Seminar 1 2011 Question Page


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Huntington's Disease: Understanding a Mutation - Questions Page

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Thank you for your contributions.  This page is now closed.




Tauranga Girls' College: Student AH 19th March 2011

Theoretically, if a person had 48 repeats of CAG but the 23rd one was CAT, because there may have been a mismatch and the 'fixing' enzyme replaced the wrong base, what effect would this have on the mutation?

A person has inherited Huntington's Disease from both parents. One parent had 42 repeats, the other 42. What effect would this have on their rate of deterioration? Would the disease progress twice as fast compared to a person heterozygous and 42 repeats?

What would happen if there was a large number of CAG repeats on another chromosome?


Pritika Narayan PhD Student, Centre for Brain Research 28th March 2011

- The problem is with the number of repeats in this instance and the change to the conformation of the original normal protein, depending on where in development this happened (i.e in germ cell line that gave rise to many other cells or in a cell that did not self renew?) would probably change the impact the mutation could have.

-Homozygosity results in a more severe disease course than heterozygosity, inferring that the normal allele in heterozygous individuals is possibly still active (Squitieri et al., 2003).

- The answer is dependent on whether it was in a gene or non coding region, and largely dependent on how ubiquitously expressed it is and the function of the protein encoded by the wildtype gene.

Colin Mak, Eric Kim and Renee Handley - PhD Students Centre for Brain Research 27th March 2011 

a) There would probably be little effect on the phenotype, if just one out of 48 CAG’s were changed, as it would still produce, by and large, a long polyglutamine tract.


b) As far as we know, there is no difference in phenotype between HD homozygotes and heterozygotes. This is called complete phenotypic dominance. This phenomenon is quite rare for dominant disorders – most dominant disorders have incomplete dominance, ie. the homozygotes have more severe symptoms and fast progression than heterozygotes, so the normal allele may confer some protection against disease. (see paper:
http://www.nature.com/nature/journal/v326/n6109/abs/326194a0.html)


c) There ARE other chromosomes that have large number of CAG repeats, eg. on the tata-binding protein (TBP) gene. Interestingly these genes may also play a role in Huntington’s disease. Also, there are many other diseases caused by problems with CAG repeats, including the spinocerebellar ataxias (SCA). So on the whole, CAG repeats may have different effects depending on the gene/chromosome they are on.


Otago Girls' High School: Student MH 18 March 2011- Hi, I have a couple of questions about the gene that causes HD and a simply random question.

If the CAG repeats was interupted by a different amino acid i.e. a mutation, will it be able to prevent the symptoms of Huntington's Disease?

And has there been any other protein found with 40 or more CAG repeats, as if the mutated huntingtin is the only protein in the body that contains more than 40 CAG repeats, couldn't there be a drug developed to specifically target the characteristics of the CAG repeats?

Also this is just a question that's a bit off topic, if the only genetic difference between a male and a female is the Y chromosome, is it genetically possible to create a female out of male DNA?

Pritika Narayan PhD Student, Centre for Brain Research 28th March 2011 

Many other polyglutamine repeat disorders exist, eg spinocerebellar ataxias (types 1-7).


Colin Mak, Eric Kim and Renee Handley - PhD Students Centre for Brain Research 27th March 2011


a) If an entire triplet were added, or a base were altered, then the DNA would still be read in-frame, and probably not much effect would occur. However if a single base were added or deleted, the reading frame would change, and wouldn’t code for glutamine anymore. It is hard to predict what effect this would have.

b) Yes there are other proteins with long CAG repeats, such as TBP. There is much recent research being performed to investigate how to specifically target the HD gene, and block the mutant allele using antisense or siRNA – the difficulty is in blocking ONLY the mutant allele and not the normal allele, as that is required for normal body function.


c) It would be difficult to create a female out of just male DNA. You would need to remove the Y chromosome and add an X chromosome, but this is probably beyond current scientific knowledge! There are also various disorders in which the number of sex chromosomes is altered to make a “female” phenotype, eg. Turner’s syndrome (XO) and Klinefelter’s syndrome (XXY)




Horowhenua College: Student JWilton 18 March 2011 Hello. I was wondering whether the epigenome would have a part to play in how the on set of different symptoms of HD are displayed and when they are displayed in identical twins? Thanks


Pritika Narayan PhD Student, Centre for Brain Research 20th March 2011

We have shown some interesting correlations between epigenetic (histone acetylation) changes and motor/motor/mixed symptoms among HD cases, however there are no HD twins in our study specifically and to the best of my knowledge, these epigenetic changes have not been studied yet in twin studies. However the fact that identical HD twins (who share the exact same CAG repeat mutation in the huntingtin gene) have definite variation in the age of symptom onset and type of symptoms, strongly suggests that genes alone are not able to account for this variation, implying a role for environment and potentially epigenetic changes in contributing to symptom type and onset in these individuals.



Newlands College: Student JKaur - 11th March 11:11 am

I am 17 years old right now and I would like to know if I have Huntington's Disease or not. Are there any tests that doctors can perform on me? I want to know this so then I can make well informed decisions now rather than later when it’s too late.


Professor Richard Faull, Centre for Brain Research, Live 17 March 2011

Theoretically a blood sample can be taken to perform the genetic analysis that would determine whether the person has the expanded CAG repeats on IT15 at a level that would cause the disease.
However it is not that simple. The international HD association has developed a process that states that it is important that a person goes through counselling to ensure that they are prepared for the outcome (whatever that may be) and have enough information to understand the outcome and cope with it. For instance if the person is in a family where HD is a question and nobody else in the family wants to take the test, the results may affect the whole family. If one person in the family takes the test and is found to be positive, this means that the parent who passed on that gene will also be positive for the disease and the siblings will have a 50% chance of being positive. If the parent finds out the result of the test for their child, they will also now know their own situation. This is complicated when we do not have a cure for the disease. People need to work with their doctors, the HD association and councillors to make sure that the testing is done in a way that will work for the whole family.


Colin Mak, PhD Student, Centre for Brain Research, 18th March 2011
Yes there is a genetics test (determining length of CAG repeats) that doctors can perform to determine if you have Huntington's Disease or not. However you must wait until you are at least 18 years old before you are eligible for genetic testing. Also you will be guided with counselling before and after the test to help you to make an informed decision.


Tauranga Girls' College: Student AH 19th March 2011

My cousins were able to get genetic testing before they were 18 (I think they might have to be 16?) to see if the had the gene mutation that causes stomach cancer. Why is that for Huntington's you must be 18 but others you do not?

Laura Fogg, Communications and Liaison Manager, Centre for Brain Research 28th March 2011

Huntington's disease is a very complex disease, both biologically and socially. The disease has a huge impact on families, affecting many generations at one time. There are many psychological impacts to consider, including life choices such as whether to have children and how the individual's future care will be planned. As a result of these psychological implications, the international HD associations have agreed that people need to be of an age to make informed choices- and this age is taken as 18.



Rotorua Boys’High School (live question 17th March)
You receive brains from all over New Zealand, how ,many of those are Māori seeing as it is forbidden to be buried without all of your body parts?

Professor Richard Faull, Centre for Brain Research, Live 17 March 2011

We receive brains from all over New Zealand for Huntington’s disease whereas for other diseases such as Parkinson’s or Epilepsy for technical reasons we can only receive brains from the Auckland region. We actually do not specifically collect data on the ethnic background of each donation. However I am Māori and we at the Brain Bank have strong ties to the Māori community as they are affected with Huntington’s disease as are any community. It is culturally a difficult for Māori to bequeath human brain tissue but the Māori community fully supports the programme. We have Māori PhD students doing some of the most exciting work in the centre which is done with the blessing and involvement of Māori communities throughout New Zealand. We work with Māori families who because of the regions they live in are unable to access support services for HD. For all people across the nation we support families with HD. We have had one donation from a family where the person with the disease was Pakeha but his wife was Māori. In this case we had a whole process with the familiy working through how to do this with their iwi. We have introduced the concept of whakanoa" for the blessing of human tissue for teaching and research when the tissue arrives. The family have visited the centre and have made the centre the guardians of the tissue. We look after all people and all people look after us.



Hillcrest High School – Cherry (livechat question 17th March)
Have scientist been able to trace the origins of where or when in the world the HD mutation first occurred


Professor Richard Faull, Centre for Brain Research, Live 17 March 2011

There are identified foci of where the disease first appeared in England and migrated out. What is interesting is that when a person has the CAG repeat at a level close to the toxic level of 36, (e.g. 30), when it is passed through the male line the mutation can jump up by say 10 repeats. So this has solved the riddle of how the disease can suddenly appear in a family - especially if this is transmitted through the paternal line. This is anticipation when in subsequent generations the mutation gets larger – which means that the disease onset is likely to be earlier.


Sacred Heart College Andrew Muller LiveChat question 17th March
If the memory section of the brain is damaged and stem cells are used to replace the damaged cells, would the memory be retained? 

Professor Mike Dragunow, Live 17th March 2011
This is a good question. There have been studies done in rodents that have shown that emotional memories of fearful events which are involved in things like stress disorders in humans are encoded in older parts of the brain – the limbic system and the amygdala. This study showed that is the cells that were responsible for the memory of the fearful event could be killed off, the animals no longer had a memory of that fearful event. One of the major challenges for stem cells is that the brain is very complex and if stem cells are going to replace damaged cells, those stem cells would have to integrate in a way that would recapitulate the circuitry that underpins that memory. For a complex memory , this is unlikely to happen. What it could do is the pathways could be reconstituted to allow new learning to occur. So I think getting back a memory would be very difficult.



Auckland Grammar School, Boris Yow (Live question 17th March)
If HD is due to a CAG repeat coding for glutamine, then can another codon coding for glutamine cause the same effect? 


Professor Mike Dragunow, Live 17th March 2011
There are a range of genetic disorders like HD that have genetic repeats in them that cause a diseased phenotype. Interestingly some of these diseases that have multiple repeat expansions can seed one other. For example the ployglutamines in Huntington’s can actually chemically seed repeat proteins from other diseases as well. There is a lot of overlap and people talk about protenographies. Neurological and other diseases caused by mis-folded proteins caused by these kind of repeat expansions.

 


Rotorua Boys’ High School (Live question 17th March)
Why is the number of CAG repeats more likely to increase in spermatogenesis rather than oogenesis

Professor Richard Faull, Live 17th March 2011
This is a great question because it is something that is unknown! We don’t know the answer however we do know that in spermatogenesis (the process of production of male gametes) there is a wide variation in the repeats in the individual sperm. We do not understand the mechanism that makes this happen. Genetics is very complex. Interestingly when for example you look at all the cells in the brain of a person with HD – you will actually find variation in the number of repeats within the one person. This is called mosaicism which is a genetic phenomena where you get a range of genotype in cells. In the areas of the brain where we see the strongest pathology (the most effect of the disease) we will find that there are higher number of repeats and greatest levels of mosaicism. Areas that are not affected by the pathology (show no damage from the disease) have less mosaicism. It is a complicated disease, and even 17 years after the discovery of the gene there is much to be learnt about the mutation and its effect. It is complicated.



Kelston Boys’ High School. Iefata Williams  (Live question 17th March)
If the excess polyglutamate chain affects the DNA by coiling it up and it easily comes off why do you not target the polyglutamate chain and just break it off and bring it out of the cell? thus stopping the coiling?
Professor Mike Dragunow, Live 17th March 2011
Protein chemistry is a very complex process and the tertiary structure of the protein (the final folding) is controlled in a very precise way. The way people are targeting this at the moment is looking at methods such as RNAi (as Pritika talked about in the seminar) to somehow silence the gene. It is possible that you could engineer enzymes that could target specific parts of the protein. You would have to work out a way of somehow chopping the unwanted part of the protein out and then have some way of ligating (joining) those sections back together again to form the normal protein. It would be very difficult of course because you would have to do it throughout the whole body. Presently impossible and even in the future extremely difficult and something that would be many many years off achieving if at all.



Jordan Carlton, Wellington Girls' College and Tauranga Girls' College Students,  LiveChat Question 17th March 
Can HD be linked to other issues or deficiencies and why? 

 


Colin Mak, PhD Student, Centre for Brain Research 17th March 2011
HD is mostly a genetic disease but it is possible that certain environmental factors, such as the level of family support or type of diet, may exacerbate/diminish the symptoms or delay the onset of symptoms.



Jenna Wilson, Waikato Diocesan School for Girls, LiveChat Question 17th March 
Why are more repeats more likely to occur in white Europeans rather than people of Asian or African descent?

Jacquie Bay LENScience 24th March 2011 

The frequency of the allele in the population will originate from the initial development of the allele in a population within evolutionary history. The variation we see in % frequency of the allele between different populations will have developed as a result of variation in the % of the allele in the founder populations in those geographic or ethnic groups. There is no evidence that the HD allele confers any fitness on carriers, so there is no selective advantage in having the allele. Because the impact of the allele usually occurs after child-bearing age, the allele is not impacting on the ability of the individual to pass on their genes, therefore it will continue in the population.




Nick B Hillcrest High School LiveChat Question 17th March
In general how much change in the phenotype could the epigenome account for as opposed to the actual genes themselves?
 

Pritika Narayan, Centre for Brain Research 24th March 2011
CAG repeat length is known to account for approx 50% of variation in age of onset (one of many phenotypic traits), so it seems plausible that environment accounts for the other 50%, however what component the epigenetics contributes to this is currently not known.


Ji Soo Kim Epsom Girls' Grammar School LiveChat Question 17th March

When the CAG repeat length increases does it increase the length of the whole DNA? Or does the CAG repeat increase in expense of another length of DNA?

Jacquie Bay LENScience 20th March 2011

The increase in the number of CAG repeats is an insertion into the gene – so the total length of the DNA is increased as a result of the mutation.



Kate Walmsley Wellington Girls' College LiveChat Question 17th March 
Can the brain make new stem cells or are you just born with all you will have?

Colin Mak, PhD Student, Centre for Brain Research 17th March 2011
The adult brain can make new stem cells, as was discovered in 1998 in the human brain, but only in certain areas (hippocampus and subventricular zone). However the adult stem cells in the brain are actually NEURAL progenitor cells, so have a more defined lineage and can only make BRAIN cells (neurons, astrocytes, oligodendrocytes).





Charlotte Duda Wellington Girls' College and Cameron Whiteman Onehunga High School LiveChat Question 17th March

Why do the CAG repeats increase from generation to generation ?

Jacquie Bay LENScience 20th March 2011

The mutation is not stable. This means that the mutation can change from generation to generation. As Professor Faull explained in the seminar, it is known that particularly in the formation of sperm, there can be a significant and unexplained increase in the number of repeats from one generation to the next. We do not know why this occurs but it does explain some of the change in the number of repeats from one generation to the next.

Colin Mak, PhD Student, Centre for Brain Research 23rd March 2011

This phenomenon is known as genetic anticipation. It may be due to the increasing number of repeats influencing the shape of the DNA, thus affecting DNA polymerase which is important in proofreading new DNA strands.



Andrew Ho Onehunga High School LiveChat Question 17th March 

Do anti-anxiety and anti-depressants work in the same way for people exhibiting the mood symptoms of Huntington's or do they respond differently?


Colin Mak, PhD Student, Centre for Brain Research 17th March 2011
The anti-anxiety/ depression drugs should work the same way (eg. blocking serotonin reuptake) but different patients may have different reactions to the drugs. so doctors must be consulted before using them.



Nick B Hillcrest High School LiveChat Question 17th March 

The genotype of identical twins are the same and the epigenome is by environmental factors if the twins were raised separately in different environment would the severity be different.

Jacquie Bay LENScience 20th March 2011

The variation in phenotype that we see in genetically identical twins is as a result of variation in the environment that they are exposed to during their lifetime. It is likely that this is the influence of the epigenome. The evidence from the twin studies that Pritika presented in the seminar has shown that identical twins with the same number of CAG repeats (identical genotype) can have differences in their age of onset of the disease and symptoms. This would suggest that it is possible that twins with HD, raised in different environments, could have different symptoms of the disease. The mechanism for this is still being explored.

The following references are provided for you by Pritika:  

Gomez-Esteban, JC, Lezcano, E, Zarranz, JJ, Velasco, F, Garamendi, I, Perez, T, Tijero, B (2007) Monozygotic twins suffering from Huntington's disease show different cognitive and behavioural symptoms. Eur Neurol 57(1): 26-30.
Friedman, JH, Trieschmann, ME, Myers, RH, Fernandez, HH (2005) Monozygotic twins discordant for Huntington disease after 7 years. Arch Neurol 62(6): 995-997.
Georgiou, N, Bradshaw, JL, Chiu, E, Tudor, A, O'Gorman, L, Phillips, JG (1999) Differential clinical and motor control function in a pair of monozygotic twins with Huntington's disease. Mov Disord 14(2): 320-325



Romeel Kumar Aorere College LiveChat Question 17th March 
Can’t they use stem cells from the umbilical cord to cure Huntington’s and if not at least repair the brain?


Colin Mak, PhD Student, Centre for Brain Research 23rd March 2011
There are still many ethical and scientific issues to overcome for use of umbilical cord stem cells before a cure is found. For example, we need to investigate which chemical signals/factors are required for the stem cells to turn into the correct neurons, to migrate to the correct area, and to functionally integrate into the existing neural circuitry. Also we need to find out how to stop the stem cells from over-proliferating, or they will turn into a tumour.
Another recent exciting finding has been that neurogenesis occurs in the adult human brain. This has the potential for therapy with fewer ethical issues (using your own cells) and rejection issues. However there is only a small amount occurring in small areas, so more research is required to harness this potential.



Kyle Tasker, Kelston Boys' High School LiveChat Question 17th March
Why doesn’t HD start straight away after birth if the CAG repeats are always there?


Colin Mak, PhD Student, Centre for Brain Research 23rd March 2011
This is unclear at present. It may be because the huntingtin protein takes some time to build up and affect cell function. However, there are often some minor mood changes occurring early in life before the chorea/motor symptoms arise.


Iefata Williams Kelston Boys’ High School  LiveChat Question 17th March 
Does Huntington have to be hereditary? Can it be caused by a mutation in non hereditary families of Huntington?

Colin Mak, PhD Student, Centre for Brain Research 23rd March 2011
Yes HD can be caused by a random mutation, ie. increasing the number of CAG repeats. However it is much more common that HD is inherited


Stephen Sit Onehunga High School LiveChat Question 17th March 
So how do CAG repeats relate to other repeat elements in DNA such as microsatellites CA for example?


Colin Mak, PhD Student, Centre for Brain Research 23rd March 2011 
There is no evidence that they are related.



Charlotte Duda Wellington Girls’ College LiveChat Question 17th March 
Can repeats of other glutamine codings also have the same effect of HD? (degeneracy)

Pritika Narayan, Centre for Brain Research 24th March 2011

The CAG repeat extension occurs by way of complementary binding (cytosine – guanine) causing a hairpin structure to form and aberrantly extend the repeat lengths on daughter strands. CAA will not bind complementarily to the same extent (no C-G binding to form hairpin).




Sophia Bicknell Wellington Girls’ College LiveChat Question 17th March  Does Alzheimer's have a genetic link like does it run in families?

Pritika Narayan PhD Student, Centre for Brain Research 20th March 2011 

Several genes have been implicated in increasing the risk of sporadic Alzheimer’s disease, including APOE4. There are also other risk factors such as getting older and being female. Also, less than 1% of all AD cases are a rare form of the disease called Early Onset Familial Alzheimer’s Disease, which is autosomal dominant, so runs much more in families (50% chance of inheriting the gene). This is caused by mutations in the APP, PS or BACE genes.



Nick B Hillcrest High School LiveChat Question 17th March

Since the repetition of CAG gets longer from generation to generation would Huntington’s disease eventually develop to an extent where foetus would just simultaneously abort by nature and therefore the disease disappears ?

Jordan Carlton Wellington Girls' College LiveChat Question 17th March 
So what happens to the final generation when the CAG is at the longest?

Jacquie Bay LENScience 20th March 2011

Repeats of more than around 100 are unusual and the longer the repeats the earlier the onset of the disease. Juvenile HD, with a large number of repeats is the most debilitating form of the disease and causes death prior to child-bearing. In cases of juvenile onset HD, the gene would not be passed onto the next generation.


Andrew Muller Sacred Heart College LiveChat Question 17th March

How is the number of CAG repeats accurately measured?

Jacquie Bay LENScience 20th March 2011

The test looks at the number of CAG repeats. DNA is isolated from a blood sample, and the region of interest (the part that contains the HD gene) is amplified using PCR. Restriction enzymes are used to cut the amplified DNA into fragments. Gel electrophoresis is then used to look at the size of the fragments of DNA and from this the number of CAG repeats can be determined.
For detailed information look here>>



Palmerston North Girls' High School: Student SP 14th March 2011

Hi. I was just wondering how the 'brain bank' was initiated and how beneficial it has been to researchers of neurological disease since its origin?

Colin Mak, PhD Student, Centre for Brain Research 24th March 2011

Prof Faull was given the brains of Huntington’s disease patients by their families in the 1980’s. He was asked to look at the brains and determine definitively with pathology whether their loved ones really had the disease (the gene was only discovered in 1993). It was in 1993 that the Neurological Foundation Human Brain Bank was formally set up, with the purchase of a -80oC freezer to store the brains. The Brain Bank now includes brains ranging from neurologically normal to Alzheimer’s, Parkinson’s, epilepsy, motor neuron and other diseases. The exceptional quality of the tissue, with little post-mortem delay, along with the dedicated commitment to informing and communicating with families before and after the donation, makes this invaluable resource highly regarded by and beneficial to researchers around NZ and overseas.

See link for further details: http://www.neurological.org.nz/About-Us/Human-Brain-Bank/ and also re-watch the seminar (especially from 26’11’’)

Laura Fogg, Communications and Liaison Manager, Centre for Brain Research 28th March 2011

Please also see the Centre for Brain Research website:

http://www.fmhs.auckland.ac.nz/faculty/cbr/about/brainbank.aspx


Palmerston North Girls' High School: Student SP 14th March 2011 

How much of an influence do psychology studies have on neurological diseases? Clearly they are currently not curable, but are there ways victims can to an extent fight back against the disease? Thanks. 


Professor Mike Dragunow Live 17 March 2011
The neuropsychological assessment is critical for understanding the disease itself. We have scanning studies to image the brain and genetic studies to look at the gene but we also have to look at the real phenotype which is the neuropsychological phenotype in the patients. That is particularly important if you are going to try and test therapies. You have to have something to test against and to measure so neuropsychology is extremely important for testing in HD, testing potential drug impacts and also understanding the progression of the disease. Psychology can certainly also help in other ways. Fro instance if you have problems with motor activity there are strategies that people can put in place in the home that can help people with neurological disease including HD. So psychology can help in terms of day to day living but also it is fundamental to understand the disease and developing treatments and hopefully one day a cure.



Epsom Girls Grammar School: Student AK 10th March 2011

Since it is a mutation in one gene that affects multiple physical characteristics, is it a pleiotropic mutation?

Jacquie Bay LENScience 20th March 2011 

A pleiotropic gene is one that produces a protein which influences a number of phenotypic traits in an organism. A mutation in such a gene may in turn affect multiple traits in the organism. In the case of the HD gene, the huntingtin protein does influence a number of biochemical pathways and of course when the protein interacts with other proteins in a pathway, the effect will flow on to these pathways. In the pathology of HD we see different effects dependent on where in the brain the disease is seen. If the mutation creates cell loss in the area of the brain responsible for movement, the phenotype is primarily related to movement or motor symptoms. If the effect of the mutation is seen primarily in the area of the brain important for mood, the symptoms are primarily around mood. The effect of the HD mutation is complex and may influence many different traits.



Epsom Girls Grammar School: Student AK 10th March 2011 

When "rare spontaneous mutations" occur in the testes, why is it that such a seemingly "large" mutation is not "caught" and fixed? Sorry i can't remember at the moment, but is it DNA or RNA Polymerase that usually "checks" and "fixes" any errors in the genetic code? Or is it precisely BECAUSE it so big, compared to smaller Point Mutations? Or am I thinking along the wrong lines?


Colin Mak, Eric Kim and Renee Handley - PhD Students Centre for Brain Research 27th March 2011

Yes, because the mutation is so big, it is difficult for the DNA polymerase to repair the error. There is also the phenomenon of slippage of DNA polymerase during DNA replication, in which the DNA polymerase III slips from the DNA template strand and reattaches at a more distant site, resulting in an expanded DNA strand.



Newlands College: Student, JB - 10th March 2011 

How much money is spent per year in New Zealand on research for cures and further information about Huntington's Disease?

Colin Mak, PhD Student, Centre for Brain Research 24th March 2011

Approximately $800,000 is spent in NZ each year on research into Huntington's disease, with funding coming from various sources including the Health Research Council of NZ and the Neurological Foundation of NZ.