Ice bucket charity supports nightmarish suffering for GM mice

The ‘ice bucket challenge’ craze that dominated social media for several weeks this summer raised £7 million for the Motor Neurone Disease Association (MNDA).[1] Many people who contributed to this impressive total were probably unaware that this British charity funds experiments on animals. At present, this includes providing more than £1 million for tests on mice, many of whom are genetically modified (GM).[2] Some of these genetic alterations can cause the highest level of suffering that it is legal to inflict on animals in UK laboratories, and a recent experiment involving MNDA-funded researchers saw GM mice being bred to suffer a range of debilitating torments and suspended by their tails to assess abnormal behaviour.[3] Yet for all the misery they cause, animal experiments into motor neurone disease have a dismal record in terms of actual medical progress, meaning that such research is ultimately a terrible waste of money donated in good faith.

Cruel breeding practices

  • The creation of GM mice generally involves several painful and invasive procedures, including castration, major surgery and ear or tail mutilation.
  • Creating just one ‘founder’ mouse with the required genetic alteration can entail the deaths of hundreds of others. These unwanted mice are often killed by being gassed or having their necks broken.
  • Building and maintaining colonies of GM mice involves drastic manipulation of the animals’ behaviour and reproductive cycles, such as housing ‘stud males’ on their own for up to two weeks, and subjecting females to overcrowding in order to synchronise their reproductive cycles.[4]

Misery in the laboratory

  • The laboratory environment is of itself a source of suffering. It has been estimated that some 50 per cent of laboratory-confined mice suffer from ‘stereotypies’, meaning that they perform abnormal repetitive behaviours such as fur or whisker plucking.[5]

Deliberately induced torments

  • Some of the genetic alterations mentioned in the charity’s summary of its research can cause terrible outcomes, including paralysis and death.[6]
  • Researchers’ own documentation indicates that the Home Office (the government department responsible for licensing vivisection) classifies these ‘paralysis models’ as being in the highest category of animal suffering.[7]
  • In recently published research that had received grant support from the MNDA, GM mice suffered muscle weakness (shown by lack of paw grip strength) and loss of body weight.[8]
  • In a further ‘study’ involving MNDA-funded researchers, GM mice were bred to suffer limb paralysis, anxiety, loss of body weight, hunched posture and motor dysfunction, which was measured by repeated use of a rotating cylinder on which the mice try to balance to avoid falling. The animals were also suspended by their tails to assess abnormal behaviour known as ‘limb clasping’.[9]

Years of failure

  • Animal experiments have repeatedly failed to deliver progress in the fight against motor neurone disease. Over the past ten years, around 12 experimental treatments that showed promise in animal ‘models’ of amyotrophic lateral sclerosis or ALS (a type of motor neurone disease) have been given to humans in clinical trials. All except one treatment failed, and the exception has only marginal benefits in terms of patient survival.[10] In terms of predicting how humans will respond to treatments, this suggests that animal ‘models’ of motor neurone disease have a failure rate of more than 90 per cent.

A flawed approach

  • The fundamental problem is that motor neurone disease is uniquely human, and it cannot be accurately ‘modelled’ in animals.[11] Mice can be genetically altered to exhibit some of the symptoms of motor neurone disease, but they do not have the underlying illness.
  • Much of the work funded by the MNDA relates to creating new mouse ‘models’ of motor neurone disease, or seeking to improve those that already exist. There are several reasons why animals cannot faithfully represent uniquely human diseases, or predict how people would respond to drugs designed to treat the conditions:
  1. There are fundamental differences between species including those relating to anatomy, organ structure and function, metabolism, chemical absorption, genetics, mechanisms of DNA repair, behaviour and lifespan.
  2. A genetically similar group of animals living in controlled experimental settings cannot predict the response of varied human patients living in natural conditions.
  3. The stress caused to animals by routine laboratory practices such as handling, blood collection, physical restraint, injections and force-feeding, as well as recovery from wounds or surgery, results in altered physiological states, which compromise test results.
  4. Some of the most common and debilitating adverse reactions to drugs are not outwardly visible and therefore cannot be detected in animal tests. These include nausea, mental disturbance, dizziness, fatigue, depression, confusion and double vision.

Ignoring current thinking

  • One of the research projects currently being funded by the MNDA involves using mice who have been genetically modified to carry a faulty version of a gene called SOD1. Yet this ‘model’ of the disease has already been heavily criticised in the scientific literature. A study published in 2011 reviewed 13 drugs that had shown potential in this particular mouse ‘model’ and found that none of these therapies showed significant success in clinical trials on humans.[12]
  • These dismal results are hardly surprising, given that the SOD1 mouse ‘model’ is an over-simplification of an inherited form of ALS that is rare to begin with. Only one in ten ALS patients have this inherited form of the disease, and less than a quarter of these cases are caused by faults in the SOD1 gene.[13] Evidence of the SOD1 gene being linked to sporadic ALS (the more common form of the disease) relates to only a fraction of cases.[14]
  • Even where it does play a role, a faulty gene represents only one part of a very complex picture. Genes interact with other genes and cellular components in ways that are unique to each species, and they are controlled by millions of ‘switches’ that regulate them in subtle and complicated ways. A study published just last month (November 19) compared the genomes of mice and humans, and found that a significant number of mouse genes were regulated in a different way from their human counterparts.[15]

Our full report into the research can be viewed here.

[1] [Accessed October 2014]

[2] Motor Neurone Disease Association (2014). Research we fund.

[3] Ricketts, T. et al. (2014) A Nonsense Mutation in Mouse Tardbp Affects TDP43 Alternative Splicing Activity and Causes Limb-Clasping and Body Tone Defects. PloS One. 9(1):e85962

[4] Stallwood A (2013). Science Corrupted. Revealed: the nightmare world of GM mice. Animal Aid.

[5] Ibid.

[6] JPND Action Group (2014). Experimental models for neurodegenerative diseases.

[7] UK Home Office (2014). Non-technical summaries granted during 2013: volume 1.

[8] Nardo G, Iennaco R, Fusi N (2013). Transcriptomic indices of fast and slow disease progression in two mouse models of amyotrophic lateral sclerosis. Brain, a journal of neurology 2013.

[9] Ricketts, T. et al. (2014) A Nonsense Mutation in Mouse Tardbp Affects TDP43 Alternative Splicing Activity and Causes Limb-Clasping and Body Tone Defects. PloS One. 9(1):e85962

[10] Perrin S (2014). Preclinical research: Make mouse studies work. Nature. Vol 507 27 March 2014.

[11] Akhtar A (2014). In Defense of Pamela Anderson. Huffington Post blog. Posted August 25 2014.

[12] Wilkins HM, Bouchard RJ, Lorenzon NM et al (2011). Poor correlation between drug efficacies in the mutant SOD1 mouse model versus clinical trials of ALS necessitates the development of novel animal models for sporadic motor neurone disease. Horizons in Neuroscience Research. Vol 5, 2011.

[13] [Accessed September 2014]

[14] Ibid.

[15] A comparative encyclopedia of DNA elements in the mouse genome, Nature, Vol 515, November 2014.


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