The Patient Researcher with Parkinson’s Disease

Dr Albert F Wright
The Patient Researcher

Learning the truth about Parkinson’s Disease

I was diagnosed with Parkinson’s disease in 2018, but had many of its invisible but debilitating non-motor symptoms for years before that. These included acute fatigue, daytime sleepiness, poor sleep with vivid dreams, confusion, balance problems and severe urinary urgency.

I was told that the causes of Parkinson’s disease were “unknown”. “Unknown to whom?” I thought. Certainly not to the most advanced researchers who I was able to contact. They shared the growing consensus that a combination of oxidative stress and mitochondrial dysfunction in neurons, were the most likely causes of the progression of Parkinson’s disease. Mitochondria are the organs that supply energy to all cells including neurons. When mitochondria in neurons do not function properly, the more distant axons of neurons suffer from energy starvation and slowly die back. This leads to a reduction of the density of the dopamine neuron network and dopamine deficiency in the regions concerned, particularly the striatum.

The cascade of events leading to neuron loss

In healthy people, a signalling protein called Nrf2 (nuclear factor erythroid-2-related factor 2), controls oxidative stress and mitochondrial function by activating the expression of hundreds of genes which release antioxidant molecules and enzymes to rapidly neutralise oxidizing molecules and free radicals (also called Reactive Oxygen Species or ROS). With increasing age, the activity of Nrf2 declines which increases oxidative stress. This leaves some types of neurons, especially those that produce dopamine, particularly susceptible to damage. Fortunately, astrocytes control Nrf2 activity, mitochondrial quality control and general housekeeping for neurons. The problem therefore comes down to making sure that Nrf2 in astrocytes is fully activated.

The Keap1/Nrf2/ARE pathway for antioxidant gene expression.

One of the best and most easily available activators of Nrf2 is sulforaphane, a molecule that can be made from broccoli seeds. Sulforaphane increases the activity of Nrf2 which in turn reduces oxidative stress and improves mitochondrial function in neurons. However, sulforaphane is unstable and must be consumed within a few hours of being made. The choice of broccoli seeds and particularly the preparation method are both critical to getting a good yield of sulforaphane. In 2022, after 3 years of research, I was able to finalise the method of preparation of a highly-reproducible, standardized Broccoli Seed Tea (BST).

The chain of reactions leading to the synthesis of sulforaphane from Glucoraphanin

Over this period of development, I was able to manage severity of my non-motor symptoms the point of total remission by consuming Broccoli Seed Tea. Consequently, despite having Parkinson’s for more than 5 years, I still enjoy excellent quality of life and have retained my full capacity to continue with my research.

Several other People with Parkinson’s with whom I shared the method have also observed rapid and concomitant attenuation of a wide range of non-motor symptoms. From a theoretical standpoint, this observation supports the hypothesis that non-motor symptoms are directly caused by oxidative stress and mitochondrial dysfunction in dopaminergic neurons.

Observations of preferential attenuation of non-motor symptoms following the ingestion of Broccoli Seed Tea.

Broccoli Seed Tea does not have the same impact on motor symptoms. The most widely accepted hypothesis is that motor symptoms occur after a long period of dopamine depletion in specific regions of the brain reduces their capacity to function properly. To work around this, neurons make new connections and form clusters of neurons which operate in a synchronized manner rather than individually. At rest, they all fire together at their own natural frequency, for example, at 3 – 8 Hz for clusters that cause tremor. Other clusters have higher frequency ranges and are associated with slowness and stiffness. Treating this aspect of Parkinson’s disease is discussed in a separate section called “Vibrotactile stimulation to reduce motor symptoms of Parkinson’s disease”.

To request privileged access to this research please use the form on the contacts page.

Dr Albert F Wright

3 thoughts on “The Patient Researcher with Parkinson’s Disease”

  1. What is a source for making broccoli tea. Could honey be added without lowering the effectiveness for Parkinson’s fatigue.


  2. I really appreciate the grit you have shown, for yourself and others, by taking arms against PD in a sea of troubles. A thought for you Dr Wright. One of the things that has been confusing to me about dopamine (DA) treatment was the specific nature of the response to dopamine (ok, L dopa). It indeed makes sense that too much DA from oral administration could cause dyskinesia because of muscle activity in response to the neurotransmitter. But shouldn’t that also occur per se when any dopamine is ingested? Some aberrant responses to DA treatment might be anticipated since DA is involved in so many aspects of motion, balance etc. There are some excellent thoughts that dopamine may be involved in more complex ways than the old concept of neurotransmitter action, but another possibility might be inherent in the hypothesis you posted here. That is, what if the need for 60 to 70 percent cell death in the substantia nigra pars compacta before PD symptoms are seen is not exact. What if the dopamine producing cells have indeed been compromised for production of dopamine but are still alive (or at least in a functional condition) whereby they might be able to produce DA if their mitochondria were again active. That would account for things like dopamine reuptake being the mode of action for the modulation provided by dopamine in the blood stream so that timing and function of particular movements could be provided by dopamine treatment but also would provide a methodology for mode of action of your treatment. Motor symptom improvement to the treatment might not occur as quickly as non-motor because a greater complexity in the coordination needed for motor actions. That is to say, that the 6 week response time for fatigue, motivation (and pain?) symptom relief might be seen in motor conditions after longer treatment with sulforaphane.


  3. Is your reference “Vibrotactile stimulation to reduce motor symptoms of Parkinson’s disease”
    the article “Focused Vibrotactile Stimulation with Cueing Effect on Freezing of Gait in Parkinson’s Disease: Two Case Reports
    Xiu Sheng Tan, 1 , 2 Floyd Pierres, 2 , 3 Alex Dallman-Porter, 2 William Hardie-Brown, 2 and Kyum-Yil Kwon”? If so, you might be interested in a glove being developed and tested at Stanford University.


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