Dementia with Lewy Bodies Scientific Essay


Dementia with Lewy Bodies Part A: Scientific Essay

Lewy Bodies : Dementia with Lewy Bodies (DLB) has been described with specific etiology, pathological development, and with specific symptomatic manifestation. DLB has been found to cause symptoms of Parkinson’s disease (PD) and Alzheimer’s disease (AD). The condition, Dementia with Lewy Bodies affects several parts of the brain including the brain’s sensory cerebral cortex and the substantia nigra. In all the affected structures, DLB manifests with impairment in the function performed by the given structure of the brain (Mayo & Bordelon, 2014). The following essay describes the anatomical brain structures about the development of Dementia with Lewy Bodies. Finally, the essay gives a reflective description of the condition (Lewy Bodies).

Dementia with Lewy Bodies is described by the presence of a protein containing structures in the central nervous system cells. The protein structures occur within the cytoplasm of the cells. The protein containing Lewy bodies is known to interfere with the electrical impulse conduction along the dendrites if the nerve cells. Dementia with Lewy bodies affects several brain structures and parts. The Lewy bodies described in dementia are Alpha-synuclein proteins. Under normal conditions, the proteins aggregate in the cells of the brain to strengthen the supporting system inside the cells. Notably, Alpha-synuclein proteins are found within the tube-like supporting structures of nerve cells. Genetic mutations interfere with the genetic coding for the assembling of the amino acids that make up the alpha-synuclein. The resulting structure of the alpha-synuclein proteins forms a helical shape. The helically structured protein does not perform the role of providing support. Also, abnormally shaped Lewy’s bodies form pores in the cell membrane of the nerve cells. The pores that are formed are permeable to toxic substances that destroy nerve cells. Further, the pores that are formed are also permeable to calcium. The excessive inflow of calcium destroys the cell as well (Abeysuriya & Walker, 2015).


Lewy Bodies
Lewy Bodies

Dementia with Lewy bodies

Aggregation of alpha-synuclein proteins and the formation of pores lead to leakage of chemical neurotransmitters that are involved in various brain functioning. The alpha-synuclein is broken down by a degradation system that utilizes protein. Genetic mutations cause the formation of abnormally shaped proteins of the degradation system for alpha-synuclein. The protein builds up in the brain, leading to the particular Lewy’s bodies observed in dementia and Parkinson’s disease.

The degradation of dopamine chemical neurotransmitter n DLB is a contributing factor to the development of the condition. Dopamine is broken down into oxide particles. The oxide particles are highly reactive and may react with iron, forming highly toxic hydroxyl complexes. The formed hydroxyl compounds react with lipids found in the layers of the cell membrane. As a result, the lipids of the cell membrane are degraded, and the entire cell membrane is destroyed Lewy bodies affect the motor regulating neurons of the brain. Additional deficiencies in DLB are; the alteration of episodes of coherent speech, alertness and competent orientation with periods of confusion and disorientation. The impairment in speech is as a result of the presence of the Lewy’s bodies on the parietal lobe which functions in the comprehension and formation of words during the speech. (McKeith, Boeve, Dickson, Halliday, Taylor, Weintraub, & Bayston, 2017).

Dementia with Lewy Bodies

DLB is associated with the interruption in the amount of dopamine and acetylcholine neurotransmitters produced in the brain. During the development of dementia with Lewy bodies, structures have impaired neurochemical processing. Therefore, amounts of dopamine produced are insufficient. In dementia with Lewy bodies, the brain cells that regulate the motor functioning are impaired. Acetylcholine neurotransmitter is responsible for conduction of electrical nerve impulses for motor function in skeletal muscles. In the occurrence of DLB, the production of acetylcholine is not controlled. Therefore, patient manifests with excessive and uncontrolled contraction of the skeletal muscles as manifested in the occurrence of Parkinson’s disease (Jones & O’brien, 2014).

Dementia with Lewy Bodies

DLB affects the nerve cells of the cortex. The cortex of the brain is known to perform the cognitive role of the brain. The cortex of the brain is involved in functions of decision making and judgment. Patients presenting with Dementia with Lewy Bodies manifest with impaired cognitive functioning such as decision making and judgment. Lewy bodies interfere with the flow of electrical impulses along nerves within the neocortex. Also, Dementia with Lewy affects the limbic system. The occurrence of Lewy‘s proteins in the limbic system affects the memory of the of the affected individual. The limbic system is significantly involved in memory processing in the brain.

Genetics are associated with the development of DLB. Genetic predisposition leads to immunological processes that begin the pathophysiology of dementia. Expression of genetics causes production cytokines, such as interleukins. Interleukins initiate an immunological process that causes the formation of Lewy’s bodies (Taylor, Collerton, LeBeau, & Perry, 2017).

Dementia with Lewy bodies

DLB predominantly presents with loss of memory. The Lewy’s bodies affect the limbic system. The hippocampus, the part of the brain that is responsible for the memory storage, is affected by the Lewy’s bodies. The hippocampus part of the brain, therefore, does not conduct electrical impulses normally. The patient presents with anterograde loss of memory in the occurrence of the disease. Hallucinations are characteristic of DLB. The Lewy’s bodies are also found in the motor portion of the cortex. The patient perceives the stimulus that is not present. DLB presents with delusions and language comprehension difficulties. The features of language comprehension are as a result of the effects of Lewy bodies to the parietal lobe of the brain (Abeysuriya & Walker, 2015).

Motor deficits that include; tremors, muscle rigidity, and involuntary movements are characteristic of DLB. Lewy’s bodies affect motor regulating neurons of the brain. Additional deficiencies in DLB are; the alteration of episodes of coherent speech, alertness and competent orientation with periods of confusion and disorientation. The impairment in speech is as a result of the presence of the Lewy’s bodies on the parietal lobe which functions in the comprehension and formation of words during the speech. Impairment in memory results from the inability of the brain to receive information and words. Also, impairment in the ability to retrieve information is another feature of DLB (Mayo & Bordelon, 2014).

A patient diagnosed with DLB presents with orthostatic hypotension. Orthostatic hypertension manifests especially during the treatment of co-occurring Parkinson Disease.

Several environmental factors are responsible for the interruption in the development of Lewy bodies. Medical conditions such as diabetes and cardiovascular diseases predispose individuals to DLB. The patient presents with significant language deficits. The common language deficits include the inability to recognize objects even with intact sensory functioning, the inability to comprehend speech, read and write even with intact motor and sensory functioning (aphasia) and the inability to carry out motor activities and movements even when the command to carry out such activities is well understood. The Mini Manual Status Examination indicators are impaired in the cases of DLB. Patients with this type of dementia have impaired memory ability to name previously identified names or objects. The loss of memory is caused by the effects of the Lewy bodies on the limbic system that is responsible for memory storage and retrieval. The patient has impaired visual-spatial abilities. DLB affects the individual’s ability to retrieve short-term memory. The patient manifests other significant cognitive functioning impairment; the patient is disoriented in time and place. The patient manifests the inability to perform organized motor. Additional cognitive deficits are; inability to recall events, inability to communicate effectively and deviation from the topic of discussion during conversations. Based on mini-mental examination, study subjects are assessed for impairment of ability to recall, orientation to place, ability to make judgments and language and naming capabilities (Bachstetter, Eldik, Schmitt, Neltner, Ighodaro, Webster, & Nelson, 2015).

Dementia with Lewy Bodies Part B: Reflection

The occurrence and development of DLB follow an abnormality in intracellular structures. DLB (DLB) is a condition that is closely associated with other conditions such as PD and AD. DLB has multifactorial etiology. DLB results from deficiencies in the genetic make for structural protein in the brain nerve cells. Alteration in the coding of the proteins leads to further intracellular processes that lead to symptoms consistent with the diagnosis for dementia Lewy bodies. During development of the DLB, there are protective far such alcohol consumption and cigarette smoking. The symptoms of dementia are consistent with other types of dementia (Mayo & Bordelon, 2014).

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Dementia with Lewy Bodies References

Abeysuriya, R., & Walker, Z. (2015). DLB. British Journal of Neuroscience Nursing, 11(3), 146-149.

Bachstetter, A. D., Van Eldik, L. J., Schmitt, F. A., Neltner, J. H., Ighodaro, E. T., Webster, S. J., … & Nelson, P. T. (2015). Disease-related microglia heterogeneity in the hippocampus of Alzheimer’s disease, DLB, and hippocampal sclerosis of aging. Acta neuropathologica communications, 3(1), 32.

Jones, S. V., & O’brien, J. T. (2014). The prevalence and incidence of DLB: a systematic review of population and clinical studies. Psychological medicine, 44(4), 673-683.

Mayo, M. C., & Bordelon, Y. (2014, April). DLB. In Seminars in neurology (Vol. 34, No. 02, pp. 182-188). Thieme Medical Publishers.

McKeith, I. G., Boeve, B. F., Dickson, D. W., Halliday, G., Taylor, J. P., Weintraub, D., … & Bayston, A. (2017). Diagnosis and management of DLB: Fourth consensus report of the DLB Consortium. Neurology, 89(1), 88-100.

Taylor, J. P., Collerton, D., LeBeau, F., & Perry, E. (2017). Cholinergic Pathology in DLB. In DLB (pp. 23-39). Springer, Tokyo.

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