person with Parkinson’s will experience a different number and combination of these symptoms.

How will it affect my life?

Parkinson’s is not fatal, and often takes years to progress. Parkinson’s is different for everyone, but often with good managementincluding exercise and medication, Parkinson’s can have little effect on life expectancy. It will however, require lifestyle changes for your individual needs.

What are my treatment options?

A combination of exercise and drug treatments can be used to help control the symptoms of Parkinson’s.

What part does surgical treatment play in Parkinson's?

Surgery is not suitable for everyone with Parkinson's. It is usually advised when medication is not of assistance or when there have been severe side effects from medication.

What support can my family and I receive?

Parkinson’s New Zealand provides support and information to people with Parkinson’s, their carers, families and health professionals. We provide help in a variety of ways:

Divisions and Community Educators

Parkinson’s New Zealand has 20 divisions and branches nationwide, as well as a National Office. Each division provides one or moreCommunity Educators who are trained to help you and your family with your Parkinson’s journey. They can provide support, information and advocacy through home visits or telephone calls.

Community Educators and divisions can also provide services to your carers and families, and can meet with your family to answer any questions.

Awe-inspiring, witty and powerful boxing champion Muhammed Ali and his battle with Parkinson’s disease


Boxing legend Muhammad Ali died in 2016 at age 74, after a lengthy battle against Parkinson's disease. Ali was diagnosed with the disease in 1984, three years following his retirement.

In 1980, ten weeks before Ali's match against Larry Holmes, a team of doctors at the Mayo Clinic submitted a medical report to the Nevada State Athletic Commission showing that there was a small hole in the outer layer of Ali’s brain. They noted that the legendary boxer reported a tingling sensation in his hands and slurred speech. He retired permanently in 1981.

Ali was instrumental in raising awareness of Parkinson's Disease. In 1997, he and his wife co-founded the Muhammad Ali Parkinson Center in Phoenix, Arizona, to provide comprehensive care for those living with the disease.  

Did boxing cause Muhammad Ali’s Parkinson’s disease?

Muhammad Ali lived with Parkinson's disease for three decades before his death on Friday (June 3) at the age of 74, and many have wondered whether Ali's boxing career caused him to develop the neurological disorder.

Although it's likely that frequent head injuries played a role in the boxer's Parkinson's disease, certain genes may have also increased his susceptibility to the disease.

In patients with Parkinson's disease, the brain cells that produce a chemical called dopamine start to die off. Because dopamine is important for the control of muscle movement, Parkinson's patients experience symptoms such as tremors, slowed movements and muscle stiffness.

In most cases, the exact reason that the dopamine-producing cells start to die is not known, However certain genes appear to increase people's risk of developing the disease at a relatively young age. For this reason, with the younger onset of Parkinson’s disease, researchers are more suspicious of the involvement of genes.

Still, head trauma has also been linked with Parkinson's disease. In a 2013 review study, researchers found that people with head trauma that resulted in a concussion were 57 percent more likely to develop Parkinson's disease, than people who never experienced such head trauma.

Head injuries can cause inflammation in the brain, which may lead to changes in cells and brain structures that contribute to Parkinson's disease.

And injuries that specifically damage the part of the brain that contains dopamine-producing cells, called the substantia nigra, can also lead to Parkinson's disease.