On April 11, World Parkinson’s Day, we invited Dr. Qiaojie Xiong, author of the article series “Alzheimer’s Disease Explained”, to once again write an article to introduce readers to Parkinson’s disease, a common disease of the elderly, and to compare and analyze the similarities and differences of the two diseases.
The first time I learned about Parkinson’s disease was when Deng Xiaoping died. I was a high school student at the time, and the disease had rarely been reported before.
In 2012, Sergey Brin, one of the founders of Google, donated a large sum of money to Parkinson’s disease research institutes in the hope of solving the problem before he developed the disease himself, because his mother had the disease and he had a high chance of developing it ($130 million from 2005 to 2012).
The total amount donated between 2005 and 2012 was $132 million!) Parkinson’s Disease
Parkinson’s Disease and Parkinsonism
The name Parkinson’s Disease comes from the English physician James Parkinson, who first detailed six cases of Parkinson’s disease in 1817.
He first reported the symptoms and progression of the disease in detail in six cases in 1817, and his birthday, April 11, has been named World Parkinson’s Day.
Parkinsonism is a clinical concept used to define a class of motor syndromes, and is commonly translated as Parkinson’s disease in China. It mainly includes trembling at rest, slow movement, stiffness of limbs and trunk, and inability to maintain a stable posture. Parkinson’s disease (PD), which we often hear about, is the most common type of this syndrome.
In addition to tremors, patients may also have other behavioral manifestations.
The patient may have a stiff facial expression (mask face), difficulty blinking and swallowing, weakness in speech, dizziness, and shuffling feet. The patient’s writing is usually small.
Although Parkinson’s disease is defined as a motor syndrome, it is often accompanied by psychiatric symptoms such as sleepy nighttime sleep, decreased sense of smell, visual-spatial awareness, attention memory, anxiety and depression.
Who is at risk for Parkinson’s disease?
As we all associate with “tremors,” people with Parkinson’s disease are generally over the age of 60, with only about 10% of cases occurring earlier than age 40. About 1 percent of people aged 60 or older have Parkinson’s disease. However, the youngest known patient was only 18 years old at the time of onset.
However, the youngest known patient was 18 years old at the time of onset. If you notice more than one of these symptoms in yourself or a loved one or friend, see your doctor immediately for a consultation and detailed examination.
Why do you get Parkinson’s disease?
In fact, there is no internationally recognized, uncontroversial research on the exact cause of Parkinson’s disease. Some studies indicate that brain injury, as well as pesticide contamination, increase the chance of developing the disease. But overall, we don’t know exactly how the disease occurs.
One thing is for sure, family history increases the chance of the disease.
Current research suggests that more than five percent of patients carry the mutated gene in question. Today, seven genes have been found to be associated with Parkinson’s disease, with the highest risk being the mutated LRRK2 carried by Google founder Sergey Brin and his mother. If you have an immediate family member who has been diagnosed with Parkinson’s disease, you can have your personal genome sequenced to check if you carry any of these known risk genetic mutations.
It is now well established that the main pathological feature of Parkinson’s disease is the death of dopamine neurons in one part of the brain. The causes and mechanisms of dopamine neuron death are still being studied.
Is Parkinson’s disease curable?
Unfortunately, as with many other neurodegenerative diseases, there is no cure for Parkinson’s disease.
Available medications, surgery and combination therapy can provide some relief, but cannot reverse or stop the progression of the disease. In principle, the currently effective treatments (and by ‘treatments’, I mean symptom relief) are designed to directly and indirectly increase dopamine in the brain or to replace it with increased dopamine function to compensate for the loss of dopamine neurons from death.
Early treatments for Parkinson’s disease include physical therapy and exercise therapy, which aim to increase dopamine secretion by stimulating the dopamine neurons remaining in the substantia nigra through massage or facial expression exercises, joint movement, and balancing.
In recent decades, there are various drugs for Parkinson’s disease, most of which are also based on the principle of directly or indirectly increasing dopamine function in the brain.
Levodopa (Levodopa) and compounded levodopa are currently the most effective drugs for Parkinson’s. Other drugs include some inhibitors of specific enzymes and some anticholinergic drugs, among others.
Each type of medication has different efficacy and side effects for patients with different conditions. What medications to use and how to take them require the advice and guidance of a medical professional after a systematic diagnosis.
Parkinson’s disease and Alzheimer’s disease
As mentioned earlier, Parkinson’s disease is a disease caused by the death of neurons in the brain. Similarly, there is Alzheimer’s disease (commonly known as “dementia”). Because of their common characteristics, they are both called “neurodegenerative diseases”. The common understanding is probably “neurological rust disease”. There are many similarities between these two diseases, but they are also very different. A brief comparison is shown in the table below.
Rejuvenating “rusty” nerves
The ultimate direction of treatment for neurodegenerative diseases is to patch up the dead neurons like a patch.
At present, unfortunately, science is unable to reverse the death of neurons or to stop the continued death of residual neurons.
Therefore, the current treatment for both diseases can only relieve some of the symptoms and cannot fundamentally cure or stop the progression of the disease. The various unreliable miracle cures on the Internet can obviously only be seen as a joke.
So, what is the ultimate cure for this “rusty nerve disease”? Naturally, it is to replenish healthy neurons in the diseased or aging brain. How to do it? Theoretically, there are two ways: through external implants, or stimulating the regeneration of nerves inside the brain.
Let’s start with the first method. For Parkinson’s disease, neuron transplantation experiments were tried in animals decades ago, but progress was very slow for various reasons. After all, it is difficult to transplant a finger, let alone transplant the most complex and delicate neurons and neural networks.
In recent years, human stem cell technology has made dramatic fundamental advances. Indefatigable scientists are constantly trying to apply these new technologies day and night.
And then there is the second approach. Activating the regeneration of the brain’s own neurons (adult
neurogenesis), which provides itself with new healthy neurons from inside the diseased brain, is also a direction of research. The human brain is very active in neuronal regeneration during embryonic and infant life, and the brain has a high potential for repair, but as soon as it reaches adulthood, these amazing regenerations stop.
At present, science already knows some molecular mechanisms that promote or hinder neuronal regeneration, and is trying to understand the mystery of brain regeneration in depth. We hope that in the near future, we will be able to find a “magic pill” to rejuvenate the brains of millions of elderly people suffering from “rust disease”!