Dementia is a serious cognitive impairment of a person who was previously normal, which is more than what is expected in the normal aging process of a person. It may be as a result of injury to the brain globally which is static or may be as a result of disease in the body or brain leading to a progressive long-term injury to the brain. The main signs and symptoms of dementia are as a result of the impairment of the cognitive function of the brain. The person is affected areas in the brain which are involved in attention, memory, problem solving and language. For diagnosis, it needs a presentation of at least six months.
Fixed cognitive impairment is caused by any injury to the brain which affects the neural function in the brain. The traumatic brain injury leads to damage of the white matter, affecting the axons of the nerves. In this case, the cholinergic system is interfered with. The brain with thus have a deficiency in the cholinergic stimulation and thus lead to decrease in the cognition. In addition, the disruption of the supply of blood to any part of blood temporally can injure these neurons. Other causes of fixed cognitive impairment include diseases such as meningitis, seizures and dementia (Mukamal, 2003).
Buy Cognitive Impairment essay paper online
Slowly progressing dementia begins slowly and progresses slowly until there is significant destruction of the neurons in the brain. This is usually caused by neurodegenerative disorders in which there is selective destruction of cholinergic neurons. This results in decrease in the number of neurons available in the brain of cholinergic system and result in decreased neurotransmitter. Alzheimer's disease is one of the diseases which cause progressive destruction of cholinergic neurons in the brain. People suffering from the disease tend to have cognitive impairment. Another cause of slow progressive dementia and cognitive reduction with time is hypothyroidism which is reversible upon treatment (Ganguli, 2005).
The relationship between the imbalance of neurotransmitters in the brain and dementia has been studied. The symptoms of dementia diseases are not purely as a result of neuro-degeneration but also as a result of alterations in the neurotransmitter interactions in the brain and some patients appear to be at more risk than others. Progressive dementia has been shown to relate very closely with the destruction of cholinergic neurotransmitters. The patients who are suffering from dementia tend to have less acetylcholine neurotransmitter and thus raising the question of the role of the neurotransmitter in the pathogenesis of dementia.
According to Fodale, (2006), disease entities such as Alzheimer's disease are associated with very significant loss of nicotinic system neurons. The disease leads to a significant decrease in cholinergic neurons in the bran. This results in the decrease in the stimulation of the brain from the cholinergic system. There are very few neurons available in the brain to stimulate the brain. The damage to the cholinergic neurons leads to severe cognition impairment raising the question of the role of the cholinergic neurons in the cognitive functions of the brain. The result in the destruction of the neurons is severe cognitive impairment and decrease in the ability of the individual to remember some things.
Anesthetic drugs which are useful in operations of patients modulate the cholinergic system. They can either decrease or increase the cholinergic transmission in the brain. Most of the drugs inhibit cholinergic transmission. This leads to a decrease in the cognitive ability of the person leading to an impairment of the cognition on that person. Most patients who have had general anesthesia administered to them suffer from brief moments of impaired cognition. This illustrates that cholinergic transmission plays an important role in the cognition. Diseases such as dementia permanently destroy the cholinergic neurons which then lead to less cholinergic transmission. Decreased cholinergic transmission decreases the cognition in that individual (Fodale, 2006).
In their research, Alloza (2005), they assessed the serotonergic and cholinergic functions in the post-mortems of both temporal and frontal cortex of twenty two dementia patients who had cognitive impairment. In their results, they established that the decrease in the cholinergic function was related to the decrease in the cognitive function of the brain. Thus, an imbalance between the serotonin and the cholinergic systems in the brain was related to the cognitive function of the person. This illustrates the role of acetylcholine in the cognitive functions of the brain. This neurotransmitter is found to be decreased in the post mortem sections of the people with dementia. The cholinergic neurons are responsible for the maintenance of cognition in the person and thus their decrease in the brain leads to decrease in the cognitive ability of the individual (Kobayashi, 2010).
Nicotinic Cholinergic systems participate in the cognitive functions of the brain. These cognitive functions of the brain which the nicotinic systems participate in include such things as, memory, learning and attention. In the brain, there are very many nicotinic receptors which imply that they have some specific functions in the brain. They enhance the brain function of an individual making him or her be able to retain the long term memory for long, a characteristic responsible for the better learning of a person who has intact nicotinic receptors. They are specifically located in special brain areas such as the frontal cortex and the hippocampus. In animal models, nicotinic receptors have been found to improve the memory tasks of the animals. This indicates that these receptors have the power to influence the mental status of an individual (Crutcher 2009).
Nicotinic antagonists have been found to impair the memory functions of the person on whom they have been administered. An antagonist sitting at the nicotinic receptor will prevent the attachment of the acetylcholine neurotransmitter and thus inhibiting its functions. This results in the inhibition of the normal functions of the neurotransmitter. The use of an antagonist leads to the decrease in the memory and cognition of the person who has used it. Since the antagonist inhibits the functions of the neurotransmitter, then, the poor learning and cognition of people who have used nicotinic receptor antagonists implies that the neurotransmitter increases them. Most of the people who have had a long term use of the nicotinic receptor antagonists are predisposed to dementia and decrease in their cognitive functions.
In dementia, there is progressive decrease in the number of acetylcholine neurotransmitters. This can result from many factors, including the normal aging process. Decrease in the brain matter leads to decrease in the specific neurons and neurotransmitters. In dementia, brain atrophy leads to decreased amount of neurons present in the brain which is manifested by decrease in the size of the brain. Decrease in the neurons globally in the brain leads to decrease in the specific neurons including the nicotinic systems. The decrease reduces the number of neurotransmitters for the nicotinic receptors and also the receptors available. Therefore, the enhancement of the cognitive aspect of the brain by the nicotinic receptors is lost. This may explain why there is a decrease in the cognitive function of the brain in individuals as they grow older because they continue loosing the nicotinic neurons (Levin, & Simon, 1998).
Malnutrition has been associated with decrease in the mental functions of individuals. Malnutrition decreases the synthesis of acetylcholine neurotransmitter. This will result in less neurotransmitter in the individual which will result in decreased stimulation of the brain. The person will be unable to synthesize enough neurotransmitter which results in decreased post synaptic stimulation and thus decrease cognitive function of the brain of that individual. This illustrates the necessity of the nicotinic system in the b rain functions, especially those concerned with memory and cognition. With decrease in the acetylcholine neurotransmitter, there is no enhancement of the brain cognitive function, a factor which is responsible for decreased mental functions of the people suffering from malnutrition. Children who have a poor nutritional status usually perform poorly in class as compared to the other children with proper nutritional status.
In the treatment of the mild cognitive impairment, the combination of Piracetam and choline has been shown to show better results than when used alone. Choline increases the ability of the drug to treat cognitive impairment especially in the older people. When the choline is not used with the drug, there is less improvement. This illustrates that choline is a very important component of the treatment of the cognitive disorders (Beglinger 2009). Choline is necessary in the synthesis of acetylcholine neurotransmitter which is the main neurotransmitter in the nicotinic system. Increased neurotransmitter levels in the brain are directly related to increase in cognitive function of the brain (Schultz, 2010). A person will respond more to the combination of the two drugs than when one drug is used alone. This therefore illustrates the important role of acetylcholine neurotransmitter and the nicotinic system in the brain functions such as cognition and memory (Health Concerns, 2010).
According to Rogers, (2007), caffeine increases the functions of the brain in the same way as acetylcholine. The author shows that caffeine increases the firing of nicotinic neurons which increases the memory functions of the brain. Caffeine is associated with an increased acetylcholine neurotransmitter in the brain and thus more stimulation of the brain (Richmond, 2010). This is evidenced by the fact that when people take caffeine containing beverages, their cognition and memory increases and thus making them understand things better (Mattsson 2009). With the use of caffeine, there is increase in the amount of neurotransmitter in the brain increasing the stimulation of the brain. As a result, people taking caffeine will tend to understand things better than their counterparts not taking drinks with the caffeine content. Caffeine has thus been used by people to enhance their cognition levels especially by students during exam times (Rogers, 2007).
Some herbal medications contain inhibitors of acetyl-cholinesterase enzyme, according to Goldman, (2001). The inhibition of acetyl-cholinesterase leads to decreased elimination of the acetylcholine in the brain. The enzyme acts on the neurotransmitter to convert it to metabolically inactive metabolite (Lambert 2009). If this enzyme is inhibited, there is decrease in the conversion of acetylcholine neurotransmitter to inactive metabolites (Greenberg 2009). As a result, there is continued activation of the post synaptic membranes of the nicotinic system. This leads to an increase in the stimulation of the brain and increased cognition in the person. This forms the basis of the treatment with such herbal drugs since they contain the inhibitor of the enzyme, (Goldman, 2001).
Jia, (2008) argue that the ability of the brain to synthesize acetylcholine neurotransmitter is a very important component of cognition. Synthesis of the neurotransmitter is depended on the availability of the nutrients and the enzymes. If the nutrient intake is decreased as in older people, there is a decrease in the substrate for the enzymes which synthesize the neurotransmitter. This results in decreased acetylcholine neurotransmitter which will then affect the cognitive functions of the brain. They argue that a good diet is important in the prevention of dementia and cognitive impairment (Desikan 2009). According to the author, the ability of the brain to synthesize the acetylcholine neurotransmitter makes the person be able to have a proper cognition and memory. However, its decrease leads to decrease in both cognition and memory of that person (Saxton 2009).
Stimulants which are composed of acetylcholine stimulate the brain in some people and in others cause psychosis. This indicates that the acetylcholine neurotransmitter increase the amount of stimulation to the brain which may result in high brain function. It can lead to the states of maniac as the person gets over stimulated (Tolboom 2009). Normally, the cholinergic agonists lead to an increase in the brain function resulting in increased brain activity and thus increased cognition. They have even been abused by people who want to increase their attention to a certain activity. University students use the drugs to increase their memory especially during exams which leads to more stimulation of the brain and thus increased memory and cognitive function (Davatzikos 2009).
Drugs such as acetyl-cholinesterase inhibitors have been shown to increase the cognitive ability of a person while those which increase the breakdown of acetyl-cholinesterase decrease the cognitive ability of a person. In the brain, acetyl-cholinestaress decreases the acetylcholine enzyme by converting the metabolically active enzyme to inactive metabolites. This results in a decreased amount of acetylcholine neurotransmitter (Mitchell, 2009). Decrease in the enzyme leads to a decreased stimulation of the nicotinic system and thus less effects of the acetylcholine. O the other hand, if there is inhibition of the enzymes which breaks down the neurotransmitter, there available acetylcholine neurotransmitter is retain in the brain which continues to stimulate the brain. It therefore uses the available acetylcholine to increase the brain activity (Symmonds, 2010). With the use of the inhibitors of the enzyme, very little acetylcholine available in the brain is able to lead to a lot of stimulation of the brain and thus make the cognitive function of the brain increase (Shinnoa, 2007).
Cortical cholinergic innervations increase the processing of information in the cortex. They increase the ability of the brain to process the information it is receiving from the peripheral receptors. The brains ability to make connections with other neurons is enhanced and thus makes more able to process the information faster. The general efficacy of the cortical neurons is increased (Williams 2009). The increase in the processing of information in the cortex is an essential component of cognition. If the cortex processes the information faster, the cognition of the person is increased and the decrease in the processing of the information in the cortex leads to decrease in the cognition of that person. The acetylcholine increase brain activity generally and thus makes the person more alert while at the same time increasing the memory of the person (Sarter, & Bruno, 1997).
Acetylcholine is a neurotransmitter in the nicotinic system. Decrease in the acetylcholine neurotransmitter has been implicated in decreased cognitive function of an individual. In addition, the decrease in the cholinergic neurons leads to decrease in the cognitive function of that person. Diseases which lead to decrease in the acetylcholine neurons lead to decreased cognitive function. In addition, diseases which lead to decrease in the acetylcholine neurotransmitter or decreasing the transmission in the cholinergic system decrease the cognitive ability of that person.
Drugs containing acetylcholine neurotransmitter increase the cognitive ability of the people who take them. Acetylcholine has been used in increasing the person's cognitive ability in people and thus makes them increase their cognitive ability. Drugs which contain acetyl cholinesterase inhibitor decrease the conversion of acetylcholine in the brain to inactive metabolites and thus increase the half-life of the neurotransmitter. This increases the amount of acetylcholine in the brain and increase brain stimulation and thus increasing the cognitive function of the brain.