Topic: Laughter is the best medicine

Delia Luo: 3417179
Sophia Tongue: 3417194
Tian Lei Wang: 3421054
Samantha Tang: 3437961

1. Introduction

Julie Power’s article, ‘Laughter and music better than drugs for dementia patients’, featured in The Age newspaper on August 3, 2013. Power discusses the results of a recent study into the effectiveness of humour therapy in the treatment of dementia, a syndrome characterised by ‘problems of short-term memory and other cognitive deficits’ (Holmes, 2012). The three-year study, which was run by the Dementia Collaborative Research Centre at the University of New South Wales, involved weekly visits to 17 nursing homes by teams from the Sydney Multisite Intervention of LaughterBosses and ElderClowns (SMILE). The experimenters tested the effect of the humour therapy session on patients’ rates of depression, agitation and behavioural disturbances, as well as their social engagement and quality of life.

Power’s article focuses on the experiences of dementia patients receiving the treatment from the Summit Care nursing home in Randwick. The article discusses how the treatment has mimicked the effect of drugs (namely, risperidone) in reducing agitation and depression rates amongst patients. The significance of the study's findings largely hinges on the fact that using laughter therapy allows patients to avoid many of the side effects associated with drug interventions. Since the article focuses on dementia amongst the elderly, we will limit our discussion to the two leading types of dementia within this group: Alzheimer’s disease and vascular dementia.

This article is of interest to us since the study it discusses paves the way for the development of non-pharmacological interventions in the management of dementia. Since this condition affects up to 1 in ten Australians over the age of 65 (Commonwealth of Australia, 2013), the need for safe and effective management programs is essential. It is important, however, to also consider how accurately the media has represented the scientific developments achieved through the study. The interpretation of scientific findings and the significance placed on personal testimonies often lead to the misrepresentation of the scientific process.

2. Neuroscientific Context

2.1 What is dementia?

Dementia is a term that describes a collection of symptoms that are caused by disorders affecting the brain. Poor memory function, reasoning and judgement are just a few symptoms that describe dementia. Brain function is affected enough to interfere with a person's normal social or normal life. Anybody can suffer from dementia, but it is more common after the age of 65. It is not, however, a normal part of ageing (What is dementia?, 2012).

Alzheimer's disease is the most common form of dementia, accounting for approximately two thirds of all dementia cases. It usually begins with memory loss then a gradual decline in cognitive abilities including lapses of judgement, personality changes, disorientation about place and time, depression and anxiety. Alzheimer's disease is characterised by two abnormalities in the brain: amyloid plaques and neurofibrillary tangles (Holmes, 2012).

Vascular dementia is the second most leading cause of memory impairment in the elderly after Alzheimer’s disease. The symptoms of vascular dementia may appear suddenly after a stroke, or appear gradually as a result of a series of mini-strokes. Vascular damage deep in the brain results in poor concentration and planning, loss of insight and apathy, and diminished motivation and initiative. If the cortex is damaged, then the patient may experience such symptoms as changes in sensory and motor functions, language impairment, memory loss and confusion (Vascular dementia, 2005).

2.2 Causes of dementia

2.2.1 Alzheimer’s disease Amyloid plaques

Although there is no clear consensus on the causes of Alzheimer’s disease, there is increasing support towards amyloid plaques as being the main contributing factor in the degeneration of neurons characterised in Alzheimer disease (Cummings, 2004). Initially, it was thought that the build up of amyloid was the origin of toxicity to brain. However, recent studies suggest that the decomposition of amyloid β (Aβ) into amyloid fibrils that clump to form amyloid plaques elicit neuronal dysfunction followed by brain atrophy (Hardy & Selkoe, 2002). A mutation in the amyloid precursor protein (APP) heightens the self aggregation of Aβ peptides into amyloid plaques and Aβ oligomers. Aβ oligomers are smaller bundles of fibrils of 2-12 peptides and are thought to be more degenerative than fibrils. The reason behind why Aβ aggregates remains unknown but what is apparent is the neurodegenerative nature of these aggregates and how it interrupts synaptic transmission between neurons (Ballard et al., 2011)

Figure 1: Formation of Aβ plaques from APP Neurofibrillary tangles

It appears that amyloid plaques are not independent in causing Alzheimer’s disease but manifest alongside neurofibrillary tangles (NFTs) as major causes of neurodegeneration. The major component of neurofibrillary tangles is Tau, a microtubule-associated protein that stabilises microtubules. Microtubules are essential expressways within neurons that allow for nutrient transportation and Tau is considered a structural protein supporting these microtubules (Ballard et al., 2011). Tau is a soluble protein; NFTs however, are formed by insoluble aggregates. Tau monomers like Aβ bind together to form oligomers that further aggregate into NFTs (Ballard et al., 2011). Under pathological conditions, neurofibrillary tangles are hyperphosphorylated causing it to dissociate from microtubules, essentially starving the neuron and causing neuronal death (Gotz & Ittner, 2008).

Figure 2: Formation of neurofibrillary tangles

2.2.2 Vascular Dementia

The main cause of vascular dementia is infarctions, areas of dead tissue resulting from oxygen deprivation due to lack of blood flow to the area. Infarctions manifest in many ways in vascular dementia, including multiple cortical infarctions, subcortical infarction and single strategic infarction (Amar & Wilcock, 1996).

Multiple cortical infarctions are distinguished by transient ischemic attacks and stroke episodes resulting in dementia (Desmond, 2004). These events cause oxygen deprivation in the brain causing universal neural death. Most vascular dementias result from multi-infarcts where cortical damage is responsible for cognitive impairment (Lee, 2011). As cognitive impairment persists, memory areas are affected causing either abrupt or gradual memory loss.

The primary types of brain lesions found in subcortical infarction (SCI) are lacunar infarcts and white matter lesions. The primary mechanism underlying SCI seems to be the white matter degeneration following prolonged infarction due to vessel wall damage caused by the thickening of vessels walls accompanied by the narrowing of lamina, in the arterioles that drain into it (Amar & Wilcock, 1996). Vessel damage creates poor blood flow to the hippocampus and surrounding areas of the brain, starving it of oxygen. This results in memory loss.

2.3 Drug intervention: Risperidone

Figure 3: Structural formula of Resperidone
Figure 3: Structural formula of Resperidone

The most problematic behavioural and psychological symptoms of dementia (BPSD) include agitation, aggression and psychosis, the latter of which has a prevalence rate of 90%(Brodaty et al, 2001). To treat these behavioural disturbances and psychotic symptoms (hallucinations, delusions), dementia patients are sometimes prescribed atypical antipsychotics such as risperidone.

2.3.1 Mechanism

Risperidone works by changing the activity of certain neurotransmitters in the brain especially serotonin and dopamine. A neurotransmitter's attachment to a receptor either stimulates or inhibits the function of the nearby nerves. Dopamine and serotonin are involved in regulating mood and shaping certain kinds of behaviour. In animal models, lower serotonin levels correlate with higher levels of voilence (Krakowski, 2003). The behavioural and psychotic symptoms that may occur in some dementia patients may be the result of an excess of serotonin or dopamine in the brain. Risperidone is a strong antagonist of the 5HT2A serotonin and D2 dopamine receptors (Janssen et al, 1988). By blocking the activity of serotonin and dopamine, excessive activity of these neurotransmitters is prevented, allowing these symptoms to be reduced. Its activity is shown in Figure 4.

Figure 4: Risperidone blocking dopamine D2 receptor
Figure 4: Risperidone blocking dopamine D2 receptor

2.3.2 Benefits

This drug has been associated with a relatively low incidence of extrapyramidal symptoms (motion disorders) compared with traditional agents (Catalan & Penades, 2011). Also the fact that risperidone is metabolised fairly quickly, any nausea that may occur usually subsides in two to three hours (Meuldermans et al., 1994). Two randomised controlled trials found that risperidone is effective in the management of psychotic symptoms and aggression in dementia (Katz et al, 1999; Brodaty et al, 2003). In Kurz, Schwalen & Schmitt’s (2005) study, risperidone improved all behavioural and psychological disturbances examined (including aggressiveness, agitation, social withdrawal, delusions). Thus, off-label uses of this drug have shown a moderate to high level of efficacy.

2.3.3 Side effects

However, it is important to note that risperidone has been associated with an increased mortality rate. (Singh & Wooltorton, 2005). Seventeen controlled studies of elderly dementia patients showed that patients that were treated with risperidone were 1.6 to 1.7 times more likely to die than patients given placebo (Lenzer, 2005). Most of these deaths were from cerebrovascular adverse events including strokes, suggesting an increasing incidence of stroke with risperidone use (Ballard, Waite & Birks, 2006). Other side effects associated with the use of risperidone including sleepiness, anxiety, dizziness and trembling (Wooltorton, 2002). Weight gain and the subsequent risk of developing diabetes is also an issue since changing the activity of serotonin receptors can affect metabolism (Newcomer, 2005).

Using risperidone as a way of relieving behavioural and psychotic symptoms is very risky and has the potential to induce adverse side effects. Although there are studies that have demonstrated its effectiveness, it is still essential to look into other treatment methods that do not result in such severe side effects.‍

2.4 Neuroplasticity and laughter therapy

2.4.1 What is neuroplasticity?

Figure 5: Increased post-synaptic excitatory responses following long-term potentiation

Neuroplasticity refers to the ability of the nervous system to reorganise its connections and structure in response to intrinsic and extrinsic stimuli (Ruge et al., 2012). This ability serves as the mechanism behind music, laughter and language therapies in their treatment of dementia (Falchook et al., 2013). A central model for the reorganisation and strengthening of synaptic connections between cells is a process known as ‘long-term potentiation’.

Long-term potentiation is a process involves two glutamate receptors: NMDA receptors and AMPA receptors. When a neural pathway is activated by a high-frequency stimulus, depolarisation causes an influx of calcium ions from postsynaptic NMDA receptors. This flux of calcium subsequently activates kinases like calcium calmodulin-dependent protein kinases II (CaMKII), which, in turn, drive AMPA receptor phosphorylation. That is, the activation of CaMKII by calcium ions increases both the conductance of existing AMPA receptors and the number of AMPA receptors in the post-synaptic membrane (Feldman, 2009). The increased activity and number of AMPA receptors strengthens the synaptic connection between the two cells by generating larger postsynaptic excitatory responses to future stimuli (Clapp et al., 2012). This can be seen in Figure 3.

It is believed that memory formation is based on this model, as neurons are wired to form small networks of cells that together create memories. In order to create new memories, these connections are broken, weakened or rewired to other neurons to form stronger connections. It is assumed that since neurons can change independently, they can make connections to multiple neurons and form numerous presynaptic and postsynaptic relations (Sossin, 1996). In dementia, neural degeneration results in the loss of memory networks, therefore resulting in such symptoms as memory loss.

2.4.2 How does laughter therapy work?

Patients suffering from dementia experience a significant loss of synaptic transmission. In Alzheimer’s-type dementia, this loss can be attributed to the neurodegenerative effects of β-amyloid plaques and neurofibrillary tangles, and is most prevalent in the hippocampus, the frontal cortex and the temporal cortex (Clare, King, Wirenfeldt, & Vinters, 2010). Laughter therapy works by enhancing long-term potentiation in these parts of the brain. This is because the therapy encourages social interaction, which has been shown to be one of the most powerful influences on neuroplasticity. (Davidson, & Ewen, 2012). Since the social interactions in which humans engage are highly varied and complex, the brain is forced to adapt to a variety of stimuli by both strengthening existing networks and generating new ones (Vance & Crowe, 2006).

The importance of social interaction in improving neuroplasticity has been revealed by a number of studies. In humans, various epidemiological studies have found that adults with stronger social experiences are significantly less prone to developing Alzheimer’s disease and dementia. This is because mental stimulation enhances synaptogenesis (Fratiglioni, Paillard-Borg & Winblad, 2004). Similarly, in a study Lu et al. (2006), for example, 22-day old rats were assigned to live either in isolation or with other rats for 4 to 8 weeks. Those reared in isolation were found to have significantly lower rates of long-term potentiation in the hippocampus, and neurogenesis in the dentate gyrus. These rats also demonstrated reduced learning and memory – symptoms that were clinically similar to those of dementia. However, when these rats were later exposed to social interaction, these symptoms were improved. From these findings, it can, thus, be inferred that laughter therapy encourages neurogenesis and LTP in the hippocampus – a region involved in memory consolidation (Graham, & Hodges, 1997).

These findings can further be corroborated by recent studies that have detected the formation of new neurons in the dentate gyrus of adult mammals. This is significant since most neurons in the mammalian brain are generated early during development and are often not replaced when lost (Kornack, & Rakic, 1999). Since atrophy in the hippocampus of Alzheimer’s patients serves as a predictor of cognitive impairment, the regeneration of synapses and neurons in this area helps to reverse this cognitive degeneration. This can explain how previously non-verbal patients began to have conversations with staff, as mentioned in the article. Long-term potentiation can strengthen the connection between the hippocampus and surrounding white matter, thus enabling for the reacquisition of language (Meinzer et al., 2010).

Neurogenesis in the dentate gyrus, an area within the hippocampus, has also been found to increase with chronic treatment with antidepressants, further illustrating how laughter therapy is able to improve mood (Malberg et al, 2000). The SMILE study found that humour therapy significantly reduced levels of agitation over time as well as behavioural disturbances. Thus, humour therapy had a similar effect to risperidone but had the added benefit of not producing any of the side effects that are associated with the use of this atypical antipsychotic (Low et al, 2013).

3. Critical Analysis

3.1 Target Audience and Aim

Firstly, the article ‘Laughter and music better than drugs for dementia patients’ was featured in The Age, which is a popular local newspaper in Victoria. The article is therefore targeting the general public, rather than those with a medical/scientific background or simply those who are affected by the disease. The pitch of the article appropriately targets this audience, avoiding the use of excessive jargon and explaining the results of the study in simple terms.

This article aims to inform the general public of humour therapy as a treatment for dementia. However, since it appears in a newspaper, it also seeks to keep readers interested and entertained. This is helped by the recent and topical subject of the article, making it relevant to current neuroscience research and the general public.

3.2 Quality of information

There exists some inconsistencies between the primary journal article and the media article. Power's article fails to
reveal any limitations of the SMILE study (Low et al., 2013) and portrays this method of treatment as incredibly successful. The study, in fact, concluded that humour therapy did not significantly reduce depression; only that it reduced agitation, social engagement and quality of life. This is not mentioned in the article, thus misleading readers and reducing the integrity of the article. Furthermore, the study did not specifically target dementia patients, as suggested by the article, but instead targets nursing home residents as a group. Laughter therapy is, therefore, falsely depicted as a specific treatment for dementia.

The article solely focuses on the effects of the treatment in one nursing centre and primarily cites evidence that is in the form of testimonies. For example, the article quotes Barry Cowing, the operations manager of the nursing home: 'We had a woman who was totally non-verbal … who started to have conversations with staff and with her family.' This claim simply serves as testimonial evidence, not scientific evidence, especially since Cowing is not an expert in the field. The article's emphasis on personal testimonies makes it highly subjective - something that could be improved by instead putting a greater emphasis on research. Citing the study that Cowling’s nursing home participated would allow the audience to read the process of conducting the study and finding out more detailed information. The discussion of more than just one study would also enhance the reliability of the article.

Although the inclusion of a statement from a psychologist, a medical professional involved in dementia research, gives the article some credibility, the article is also misleading in how it explains the mechanism behind laughter therapy. The title, although engaging and appealing is ambiguous. It is only towards the end of the article, with the statement from the psychologist that we realise that it is not actually humour and music that are the driving factors for this treatment but the role of interaction. This area is not sufficiently emphasised in the article, therefore misinforming readers, particularly those who do not read the entire article.

4. Appendix

Initially, the members of our group were unsure which topic under neuroscience would best fit the criteria of this project; therefore, we decided to conduct generalised research where we individually suggested topics and communicated which to address. This investigation exploited assorted media search engines including YouTube and newspaper websites. To allow for further discussion, a Facebook group page was set up where ideas could be shared and commented on. A few topics were brought to light however; the choosing of the topic ‘Laughter is the best medicine’ was a unanimous decision by the members after in-depth discussion. It was apparent that all members were drawn to the chosen article due to its relatable nature to the modern context.

Following the selection of Dementia as our main focus, we began more comprehensive research through using the ‘SearchFirst’ function on the UNSW library website. After understanding the general theories behind dementia, the main areas of focus were gathered and allocated to each member. Subsequently, our members conducted thorough investigation on the topics that had been allocated, utilising the ‘Google scholar’ as an initial search engine and further directing research into UNSW’s various databases where further detail could be attained. The articles contained studies conducted in the area that both supported and contradicted past research. Therefore, it was important to assess all articles objectively.

While writing up our findings, group members found it beneficial to share articles with each other that they thought were more explicit and centred on our groups focal points. Some members found areas of overlap but overcame these issues by clearly allocating sections to revise. Throughout the entire process, the group organised meetings to improve what had already been completed while progressing to what was still to be completed. Meanwhile, we maintained communication through the Facebook group.

An overall consensus emerged that our wiki was well above the word limit and lacked sufficient explanation of the mechanisms behind laughter therapy. It was, however, difficult to both significantly cut down whilst adding additional information. To overcome this issue, the group chose not to expand the drug therapy section, but instead link it more to laughter therapy. To further tackle the mechanisms behind laughter therapy, we focused on the neuroscience behind laughter therapy, expanding on the parts of the brain undergoing long-term potentiation.

Another major area of critique was the need to compare the media article to the original journal article in the critical analysis. We dealt with this by locating the original article and assessing the media article's representation of the journal article's findings. The misrepresentation of various parts of the study by the media article were discussed. To accommodate for adding to these sections, areas in the scientific context that were unnecessary or repetitive were removed and sentences were made to be more concise. We also reviewed any grammatical or spelling errors.

5. References

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Looks good - you seem to have identified a good range of contextual material to cover for the neuroscientific background.
Good luck.


Samantha: Effect of social interaction on neuroplasticity/Introduction
Stanley: What is dementia/Critical analysis
Delia: Current pharmacological interventions/Critical analysis
Sophia: Causes of dementia/Appendix
All members keep track of the references they have used and will compile together at the end.