Category - Getting the Knowledge

Main section – PD Knowledge

A-B-C of PD – Glossary of Terms

At Spotlight YOPD, we believe that knowledge is power and would like all Parkies to be in a position to make informed decisions as to their health and wellbeing. While a cure may still be proving itself elusive, there is much that the individual can do to manage their own symptoms and improve their quality of life.

We know that one size does not fit all – so urge Parkies to work collaboratively with their neurologist, PD nurses and fellow Parkies to find out what works for them. Ask questions, make notes, keep a diary, track your good days and bad, look for patterns – help find the solutions to your specific problems and manage your PD and your life better.

We want this site to be as user-friendly as possible and have tried to keep to plain English. However, there are some biological and medical terms without a layman’s alternative. We have included them in the glossary below – along with other words that may be relevant to PD.

Remember PD – is a very individual condition – so symptoms listed may not affect everyone diagnosed. Similarly, what works well for one person in managing their symptoms may not work for someone else.

Please email us with suggested addition and/or corrections.

For a website and charity that’s all about Parkies helping themselves, apathy – a side effect of the condition is a tricky non-motor symptom to cover off. In fact, we’re not sure we can be bothered…
Just kidding – apathy is defined as a lack of interest, emotion and motivation. Common in patients with stroke, Parkinson’s disease (PD), traumatic brain injury, Alzheimer’s disease (AD) and depression.
There’s little info out there specific to Young Onset and apathy. It tends to sit alongside fatigue and depression and can be tricky to differentiate. We know PD is caused by reduced dopamine – the chemical that makes us strive to achieve.
Also known as ‘Eggplant’, it is part of the ‘nightshade’ family – along with potatoes, peppers and tomatoes – and contains nicotine, thought to be beneficial in alleviating PD symptoms. A Mediterranean diet featuring these vegetables is similarly thought to have a positive effect. However, method of storage, cooking and other factors can hugely impact on their nicotine content.

Science bites are fascinating, but they require a basic knowledge of chemistry and biology to understand how and why R&D (Research & Development) is important to us. Whether is cellular, genetic, microbiological or chemical; we need to know how things work to really grasp it.

All living things are made of cells. For us humans it takes 10 trillion cells to make a working body. They come in a variety of sizes and shapes but it comes down to only really two main types: eukaryotic cells and prokaryotic cells. While prokaryotic are much smaller, there are about 10 to 20 times more of them than eukaryotic cells.

Bacteria are prokaryotic single-celled organisms – good and bad – making us veritable petri-dishes of ‘germs’.Like eukaryotic cells, prokaryotic cells contain DNA, but not in a true nucleus. We cannot live without bacteria.

Eukaryotic Cell Structure

Ribosome (little dots)
Rough endoplasmic reticulum
Golgi apparatus (or “Golgi body”)
Smooth endoplasmic reticulum
Cell membrane*fluid that contains organelles, comprising the cytoplasm.

Prokaryote Cell Structure

As you can see, prokaryotic cells are a lot simpler than eukaryotic cells.

Generally  considered the bad guy in a PD diet.
Dopamine Agonist
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Recent research has found that estrogens may protect the nigrostriatal dopaminergic pathway affected in PD. A chemical present in both sexes, there have been anecdotal accounts from YOPD women that just prior to and during their monthly period their PD symptoms become more pronounced – which coincides with the natural drop in estrogen.
Levodopa or L-dopa
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One the more bonkers revelations about PD is that smokers don’t tend to get it. This has led to subsequent mixed research into the use of nicotine patches and consumption of vegetables from the nightshade family.
The nightshade family of plants includes tomatoes, potatoes, peppers and aubergines. All contain nicotine and are allegedly beneficial in alleviating PD symptoms.
On-off effect
Side-effect of levodopa. Parkie can suddenly freeze, unable to move – as if switched ‘off’.
PD symptom – repetition of a word or syllable.
PD symptom (and beyond) – Tremor, rigidity, bradykinesia, stooped posture and shuffling gait – all associated with PD but also symptomatic of striatonigral degeneration, and a reversible condition induced by certain drugs (including those used to treat schizophrenia).
Another member of the nightshade family – possibly positive for Parkies.
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Insomnia is often an early symptom pre-diagnosis. Later on the meds can also contribute to sleep problems. The nightmare of a list includes: excessive daytime sleepiness/fatigue, vivid dreams/nightmares, sleep attacks (a sudden involuntary episode of sleep), REM sleep behavior disorder (acting out dreams during sleep), periodic leg movement disorder (PLMD), restless legs syndrome (RLS), sleep apnea, and nocturia (frequent night-time urination).
Another member of the nightshade family – containing nicotine. Unripened green tomatoes contain considerably more than red.


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The MS drug and its promise for Parkinson’s

Some in the world of Parkinson’s may have heard about the possibility of a drug currently used for Multiple Sclerosis having another application; in Parkinson’s (PD). Here’s the published report. Lisa Vanderburg  recently spoke with Neuroscientist Dr. Bobby Thomas – the Lead Scientist on the research being done in this area. He’s Associate Professor of the Departments of Pharmacology, Toxicology and NeurologyMedical College of Georgia, Augusta University; his (et al) results are very promising for PD. Hopefully this will explain why.

DMF (dimethylfumarate) is an FDA-approved drug used in the treatment of MS (multiple sclerosis). It’s the metabolite part of DMF that’s the focus of attention here; the active metabolized bit. Rather like L-Dopa contains an active metabolite to transition into much-needed dopamine in Parkinson’s, it is a process… a chain of events that lead to the best possible effect.But like L-Dopa, introducing pharmaceuticals can often lead to unwanted side-effects. In the process of metabolisation we have to – basically – persuade the brain that what’s being introduced has a plausible function. However, our brains are pretty savvy… We need to think of all products and processes in our brain like an ever-moving conveyor belt of evolving motion; each stage needs to do its part to create the next step. In a normal state of affairs, the metabolite MMF (monomethylfumarate) buddy up with DMF for optimum function.Metabolites work as both products of and intermediates (precursors) to metabolism. As always, crossing the BBB (blood/brain barrier) is a costly and difficult business, so we have to trick the brain into accepting this mimic; that creates a pay-back. Cause and effect.Now that’s all very science-y, so let me draw you and analogy: Dr. Temple Grandin, Professor of Animal Science at Colorado State University has spent the last 30 years re-vamping slaughter house techniques. Why? Because she was diagnosed as Autistic and that ‘disability’ transformed her abilities to see what others could not: the unnecessary suffering of our livestock. Spending years observing and living with the animals led to one of her many achievements; she developed a process to lead bovines to their inevitable end that was not only much more humane, but prevented the animals from releasing adrenaline and cortisol hormones to flood their muscles as a result of panic and stress.She saw a broken system (think: Brain), and fixed it with an ingenious solution… By creating a looping walkway that not only hid the animals from each other, but it wound round (as an animal would naturally do), gently picking them up with a conveyor belt from under their flanks so that, as they arrived to the stun-gun the chance of a near-miss or worse was significantly lessened – and the animal behind didn’t see what was happening.With the idea of process rather than mere static ‘function’ established, let’s move on.Researchers led by Dr. Thomas at the prestigious Medical College of Georgia’s Augusta University have found that the metabolite ends of the oral drug DMF, as well as MMF, both increase the activity of a protein called Nrf2.This is a BIG discovery, and here’s why: Nrf2 is a major player in cellular defence from oxidation, free-radicals and inflammation, and that’s what keeps coming up as a leading factor in degenerative and neurological disease. As I mentioned before, the last thing we want unchecked in our brains is oxygen. It’s toxic as all hell when it is not contained solely at a cellular level as fuel. It comes up time and again in Parkinson’s as the crucial cause for this catastrophic disease.

The downside of DMF as a ‘parent drug’ treatment is its side-effects. These can be pretty hellacious; anything from ‘flushing, diarrhoea, nausea, vomiting, abdominal pain and the brain infection encephalopathy’ said Dr. Thomas, corresponding author of the study in The Journal of Neuroscience. Dr. Morgan points out that ‘the gastrointestinal side effects can exacerbate some problems patients with Parkinson’s already experience’. As I know full well the ravages to the autonomic system in PD in my own husband, I get it that Parkinson’s causes nerve cell death in the gastrointestinal tract and related problems such as severe constipation.But you can’t throw the baby out with the bath water. In this case, what they’re after is the increased production of that super-scrubber deoxygenating Nrf2 protein that both DMF and MMF afford. Nrf2 is a natural protective mechanism we have for oxidative stress. It is also the declining activity of the Nrf2 pathway that is found in both MS and PD – the link between these diseases. Interesting, eh?Certainly in Parkinson’s, once you realize you have it; the horse has bolted, Elvis has left the building and all hell has broken out because, as Dr. Morgan says, “by the time they seek medical care, patients may have lost 30-50 percent of their dopaminergic neutrons.”I have rated this as eight out of ten dopamine production-marbles in the past, based on the work of Bernheimer and colleagues, which was later contested. It depends on what area of the brain you’re talking about, and really; it’s moot – you’ve lost too much by then. More about that in a minute….Here’s a good paper – if you want to see how complicated the matter truly is.


Dopamine-producing neurons are located in that iddy-biddy part of the brain called the substantia nigra.

Dopamine-producing neurons are located in that iddy-biddy part of the brain called the substantia nigra. “Even in the absence of disease, making dopamine is a stressful job for these neurons that makes them generally more fragile and actually results in oxidative stress, even in a healthy scenario,” Dr. Morgan said. “To make a difficult situation worse, increased oxidative stress can make dopamine toxic to neutrons,” he added.Moreover, Dr. Thomas stated, “To increase Nrf2 activity, the parent drug DMF also appears to first make bad matters worse. DMF increases oxidative stress by depleting the natural antioxidant – glutathione. It also reduces the power of cell powerhouses – called mitochondria – by limiting their ability to use oxygen and glucose to make energy leading to reduced viability of dopamine-producing cells.”Now I know glutathione – my hubby had many IV pushes of the antioxidant as well as phosphatidylcholine, a lecithin (to theoretically break down long trains of trans-fatty acids in the brain). These didn’t work – that comes down to the problems of introducing a mimic again.So, how to get round this problem of side-effects and still keep the Nrf2? It’s actually brilliant; our prestigious researchers switched to MMF… clever dudes. MMF is not quite as potent as the parent drug (DMF) in increasing Nrf2 activity, but (yup, it’s a BIG but) – no side effects.Conversely, the metabolite MMF appears to more directly activate Nrf2, and does not deplete glutathione and improves mitochondrial function, brain cell studies showed. While the parent drug DMF ultimately produces a higher Nrf2 activation, the researchers found the MMF effect was sufficient to stop the dramatic neuron loss in the animal model.Both DMF and MMF slowed neuron loss to a more normal level, and the neurons that survived continued to make dopamine. Inflammation and oxidative stress levels also were significantly reduced, the researchers said.Furthermore, the new study indicates that MMF action is sufficient to dramatically slow the loss of dopamine-producing neurons as well as the parent drug, in an animal model of Parkinson’s.The really relevant bit for those with Parkinson’s:Because DMF is already an FDA-approved drug,we won’t have to wait around for decades – it’s more a matter of re-classification. As DMF’s active metabolite is MMF, both are basically interchangeable by the process of esterase, making them interdependant. What that ultimately means is human trials could start in as little as two to three years. Clinical trials are in planning stage in the UK (because EVERYBODY does that – the US takes too long, even in reassigning drugs).In mid-April I heard from Laurie Hawkins about a small (38 peeps – 29 with PD) trial in Australia for the World’s first blood test for Parkinson’s, led by Professor of Microbiology, Paul Fisher. Now, with MJFF funding, La Trobe University will trial 100 peeps (70 with PD, control of 30).My first thoughts were along the lines of ‘who on earth would wanna know?’ That’s because, since discovery nearly 200 years ago, all we have is L-Dopa and DBS. If you’re not able to have DBS (or elect not to), your PD life is going to be pretty miserable. I have to say here that I’ve recently come under some flak from people with Parkinson’s, who tell me that a good advocate is one that sugar-coats the truth. I don’t agree. I think it rather insulting to those who want the truth.PD will be a long road… downhill all the way. The public needs to be aware just how little we have advanced after two centuries. We need their outrage. The only way I have gotten anywhere (like talking to Dr. Thomas) is because I tell it how it is.In conclusion, if you tie this blood test with what these extraordinary guys from Augusta University are doing, you’ll see the potential for real progress – at the very least for those pre-Parkinson’s. In a touching eulogy to Muhammad Ali, Dr. Peter F. Buckley, Dean of Augusta University, Georgia, adds his weight to this achievement.Many thanks to Dr. Bobby Thomas for helping me understand this very important discovery. We live in hope. 

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