Answer to Question #188048 in Psychology for Alberta Adjoa

Question #188048

Describe the basis for Parkinson's disease


1
Expert's answer
2021-05-07T10:33:54-0400

Basis of Parkison’s Disease

Parkison’s disease is a neurodegenerative disease. Aetiopathological factors in the causation of PD are listed below.

●      Environmental factors.

●      Genetic factors.

●      Age.

●      Drugs.

●      Metabolic derangements.

●      Infections.

Pathophysiology

It affects the basal ganglia majorly in the brain and direct and direct pathways signaling the motor system. The disease also affects the sympathetic and autonomic nervous systems of the brain. The destruction of the basal ganglia that contains the substantia nigra causes a decrease in the amount of dopamine in the body. A reduction in the amount of dopamine leads to the production of motor symptoms such as resting tremors. The neurons in the brain cause clump-like structures. The clump-like forms are attributed to a protein called alpha-synuclein that causes aggregates that are visualized under a microscope as Lewy bodies (Raza & Anjum, 2019).

The net effect of the destruction of the basal ganglia results in the pathways that originate from the basal ganglia being affected adversely. The pathways involved are:

●      Motor (direct and indirect pathways)

●      Nigrostriatal pathways.

Infections and metabolic derangements of electrolytes cause the death of the basal ganglia cells leading to microgliosis, astrocytes death, dysfunction of the mitochondrial cells, and generation of reactive oxygen species (ROS). ROS is attributed to the dying of the mitochondria because it releases ROS as it dies. The ROS causes oxidative damage to the cells of the basal ganglia. The ROS gains access into the nucleus of the cell, altering the regulatory genes for apoptosis. The genes for apoptosis are upregulated, and apoptosis of the cells of the basal ganglia die. Caspases regulate apoptosis (Blauwendraat, Nalls & Singleton, 2020).

           Dopamine hormone regulates muscle activity by causing inhibition of hyperreflexia. Dopamine ensures that muscle tone is controlled. The regulation of the muscle tone is regulated and only exhibited at appropriate times. Insufficient dopamine causes the symptoms of Parkison’s disease (Verschuur et al., 2019).

Ball et al (2019) argue that environmental factors compound the generation of ROS by the generation of toxins that alter the DNA of the brain’s cells. Environmental factors include herbicides, head injury. The environmental factors cause alteration in genes that regulate apoptosis, destroying brain cells.

Certain drugs are implicated in the causation of Parkinson’s. The cause would be drug-dependent. Once the drug is withdrawn, the symptoms are reversed. Typical and atypical antipsychotics are implicated. The basis of antipsychotics is that they cause depletion of the hormone dopamine in the brain causing Parkison’s disease. The therapy of these drugs should thus be monitored whenever instituted.

The aging process is implicated because as a person ages, cells of the body begin to die via programmed cell death. The brain cells die in the process of aging, which results in the manifestation of Parkison’s symptoms. The motor symptoms associated with dopamine insufficiency in Parkison’s disease include resting tremors, difficulty with gait, bradykinesia, speech difficulties, mask-face, cogwheel rigidity, akathisia.



References

Ball, N., Teo, W. P., Chandra, S., & Chapman, J. (2019). Parkinson's disease and the environment. Frontiers in neurology, 10, 218.

Blauwendraat, C., Nalls, M. A., & Singleton, A. B. (2020). The genetic architecture of Parkinson's disease. The Lancet Neurology, 19(2), 170-178.

Raza, C., & Anjum, R. (2019). Parkinson's disease: Mechanisms, translational models and management strategies. Life sciences, 226, 77-90.

Verschuur, C. V., Suwijn, S. R., Boel, J. A., Post, B., Bloem, B. R., van Hilten, J. J., ... & de Bie, R. M. (2019). Randomized delayed-start trial of levodopa in Parkinson’s disease. New England Journal of Medicine, 380(4), 315-324.



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