Parkinson’s Disease

Parkinson’s Disease

Introduction

Parkinson’s disease is a progressive neurodegenerative condition of the central nervous system that affects movement (Lai, Chou, Lin, and Kao 869). It is characterized by rigidity, tremor, bradykinesia and postural changes (Lai et al., 869). The loss of nerve cells in substantia nigra is implicated in Parkinson’s disease. Degeneration of substantia nigra causes dopamine deficiency in the striatum. By the time Parkinson’s disease is diagnosed, about 80% of dopamine-producing neurons have ceased functioning. The purpose of this essay is to discuss the etiology of Parkinson’s disease.

Clinical Symptoms of Parkinson Disease

It is a progressive neurodegenerative disorder characterized by tremor, bradykinesia, rigidity and postural instability. However, not all people with this condition present with all of these clinical signs. Motor weakness is often the initial complaint. Soon tremor and postural deficits emerge, prompting the examiner to look at the medical history and conduct neurological exam. In addition to these clinical symptoms, patients with Parkinson disease have disturbing pain and sensory symptoms in affects affected limbs.

Prevalence

The prevalence of Parkinson’s disease increases with age.

Parkinson is the second most common neurodegenerative disease after Alzheimer’s disease. It is also the second most common movement disease after tremor. It affects 100-200 per 100,000 people in the United States (Lai et al. 869).  The disease affects people of all socioeconomic levels, races and geographical regions. It affects men more than women. According to the Global Burden of Disease Study, the number of cases of Parkinson’s disease will reach 13 million by 2040 (Dorsey et al. 940). This projection highlights the heavy burden that Parkinson’s disease can present for society.

Parkinson’s disease is characterized by symptoms that affect the ability to move on one hand and non-motor symptoms on the other hand (Obeso et al, 1266). Non-motor symptoms include dementia, smell loss and pain in affected limbs. A person with this disease may not develop all of these symptoms. One patient may have severe dementia but no tremor. Another patient may have tremor without accompaniment of memory issues. In addition, it is difficult to predict how fast the symptoms will get worse. Parkinson’s disease progress at different paces for different patients and changes come gradually. Symptoms worsen over time while new ones come up along the way. The initial symptoms of rest tremor, bradykinesia, and rigidity are followed by disability and even death.

 Etiology

The substantia nigra in the brain secretes dopamine -neurotransmitter substance that controls muscle movement. The nerve cells (nigra) that manufacture dopamine substance are damaged in Parkinson disease. The degeneration of these nerve cells reduces the amount of dopamine. As a result, the region of the brain that control muscle movement cannot work normally, causing low movements (Jankovic and Tan, n.d). It is not known what causes degeneration of substantia nigra and other neurons. However, the role of genetic and environmental factors in the development of this disease has been debated.

Neuron Loss

Loss of neurons is important for the diagnostic features of Parkinson. The loss of dopamine-producing neurons in the substantia nigra is the main pathological feature in patients with Parkinson’s disease. In many cases, Parkinson diagnosis is made when a person has lost about 60% of dopamine-producing neurons. The loss of these neurons accounts for 80% loss of dopamine-producing neurons in the corpus striatum (Surmeir 3660). Mitochondrial dysfunction and alpha-synuclein pathology contribute toward the pathogenesis of Parkinson disease (Surmeir 3660).

Genetics

While Parkinson’s disease is an idiopathic disorders, studies have found minority of cases running in families. In certain families, Parkinson disease occurs in more than on generation, meaning that parents pass down the faulty genes to their offspring. This suggests that a person’s risk of Parkinson’s disease is partially due to genetic factors. Genes may be playing a role in the onset of Parkinson disease have been identified. These genes have been named as PARK genes. Mutations in the PARK genes have been linked to Parkinson’s disease. Mutaions in PARK 2, PARK7 and PINK1 have been reported in affected persons who had siblings with Parkinson. Similarly, studies have reported mutaions in LRRK2, SNCA, and UCHL 1 genes in families with dominant inheritance (Jankovic and Tan, n.d).  It worthy to note that rare cases of Parkinsonism are inherited this way.

Carbon Monoxide Intoxication

Carbon monoxide intoxication (CO) happens following inhalation of sufficient amounts of CO. inhaled CO quickly enters the bloodstream and binds to hemoglobin to form irreversible carboxyhemoglobin. This reduces oxygen-carrying capacity leading to hypoxia. COI results in 40,000 EM consultations and over 5000 deaths annually in the United States (Lai et al. 869). Additionally, CO causes cellular injuries, including lipid peroxidation. Clinical symptoms of COI include nausea, weakness, headache and dizziness. Some patient can develop typical delayed neuropsychiatric manifestations, such as Parkinsonism, dementia, incontinence and psychosis, weeks after acute COI (Lai et al., 869). However, the mechanism of delayed neuropsychiatric manifestations is yet to be determined.

CO-induced Parkinsonism is unclear albeit the combined direct CO toxicity to cells and tissue anoxia results in necrosis in substantia nigra (Lai et al., 869). Studies have found elevated levels of the CO-producing enzyme in patients with Parkinsonism, and reduced oxygen levels in the brain regions associated with Parkinsonism, including the substantia nigra and basal ganglia (14).

Aging

Age is considered biggest contributing factor for Parkinson disease, with average age of onset being 60. The risk increases with age. Parkinson’s disease usually occur in late middle age and increases significantly in its prevalence with advancing age (109). Majority of people with this disease are diagnosed between ages of 40 and 70. The disease incidence increases with age to 93 per 100,000 people in 70 to 80 age-group (). Studies have shown that the loss of striatal dopamine-producing neurons increases with age (Chaudhuri and Sauerbier 10). This suggests that aging plays a role in the degenerating process.  The rate appear higher in men than women. However, this rate may be affected by variations in prevalence of factors such as caffeine intake, smoking behavior and use of postmenopausal hormones (Ascherio and Schwarzschild 1260).

Herbicides and Pesticides

The association of heavy metals and toxic chemicals in Parkinson’s disease has been studied but the findings remain inconclusive. These chemicals have been evaluated against the standard of 1-methy-4-phenyl-1, 2, 3, 6-tetradropyridine (MPTP). MPTP had been found to be responsible for nigrostriatal degeneration (Kouli, Torsney, and Kuan, n.p). In 1983 several individuals developed characteristic symptoms of Parkinson disease after receiving injections contaminated with MPTP. Injected MPTP metabolizes into a neurotoxin that selectively damages dopaminergic cells (Kouli et al. n.p). The implication of MPTP in the degeneration of nigra led to the notion that Parkinson disease could be triggered by environmental toxins. Consequently, many studies have established a relationship between Parkinson disease and chemicals. Some chemicals cause toxicity of neurons while others cause brain inflammation. A number of chemicals have been linked to parkinson’s disease in animal models. For example, rotenone (pesticide) and paraquat (herbicide) have been found to induce dopaminergic degeneration in animal models with Parkinson’s disease in lab animals (Kouli et al. n.p). Maneb (fungicide), which contains manganese has been implicated in Parkinson-like symptoms. Heavy metals, such as lead, iron, aluminium, and manganese, all have lethal impacts on dopamine-producing neurons. Autopsy studies of brains of patients with Parkinson have found increased levels of iron and aluminium. Welding fumes carry many heavy metals, and studies show that extended exposure to welding fumes can trigger Parkinson’s disease (Cersosimo and Koller 27). Although studies have suggested an association between chemicals and the development of Parkinson’s disease, the evidence is scant due to inability to single out the specific agent that induce this risk. Environmental risk of developing this disease from chemical and heavy metal exposure is not mutually exclusive.

Other risk factors associated with the development of Parkinson’s disease include rural living, traumatic head injury, agricultural occupation, intake of dairy products, history of melanoma and type 2 diabetes (Ascherio and Schwarzschild 1260). While these associations are supported by biological plausibility, it is difficult to replicate many of these observations.

Oxidative Stress

Parkinson’s disease results from the loss of dopamine-producing neurons. One school of thought attribute the cause of this condition to unstable free radicals that cause the death of nerve cell. These free radicals are a byproduct of chemical reactions that occur in the mitochondria. Often called reactive oxidative species, free radicals cause oxidative stress when their production exceeds the ability of removal mechanisms (Mayeux 89). Oxidative stress results in the cascade contributing to degeneration of dopamine cells in Parkinson’s disease. Oxidative stress is associated with other aspects of the degenerative process, including inflammation, excitotocity, and mitochondrial dysfunction.

Viral Infection

Contracting viral infections early in life increase the risk of Parkinsonism. Viral infections cause inflammation, which in turn affects the ability of the brain to effectively respond to other infections. In addition, early viral infection compromises the quality and integrity of dopamine-producing neurons.

Substance abuse

Abuse of methamphetamine has been associated with Parkinson-like symptoms. In animal models, methamphetamine exposure has been shown to damage dopaminergic neurons in the striatum and cell bodies in the niagra, resonating with the degeneration witnessed in patients with Parkinson’s disease.  Studies have also observed selective degeneration in dopaminergic terminals in the striatum among methamphetamine users (Granado et al. n.p).

Conclusion

This paper has examined the etiology of Parkinson disease, a progressive neurodegenerative disorder characterized by rigidity, tremor, bradykinesia and postural changes. The exact cause of this disorder is not known but genetic and environmental factors are debated as contributing to its development. Among the risk factors discussed include aging, neuron loss, pesticides and heavy metals, carbon monoxide intoxication, viral infection, and genetic factor. Although many studies have investigated these factors, the findings are not conclusive. Hopefully, next studies could find a strong association in these factors and the development of Parkinson’s disease.

Works cited

Ascherio Alberto , Schwarzschild Michael A. The epidemiology of Parkinson’s disease: risk factors and prevention. Lancet Neurology, 15(2016): 1257–72

Cersosimo, Maria and William C Koller. “The Diagnosis of Manganese-induced Parkinsonism.” Neurotoxicology, 27(2006), 340-6.doi: 10.1016/j.neuro.2005.10.006. https://www.sciencedirect.com/science/article/abs/pii/S0161813X05001853

Chaudhuri KR, Sauerbier A, disease P. Unravelling the nonmotor mysteries of Parkinson disease. Nat Rev Neurology; 12(2016), 10–11

Dorsey Ray E. et al . Global, regional, and national burden of Parkinson’s disease, 1990-2016: a systematic analysis for the global burden of disease study 2016. Lancet Neurology, 17(2018)939–53.doi:10.1016/S1474-4422(18)30295-3

Granado Noeli, Sara Ares-Santos, Rosario Moratalla R. (2013). Methamphetamine and Parkinson’s disease. Parkinson’s Disease, 2013(2013), ID 308052, https://doi.org/10.1155/2013/308052. http://www.hindawi.com/journals/pd/2013/308052/.

Jankovic, Joseph, and Eng King Tan. Parkinson’s disease: etiopathogenesis and treatment. Journal of Neurology, Neurosurgery, and Psychiatry, 91.8(2021). http://dx.doi.org/10.1136/jnnp-2019-322338

Lai, Ching-Yuan, Mei-Chun Chou, Cheng-Li Lin, and Chia-Hung Kao. “Increased risk of Parkinson disease in patients with carbon monoxide intoxication: a population-based cohort study.” Medicine, 94.19(2015): e869. doi:10.1097/MD.0000000000000869

Mayeux Richard.  Epidemiology of neurodegeneration.  Annual Review of Neuroscience, 26(2003), 81–104

Obeso JA et al . Past, present, and future of Parkinson’s disease: a special essay on the 200th anniversary of the shaking palsy. Movement Disorder, 32(2017):1264–310

Surmeier, Dalton James. Determinants of dopaminergic neuron loss in Parkinson’s disease. FEBS Journal, 285(19(2018):3657-3668.doi: 10.1111/febs.14607; https://febs.onlinelibrary.wiley.com/doi/full/10.1111/febs.14607

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