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Parkinson’s Disease Etiology Research Paper

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Updated: May 12th, 2022

Abstract

Parkinson’s disease is the second common neurodegenerative disorder. The main characteristics of the disease are muscle rigidity, tremors, and weakness of emotional expressions. The literature explains many etiologies of the disease, disturbance of dopaminergic neurotransmission, neurodegenerative changes of the substantia nigra, and genetic mutations are possible causes. This essay aims to describe in brief what causes Parkinson’s disease.

Parkinson’s disease, named after James Parkinson who first described the disorder in 1817, is a disturbance of motor function. Slowing and weakness of emotional and voluntary movements, muscular rigidity, and tremors are the main characteristics of the disease. A multiplicity of different pathological conditions produces Parkinson’s disease and the main pathological changes are due to lesions of the corpus striatum and substantia nigra (Brain and Walton, 1969).

Parkinson’s disease is the second most common neurodegenerative disorder (second to Alzheimer’s disease). It affects 1% of Americans above the age of 60 years (as it is rare before the age of 40). Disease incidence is higher in males, with no race or ethnic difference. The main pathological features of the disease are disturbances of the dopamine-dependent neurotransmission, presence of Lewy bodies in the remaining neurons of the substantia nigra. Recently genetic evidence of Parkinson’s disease etiology has been suggested (Nutt and Wooten, 2005).

Parkinson’s disease and disturbances of dopaminergic neurotransmission

The corpus striatum and the substantia nigra

The corpus striatum is, phylogenetically, the oldest part of the cerebrum. It lies deep in the substance of the cerebral hemisphere between the lateral ventricle and the insula. It contains many fibers among which are the efferent fibers running from the corpus striatum to the substantia nigra. The substantia nigra is a gray mass lying between the crus cerebri and tegmentum of the midbrain at the level of the superior colliculi. It consists of a zona compacta lying dorsally, and a zona reticulate. This part of the brain is responsible for the control of muscle tone, posture, and muscle tone (extrapyramidal functions). The neurotransmitter for the neurons that pass from the substantia nigra to the corpus striatum (dorsal part) is dopamine. These neurons are responsible for the commencement and carrying out of movements (Volkow and others, 1996).

The dopaminergic deficiency theory of Parkinson’s disease

It assumes the main characteristic symptoms of Parkinson’s disease (muscle rigidity, tremors, and postural instability) are the product of the marked disappearance of the dopaminergic neurons in the zona compacta of the substantia nigra because of cell death. Dopamine neurons in the ventral tegmental area are responsible for motivation, mood, and thought orderliness, thus dopamine lack explains the psychological disturbances occasionally present in Parkinson’s disease patients (Moore and others, 2005).

Mechanisms of neurodegenerative changes (Biological changes)

The exact mechanism that leads to substantia nigra cell death is still not fully known, several mechanisms are assumed to play a role.

Alpha-synuclein and cell death

Alpha-synuclein is a small soluble protein available at the pre-synaptic ends of the central nervous system. Dysfunction of alpha-synuclein relates to neurodegenerative diseases, among which is Parkinson’s disease. The physiological functions of this protein still need more explanation, although data suggest it may have a role in regulating neural membrane stability and neuronal ability to keep shape and function after a minor change. Variable causative biological agents, environmental or genetic, may lead to a succession of incidents including loss of normal function of alpha-synuclein. In dopaminergic neurons, this may trigger a hurtful sequence of events in which elevation of dopamine level in the cytoplasm, oxidative stress, neuron membrane dysfunction, and interference with vesicle function occur. These events eventually result in dopaminergic cell death and subsequently Parkinson’s disease. Alpha-synuclein brings on neuronal cell dysfunction through more than one conduit, such as cell amassing or interaction with other proteins molecules, as synphilin-1, chaperone 14-3-3 protein, and dopamine (Recchia and others, 2004).

Lewy bodies

Lewy bodies are a histopathological characteristic of Parkinson’s disease. They are circular eosinophilic (because of a protein core) structures surrounded by a peripheral nimbus identified in the cytoplasm of the neurons. Recent research recognized that Lewy bodies participate in neurodegenerative processes including Parkinson’s disease and not by-products of the degenerative process (Loutharius and Brundin, 2002).

Mitochondria and oxidative stress

Mitochondria are the main source of cellular energy; in addition, it contains an enzyme system called NADH-quinone oxidoreductase shortened as I complex. This enzyme system is the portal for the main part of electrons that pass through the respiratory chain ending in oxygen reduction. Some patients with Parkinson’s disease present low levels of this enzyme. Researchers assume that such low enzyme levels expose nerve cells to the insult of oxygen free radicals (oxidants), which are the result of some natural chemical processes in the body. Increases oxidants production occurs on exposure to environmental stresses (imbalance between body adaptive mechanisms and an external or internal insult). In case of decreased levels of complex I, or increased oxidants production, they can injure any human cell, including nerve cells in substantia nigra, causing Parkinson’s disease (Loutharius and Brundin, 2002).

Genetics of Parkinson’s disease

The observation that 10 to 15 % of Parkinson’s disease patients have a positive family history for relatives of the first or second-degree suffering from the disease pointed out to study possible genetic factors of the disease (Nutt and Wooten, 2005). Mutant genes on chromosome four responsible for the control of alpha-synuclein protein (in dopamine secreting nerve cells) may be the cause of autosomal dominant Parkinson’s disease. Failing genes on chromosome six, responsible for the control of parkin molecule (needed for cell self-destruction of alpha-synuclein) may be responsible for autosomal recessive Parkinson’s disease. Research suggests that in cases with a positive maternal history of Parkinson’s disease, nerve cells mitochondria DNA defects are worthy of further investigation. A mutant tau gene has been recently described; this gene control controls the support system responsible for transferring nutrients through nerve cells. This gene defect may be specifically responsible for late (old age) onset Parkinson’s disease (Klein and Schlossmacher, 2006).

Conclusion

Parkinson’s disease is a disabling neurological condition that affects 1% of Americans above the age of 60 years. A noticeable characteristic is the selective loss of dopamine-producing neurons in the substantia nigra. Parkinson’s disease links to many causes, including genetic alterations, alpha-synuclein dysfunction, and cell death, and the role played by Lewy bodies and oxygen-free radicals. Although the series of events that lead to nerve cell death is somewhat unspecified, yet recent research spotlighted the possible pathogenic mechanisms that trigger the degeneration of these cells. It seems the key event in the presynaptic ends of dopaminergic neurons in Parkinson’s disease is the faulty appropriation of dopamine into vesicles. This leads to the generation of reactive oxygen species in the cytoplasm irrespective of genetic or environmental triggering factors.

References

Brain, L, and Walton, J N. (1969). Brain’s Diseases of the Nervous System (7th edition). London: The English Language Book Society and Oxford University Press.

Klein C. and Schlossmacher, M G. (2006). The Genetics of Parkinson Disease: Implications for Neurological Care. Nat Clin Pract Neurol, 2(3), 136.

Lotharius J. and Brundin P. (2002). Pathogenesis of Parkinson’s Disease: Dopamine, Vesicles and &-Synuclein. Neuroscience, 3, 1-11.

Moore, D J., West, A B., Dawson, V L. and Dawson, T M. (2005). Molecular Pathophysiology of Parkinson’s Disease. Annu. Rev. Neurosci., 28, 57-87.

Nutt, J G. and Wooten, G. F. (2005). Diagnosis and Initial Management Of Parkinson’s Disease. N Engl J Med, 352, 1021-7.

Recchia, A, Debetto, P, Negro, A. et al (2004). α-Synuclein and Parkinson’s disease. FASEB J., 18, 617-626.

Volkow, N D., Fowler, J S., Gatley, S J. et al (1996). PET Evaluation of the Dopamine System of the Human Brain. J Nucl Med, 37, 1242-1256.

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