關於愛，我是個小學生。

As people live longer and the world population grows older, late-onset disorders such as Parkinson’s disease and Alzheimer’s disease will affect more and more individuals. Both of these diseases are neurodegenerative and typically begin late in life, so many people assume that they are related or linked in some way. Let’s take a look at how much truth there is to that idea.

First of all, the two diseases are not related but they do share some similarities. Both Alzheimer’s and Parkinson’s disease have an onset that is late in life, usually after the age of 50. Both diseases are neurodegenerative, meaning that brain cells (neurons) become damaged and die during the course of the disease. They are also both progressive, so they get worse over time. In the late stages of both diseases, the neurodegeneration can ultimately lead to dementia – a severe impairment in memory, judgment, orientation, and executive functioning. Approximately two out of every three dementia cases are caused by Alzheimer’s disease, making it by far the most common cause. Meanwhile, dementia due to Parkinson’s accounts for a much smaller portion of all dementia cases.

Despite all of these similarities, Alzheimer’s and Parkinson’s disease are completely separate illnesses with different mechanisms, symptoms, and treatments. Parkinson’s disease is primarily a movement disorder that can eventually result in memory problems and dementia in about 50% of patients. Many individuals with Parkinson’s will never have memory problems during the course of their illness. On the other hand, Alzheimer’s is primarily a memory disorder that rarely includes any type of movement impairments. While both diseases are progressive and neurodegenerative, their disparate symptoms come from differences in etiology. Parkinson’s disease results from the loss of dopamine-producing neurons in an area of the brain called the substantia nigra. Dopamine is needed in that part of the brain to control movement and coordination, and it is estimated that it takes a 60-80% loss of these dopaminergic neurons before symptoms become outwardly apparent. These symptoms include a resting tremor (shaking at rest), muscle rigidity, slowed movements, and impaired coordination. Since the primary cause for Parkinsonian symptoms is a loss of dopaminergic neurons, approved drug treatments work to increase the amount of dopamine available within the brain. Over time, as the disease progresses, the benefits of the drugs often diminish or become less consistent.

Now with Alzheimer’s disease, the initially affected brain areas are the hippocampus and the entorhinal cortex, which are critical for learning and memory. Therefore it follows that the early symptoms of Alzheimer’s are cognitive in nature. In Alzheimer’s it is the neurotransmitter acetylcholine that is progressively diminished over the course of the disease. This worsening of memory and general intellect can progress and become severe without any effect on the patient’s coordination or movement ability. Since acetylcholine depletion is a root cause for the Alzheimer’s symptoms, a class of drugs called cholinesterase inhibitors (brand names: Aricept, Exelon, Razadyne) has been shown to be effective in slowing cognitive decline by preventing the breakdown of acetylcholine. Essentially they work to maintain the acetylcholine that is present in the brain but they do not prevent the loss of neurons or increase the amount of acetylcholine available. In 2003, the F.D.A. approved another Alzheimer’s drug called Namenda for treating moderate-to-severe cases. This drug works by regulating receptors of yet another neurotransmitter in the brain called glutamate. While pharmacological treatments for both Alzheimer’s and Parkinson’s disease currently work by altering chemicals within the brain, they differ in their mechanisms of action and in their effects on the brain. This is why it is paramount that a proper clinical diagnosis be obtained for individuals at the very onset of noticeable symptoms. With both diseases, drug treatments are most beneficial at combating the early to middle stages of disease.

adapted from an article by dr. eric chang in alz.org