Compare and contrast different neuronal and neurotransmitter abnormalities on behaviour

University Degree Medicine and Dentistry

The brain is an incredible organ, and the most complex computer in existence. It contains billions of brain cells, or neurons, with multiple connections to one another. Information is sent between neurons via chemical messengers called neurotransmitters, which cross the small synapse, the miniscule gap between two neurons. All of the body’s functions, from the most simple to the most complex, depend on the transmission of these chemical messengers between the cells of the brain. Therefore, the health of neurons in the brain and the way they transmit their array of neurotransmitters crucially affects behaviour.

Damage to neurons, both to the neuron itself and to the quantities of neurotransmitters released into the synapse, has been linked with a number of disorders. Many of these are characterised by a variety of abnormal behaviours. This essay will examine the neuronal and neurotransmitter abnormalities of two well-known disorders, Alzheimer’s disease and Schizophrenia, and compare the abnormal behaviours sufferers of these diseases exhibit.

Alzheimer’s disease belongs to the class of senile dementia disorders, and accounts for fifty per cent of all cases (Wilson 2003). It was first officially recognized in a fifty-one year old lady by Alois Alzheimer in 1906, by the identification of various abnormalities in the cerebral cortex (Kolb & Whishaw 2001). It is characterised by memory and related cognitive deficits, disorientation for time and place, inappropriate emotional responses, and in some cases hallucinations, hostility, and paranoia.

Schizophrenia on the other hand tends to appear in late adolescence to early adulthood (Pantelis et al 2002). It is an extraordinary disease, with symptoms which are hard to generalise. Some researchers have suggested that Schizophrenia is not in fact one, but a group of diseases which should be treated as such (Wilson 2003). There exist within schizophrenia two widely set of symptoms, sometimes called Type I and Type II, or positive and negative symptoms. Positive or Type I behaviours include delusions, hallucinations, and thought disorders; while Negative or Type II behaviours include social withdrawal, lack of effect, and reduced motivation (Carlson 1998).

Although it is relatively unknown in the lay world, there exist some similarities in the neuronal and neurotransmitter abnormalities seen in Alzheimer’s Disease and Schizophrenia (Spitzer 1999) and in the subsequent abnormal behaviour they give rise to (Spitzer 1999). In fact, Kraepelin, one of two psychiatrists who discovered schizophrenia in the early 20th century, was so struck by the ‘progressive intellectual deterioration’ of his patients, that he termed the disorder dementia praeox, believing it to be due to a deterioration of the brain often seen in dementia disorders such as Alzheimer’s. This belief has been questioned by the other discoverer of schizophrenia, Bleuler, who did not believe that schizophrenia was due to degeneration of the brain, and was not a progressive disease. However, he was struck by the dissociation of thoughts, words, and emotions in schizophrenia, disruptions which are also present in sufferers of Alzheimer’s (Wilson 2003).

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It has been found that levels of the neurotransmitter AcH is particularly low in people with Alzheimer’s due to a destruction of cholinergic, or AcH producing neurons in the basal forebrain. This is thought to contribute to the deterioration of memory seen in sufferers, starting with a gradual loss of memory, leading to sufferers being unable to carry out every day tasks. (Wilson 2003). (Carlson 1998). Glutamate, an amino acid that acts as a neurotransmitter, is also low in sufferers of Alzheimer’s, as a result of the disruption of glutamatergic neurotransmission. This deficit also contributes to poor memory, as well as learning difficulties. (Greenamyre et al 1988). Deficits in memory have also been observed in Schizophrenia patients, although such deficits have not been adequately characterised. Unlike Alzheimer’s however, such deficits are not degenerative (Pantelis et al 2002). Also, AcH is not thought to play a role in the memory deficits of schizophrenia, rather a reduction in size of the Hippocampus with a haphazard arrangement of it’s neurons is thought to cause this (Wilson 2003).

A further feature of Alzheimer’s is a loss of cortical neurons beyond that normal with ageing (Hart & Semple 1990), which affects a person’s perceptions, memories, and the way they formulate and execute plans (Carlson et al 2000). As in Alzheimer’s, disturbances of the cortex have been documented in Schizophrenia, particularly of the dorsolateral prefrontal cortex. This has been linked with deficits in tasks of executive function, (Pantelis et al 2000), such as attention, freedom from distractibility, mental flexibility, and abstract reasoning (NAN 2000) . The prefrontal cortex is responsible for formulating plans and strategies (Carlson 1998), and in some cases damage has led to thinking so disorganised in schizophrenics that it resembles ‘the cognitive decline of dementia’ (Wilson 2003).

There is also a development of neuritic plaques concentrated in this region, particularly the temporal lobe (Kolb & Whishaw 2001). These are extremely large masses of extra cellular protein and swollen neuronal processes. Damage to the temporal lobe affects the auditory association cortex, the visual association cortex, and the hippocampus, affecting the recognition of objects by sight, the perception and production of speech, as well as learning and memory (Carlson 1998). There is no incidence of neuritic plaques in schizophrenia. However, the temporal lobe is affected, particularly the parahippocampal gyrus on the median side. This too has an effect on memory, with a difficulty in linking stored memories to current stimuli (Pantelis et al 2002).

Neurofibrillary tangles are also characteristic of Alzheimer’s disease, consisting of tinted masses of protein in the cytoplasm of neurons (Wilson 2003). As the disease progresses, neurons begin to deteriorate (Whishaw 2001), with a restriction in dendrite branching (Taylor & Francis 1990). This results in a progressive decline in all physical and intellectual functions that eventually result in death (Wilson 2003). These abnormalities do not feature in Schizophrenia, meaning it is not a degenerative pathogenic disease.

Famously, sufferers of Schizophrenia often experience auditory, visual, and olfactory hallucinations (Carlson 1998), however this is also the case with some sufferers of Alzheimer’s, although incidences are not as prevalent (Wilson 2003).

As mentioned previously, schizophrenia consists of two groups of widely different symptoms, termed Type I and II, which can exists separately or together. The existence of such differing symptoms in the same disease suggests that disturbances must exist in ‘widely different parts of the brain’. (Wilson 2003). Research suggests that positive symptoms are to do with abnormalities in neurotransmitter pathways, while negative symptoms are due to brain damage. However, some believe there to be a common set of underlying causes which can explain both. (Carlson 1998). This provides evidence of similarities in Alzheimer’s and Schizophrenia, in that that there is evidence of both brain damage and neurotransmitter abnormalities in both.

One of the most influential theories of schizophrenia is the dopamine hypothesis, which stipulates that excessive levels of dopamine are responsible for at least the positive symptoms of schizophrenia (Wilson 2003, Carlson 1998). This has been proven by the fact that Amphetamine and Cocaine use produce or exacerbate Type I symptoms stimulate dopamine receptors in the brain. Further, drugs which lessen these symptoms act by countering the action of dopamine (Wilson 2003).

There is also a link between dopamine and Alzheimer’s disease, although in the case of Alzheimer’s it is a deficit in the neurotransmitter which seems to cause the problem. The drug Aniracetam has recently been shown to increase extracellular dopamine in rats (Shirane & Nakamura), and is beneficial in sufferers of Alzheimer’s showing mild to moderate cognitive impairment (Lee & Benfield 1994).

A further theory of the development of schizophrenia suggests that sufferers start to show brain abnormalities before birth, in the form of a lesion in the prefrontal cortex caused by abnormal gene activity. This is likely, considering that the concordance rate for schizophrenia in monozygotic twins is at least four times higher than it is in dizygotic twins

Although it’s seeds are sown before birth, Schizophrenia does not usually appear until adolescence or early adulthood. The explanation for this is that the prefrontal cortex only completes development during this period. Emotional, social, and cognitive abnormalities often present themselves in children who will go on to develop Schizophrenia as adults, which act as precursors to the disease (Pantelis et al 2002). If we assume that genes affect schizophrenia development, then that provides us with a further comparison with Alzheimer’s Disease; as two genes have been isolated which are thought to carry the disorder. However, there are no childhood warning signs for Alzheimer’s as there are in Schizophrenia.

To conclude, sufferers of Schizophrenia and Alzheimer’s share a surprising neuronal and neurotransmitter abnormalities, which leads to common behavioural symptoms in the two in areas such as memory, perception, and the organization of thoughts. Such similarities are surprising, as it is the very stereotypical symptoms of hallucinations in Schizophrenia and memory loss in Alzheimer’s which are well known. However, there also exist significant differences between the two diseases, such as the non degenerative nature of schizophrenia, an absence of Neurofibrillary tangles and neuritic plaques, and the different role dopamine plays in each disorder. A last similarity is the devastating effect both diseases have on the sufferers and their families, and the need for further research to enable a greater understanding.

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