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Parkinson’s FAQ’s

Parkinson's primarily affects a region of the midbrain called the substantia nigra. Brain cells in this region produce high concentrations of the neurotransmitter dopamine and help initiate and control voluntary movements. Early-stage Parkinson's patients can also show evidence of the disease in the brainstem. Late-stage Parkinson's patients may show evidence of the disease in the hippocampus, which controls memories, and the cerebral cortex, which controls higher-level thinking and planning.
Parkinson's disease is not a death sentence, and otherwise healthy Parkinson's patients can expect to live a normal lifespan. According to the Parkinson's Foundation, Parkinson's patients tend to die "with the disease rather than of the disease.
Approximately 10% of patients with Parkinson's disease are believed to have inherited genetic forms of the disease. The vast majority of patients do not appear to have any genetic or familial predisposition. Genes that can increase the probability of Parkinson's include SNCA, LRRK2, PARKIN, PINK1, and GBA.
Parkinson's Disease is caused by the loss of neurons in the substantia nigra region of the midbrain. At present, there are no treatments that can restore these cells or their connections. However, several treatments can substitute for the lost cells, at least temporarily. Cells of the substantia nigra produce and release large amounts of the neurotransmitter, dopamine. L-DOPA is a precursor drug that is converted in the brain to dopamine and can restore some lost functions in Parkinson's patients. In addition, the electrical activity of cells in the substantia nigra can be mimicked by sending electrical pulses through thin wires embedded selectively in brain regions where signals from the substantia nigra have been lost.
Patients with Parkinson's Disease can progress over time to dementia that further complicates the usual motor symptoms. In addition, some Parkinson's patients show signs of early dementia at the same time that the typical motor symptoms present. In some patients, the dementia associated with Parkinson's is difficult to distinguish from Alzheimer's Disease. For these reasons, it may be helpful to view Alzheimer's and Parkinson's as two diseases along a spectrum of related diseases, which has been referred to as the Parkinzheimer Spectrum.
Parkinson's Disease appears to have different causes in different people. In approximately 10% of cases, the cause appears to be genetic or familial. Other patients with Parkinson's share a history of repeated head traumas, as seen in boxers and some soldiers. Still other patients appear to show a link to abnormalities in the gut and possibly the bacteria that colonize the gut. Once Parkinson's has been started, it slowly progresses and moves through different regions of the brain including the substantia nigra of the midbrain, which is responsible for the classical motor symptoms of the disease.
Parkinson's symptoms result from the destruction of brain cells (neurons) in the substantia nigra of the midbrain. Since neurons are not naturally replaced after injury or death, these cells and their functions are permanently lost. A cure would require either prevention of neuron cell death or replacement of the lost cells from outside of the body. Prevention may be possible with early detection before most cells have been destroyed. Replacement may be possible one day by either injecting stem cells from other regions of the body or by inducing existing brain cells to replicate and migrate to the substantia nigra. There is considerable interest and activity in both of these areas.
The diagnosis of Parkinson's is currently performed by an experienced professional based mainly on clinical symptoms. Since Parkinson's can resemble other diseases at the early clinical stages, a definitive clinical diagnosis may require multiple visits over a 6 month to 2 year period. In many cases, an experienced physician will treat suspected Parkinson's patients with L-DOPA and look for significant improvement, which strongly supports a definitive diagnosis of Parkinson's. In some cases, a physician may order a radioactive DaT Scan, which looks for loss of dopaminergic neurons in the area of the substantia nigra. DaT Scan changes indicate relatively late stages of disease.
Parkinson's affects the nervous system in several different ways. First, Parkinson's disrupts normal protein metabolism by converting synuclein, an essential protein, into a misfolded prion form, thus reducing the normal cellular activities of synuclein. Second, the misfolded synuclein prions are toxic to the cells and cause irreversible damage and cell death. Third, the synuclein prions can infect other connected neurons leading to extensive cell loss and further spread of the disease. The symptoms of Parkinson's begin to appear only after most of the connected cells in the substantia nigra of the midbrain have been lost.
At present, Parkinson's can only be detected by clinical symptoms and only after significant irreversible damage to the brain. However, damage to regions in the brainstem may precede the movement disorders associated with damage to the substantia nigra region of the midbrain and may represent the earliest stages of the disease. The early damage tends to affect regions of the brain responsible for taste and smell, normal sleep patterns, and normal gut motility. As a result, the earliest signs of Parkinson's are related to loss of smell, sleep disorders and constipation. Since these are relatively non-specific symptoms associated with many different diseases, they may lead an experienced physician to look for other signs of early Parkinson's.
The earliest clinical signs associated with Parkinson's disease tend to be distinct from the motor symptoms most commonly associated with Parkison's. These "prodromal signs" include constipation not linked to other known problems, sleep disorders mainly associated with the rapid-eye-movement (REM) phase of sleep, and loss of sense of smell and taste. For individuals with one of these symptoms, approximately 60% go on within 10 years to develop clinical symptoms associated with Parkinson's. It is possible that treatment of patients at this prodromal stage may slow or prevent the eventual onset of Parkinson's symptoms.
We consider Parkinson's and Alzheimer's as similar diseases on the same spectrum--the ParkinZheimer spectrum. These two diseases overlap, resulting in irreversible cognitive, motor, and autonomic dysfunction. The spectrum includes the two most common members, Alzheimer's and Parkinson's Diseases, but also Amyotrophic Lateral Sclerosis (ALS), FrontoTemporal Dementia (FTD), Progressive Supranuclear Palsy (PSP), and Multiple System Atrophy (MSA). While originally described as distinct diseases, they now appear to have common elements underlying their causes, progression, and late-stage symptoms.
Both Alzheimer's and Parkinson's are now believed to result from the destruction of brain pathways caused by proliferation of prion-like particles composed of misfolded synuclein and tau proteins. These prion-like particles are responsible for irreversible cell death that spreads from cell to cell through established connections. Almost all cases of Alzheimer's contain tau prions, but up to 40% may also contain synuclein prions. Conversely, almost all Parkinson's cases contain synuclein prions, but tau prions appear to be present in a significant percentage as well. While Parkinson's initially presents as a motor disease and Alzheimer's presents as a cognitive disease, these differences may blur as both diseases progress. At Amprion, we refer to these diseases under a common classification, the ParkinZheimer Spectrum.
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