Describe the impact of neuronal and neurotransmitter abnormalities on brain function Essay

This essay will explain the effects of neuronal and neurotransmitter defects on brain functions. There will be a brief overview of the brain functions describing the individual functions and structures. This essay will discuss four types of disease explaining how brain disorders affect either the neuron or the neurotransmitter. The diseases being discussed affecting the neuron will be Multiple Sclerosis and Alzheimer’s. The areas discussed will show how the disease affects neurons, symptoms and how treatments alleviate symptoms or target the mechanisms.

The next two diseases to be discussed which affect neurotransmitters will be Parkinson’s disease and Schizophrenia. The essay will focus on the main areas including how these diseases affect the neurotransmitters, symptoms and various treatments that aid symptoms or treatments that target brain mechanisms. The neurons are the building blocks of the brain, which are unique and have the ability to communicate specifically, briskly and over long distances reaching target cells such as gland cells and muscles (Bernstein, Clarke-Stewart, Penner & Roy, 2008, p. 5).

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The neuron is a generic name that represents the entirety of the whole cell and is unique due to containing the ability to generate electrical impulses, allowing neurons to communicate with each other. These impulses are known as action potential, when these impulses become active they fire off their own action potential. The neuron receives information in through the dendrites, processes the information in the soma and then executes the information down the axon and onto other neurons.

There is a gap between each neuron known as the synaptic cleft, this allows for the chemical, neurotransmitter, to release and fuse onto proteins of the dendrites on the next neuron. The previous neuron returns to its own resting state when enzymes within the synaptic cleft obstruct remaining neurotransmitters (Marc Breedlove, Rosenzweig & Watson, 2007, pp. 23-33). However when damage occurs to the neuronal structure, degenerative diseases can occur such as Multiple Sclerosis (MS).

The primary location of MS is found in the central nervous system (CNS) and is a multifocal demyelinating disease that causes damage or loss of myelin throughout the CNS (Graham Beaumont, Kinealy & Rogers, 1999, p. 505). MS is considered as an autoimmune disease where the immune system attacks its own tissue; therefore, its own immune system attacks the myelin that insulates the axon. The damage to the myelin stops nerve cells from efficiently conducting action and synaptic potentials, losing the ability to send signals throughout the body and resulting in incapacitating symptoms.

This disease mostly affects motor and sensory neurons that possess long axons carrying information to different parts of the body. Therefore the length of these axons provide a greater need for insulation of the myelin to transmit this information so greatly affected by the destruction this disease causes (Longstaff, 2000, p. 12). The breakdown of motor and sensory functions produce several symptoms, most common include vision, coordination, sensation, speech and bladder control.

These symptoms are a result of the neurons inability to process the transmissions due to breakdown of functions that carry signals from the brain and spinal cord to the muscles (Kingsley, 2000, pp. 24-25). Different treatment therapies as with all neurological disorders can divide into either treating symptoms or targeting the mechanism that initiates the disease. Several drugs and treatments are available to help alleviate some symptoms; however, some symptoms are difficult to control such as overwhelming tiredness.

There are also various drug treatments available to alter the immune response within this disease by reducing the frequency of relapses, although these provide some relief they do not prevent progression of the disease. Other research currently been carried out suggests that stem cell transplantation can induce remission in severe cases. The stem cells segregate into glia and neurons to enable remyelination and axonal repairs at the plaque sites (Rog, Burgess, Motterhead & Talbot, 2009).

Other degenerative diseases include Alzheimer’s disease (AD) which is progressive and is the most common neurodegenerative disease. AD is the most common cause of dementia that is irreversible and occurs when the brain is damaged by this condition. AD affects the brain by shrinking or deteriorating brain tissue, which is most evident in the temporal lobe. The ventricles begin to grow larger and the sulcus becomes wider resulting in neuron loss, therefore symptoms forming.

This causes less tissue and less processing capacity compared to a healthy brain (Nagy, 2007, p. 139). The cortex shrinks leading to areas of thinking and remembering becoming damaged, especially in the hippocampus where formations of new memories exist (Kingsley, 2000, pp. 546-547). The main pathologies for AD are developments of extracellular amyloid plaques and intracellular neurofibrillary tangles. Amyloid plaques are mostly made of proteins, which in a normal brain are made in the cell, transported to the membrane and broken down.

These proteins however, stick together and cause problems communicating between neurons, which results in amyloid plaques. These plaques insert themselves into the membrane causing a leak of substance outside the cell that causes further damage resulting in neurone dysfunction and death. The neurofibrillary tangles are made of an abnormal form of tau protein that is crucial for the structure of the neuron. In AD, tau protein becomes overactive and produces enzymes that result in formation of neurofibrillary tangles causing death of cells (Nagy, 2007, pp. 140-142).

Scientists are not sure what causes cell death in the Alzheimer’s brain, but plaques and tangles are the main thoughts (Nagy, 2007, p. 144). Symptoms of AD start slow and gradually increase as the disease deteriorates, progressing from mild poor memory to widespread brain destruction. As the cells die within the brain, the more the disease takes hold (Nagy, 2007, pp. 132-133). The new treatments available for AD aim to slow this disease but are unable to prevent. However, the drugs what are available only help a fraction of the patients with their symptoms.

Nonetheless, measures such as retaining education, physical exercise, good diet and vitamin supplements have shown improvements against some of the risk factors associated with AD, although their true effectiveness remains to be proven (Nagy, 2007, pp. 147-149). A neurodegenerative disease is an umbrella term, which primarily effect neurons that die within the brain over long periods, which then become slowly progressive. Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease; both of these diseases are debilitating (Clark ; Morrison, 2007, p. 51). The deaths of the dopamine releasing neurons are the main pathological process in PD.

The network that uses dopamine starts in the midbrain, the substantia nigra then projects forward into the cortex and into the basal ganglia (Clark ; Morrison, 2007, p. 153). The neurotransmitter is processed in the cell and passed down the axon onto the vesicles by the pre synaptic axonal button. If the brain cells die which produce the dopamine in one part in the midbrain, the neuron does not receive any input, as the neuronal transmitter is not there.

This is the process of PD as neurons in the midbrain are projecting to neurons that are responsible for controlling movement in the forebrain are not receiving input so unable to function properly which ultimately leads to symptoms of PD (Kingsley, 2000, pp. 300-305). The symptoms of PD are difficulties initiating movement, tremors and falling over frequently (Bernstein et al, 2008, p. 100). The treatments available for PD individuals aim to improve symptoms and signs but there is no treatment available to slow or halt the process of PD.

The antiparkinsonian drugs work by becoming a building block to enable the brain cells to manufacture and produce more dopamine. This helps to normalise symptoms to allow for more movement and less stiffness (Bernstein et al, 2008, pp. 100-101). Another treatment that is used are dopamine agonists, these stimulate the cells that produce dopamine. They mimic the effects of dopamine to enable binding with the postsynaptic dopamine receptors. The agonists target certain areas in the brain to stimulate receptors required to help with symptoms (Clarke ; Morrison, 2007, pp. 58-160). Drugs change over the course of the illness to try to support the failing neurotransmitter system.

This could result in drugs being increased or decreased, or new drugs being used to compensate for changes that occur throughout the disease (Bernstein et al, 2008, p. 100). Schizophrenia is a syndrome, considered as a major psychosis, which affects the behaviour of the individual. Schizophrenia is a serious mental disorder that is bewildering, common and incapacitating condition that causes the individual distress and torment (Jones ; Oyebode, 2007, p. 05).

According to Jones and Oyebode (2007, p. 311) this syndrome is caused by several different factors that are complex; however the actual cause is still unknown. There are strong indications that the aetiology of Schizophrenia varies from biological roots such as genetics or environmental causes such as excessive use of cannabis or complications at birth. Michael-Titus, Revest ; Shortland (2010, p. 271) explains the biochemical abnormalities which led to a theory that dopamine is the main neurotransmitter in schizophrenia.

This theory was largely based on pharmacological evidence that a dopamine receptor antagonist was the first drug that provided an improvement in schizophrenic sufferers. However, side effects to dopamine treatments can lead to symptoms relating to PD, if the dopamine levels were reduced too much. Clinical features of schizophrenia are classified into positive and negative symptoms. Positive symptoms include hallucinations and delusions, whereas negative symptoms include lack of drive and interest (Jones ; Oyebode, 2007, pp. 306-311). Subtypes are defined by symptoms using current classifications of schizophrenia.

There are five subtypes including paranoid, hebephrenic, catatonic, undifferentiated and residual. These classifications and subtypes are crucial for diagnosis and essential treatments (Michael-Titus et al, 2010, p. 275). Treatments available include antipsychotic medications that are most effective in acute psychosis. This medication blocks dopamine receptors but has serious side effects. Other treatments can include Cognitive Behavioural Therapy, to encourage the individual to understand alternative explanations of their symptoms such as hallucinations and delusions.

Basic treatments such as providing social care enable sufferers to live in the community to help with rehabilitation. However, support is required from a multidisciplinary team to ensure each patient is tailored for and supported in their environments (Jones ; Oyebode, 2007, pp. 318-320). In conclusion, this essay has focused on four brain abnormalities which either effect the neuron or neurotransmitter. It has described how each of these brain abnormalities effect the mechanisms of the brain by either providing outward signs such as tremors or inward signs such as cell death.

The diseases discussed relating to neuron damage, which include MS and AD have shown that treatments are unable to cure but drugs are available to manage symptoms. Neurotransmitter abnormalities discussed include PD and schizophrenia showing how neurotransmitter abnormalities affect individuals and how the drugs are able to target the mechanisms that are abnormal to alleviate outward symptoms. In all four diseases, the use of drugs helps to provide the individual with some quality of life and to prolong the inevitable, death.

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