Why Using Animals in Alzheimer’s Research Isn’t Working

Why Using Animals in Alzheimer’s Research Isn’t Working

Sadly, around 70,000 Kiwis are living with dementia today. Alzheimer’s is the most common form of dementia and accounts for around 60-80% of all cases. It is also estimated that at least 170,000 people will be living with dementia by 2050.

Globally, we see a similar trend. As of 2020, there were over 50 million people worldwide living with dementia. Just think about the true extent of this - every 3 seconds that pass, someone, somewhere in the world, has developed dementia.1

So, the problem is huge – there are millions of people who are suffering from this and need help. 

Countless animals are still being subject to cruel experiments for research into Alzheimer’s. The pursuit of finding a treatment and cure for Alzheimer’s is a noble one that we are fully behind. However, using mice and other animals is not the solution.

The biggest injustice is that the suffering animals endure in these types of cruel experiments is all for nothing…


A shocking 99.6% of Alzheimer’s drugs that test successfully in animals fail in human trials.2

To make this failure even more obvious, in the last decade, no new drugs have been developed that can treat Alzheimer’s effectively.3


Why using animals doesn’t work

Mice only teach us about Alzheimer's-like symptoms in mice, so any results from animal experiments can't be transferred over to humans. We can’t use the findings of these animal studies to find out more about treatments or causes of Alzheimer’s in humans!For example:

  • Researchers can destroy parts of the brain or use transgenic mice, resulting in Alzheimer-like symptoms, but this tells you nothing about the true locations of lesions in this disease or the causes (and therefore pathological mechanisms and treatments).
  • Researchers can cause lesion formation in the same way as seen in human Alzheimer’s patients, but this does not necessarily result in the same symptoms and still doesn't tell us anything about the true causes of Alzheimer’s in humans.
  • Creating genetically modified mice can result in brain lesions similar to Alzheimer’s in humans too, but again this doesn’t create a true reflection of complex human mechanisms.

Important fact: The huge failure of animal experiments to produce results relevant to people has led one of the world’s largest pharmaceutical companies (Pfizer) to end research for new Alzheimer’s drugs.5


An example of Alzheimer’s research involving animals in NZ

In an experiment6 published in 2022, conducted by the University of Otago twenty-five mice were subject to something unfathomable…

They were anaesthetised and put through stereotaxic surgery. Their heads were mounted to a frame so that their skulls could be exposed and drilled into. A drug (or control solution) was then injected through the hole in their skull, directly into their brain. The researchers were trialling a “rescue” medication that was meant to build new brain cells.

Six weeks later, the mice were injected with a marker substance twice daily for 5 days so that researchers could distinguish between newly formed cells and older ones. Eight weeks after this, the mice were injected with another marker. All were killed the following day by having their hearts flushed with saline solution and paraformaldehyde. This method of euthanasia is used to try and preserve the animals’ brains so they can be dissected. 

All twenty-five animals lost their lives for research that does not translate to humans.

Animals can’t reliably predict how humans will respond and this is the fundamental issue with a vast majority of Alzheimer’s research happening in NZ and around the world


A better way forward

There are already viable animal-free and human-relevant research methods that can be used and there is a lot of space for more to be developed! Examples include:

  • 3D cell models out of human stem cells that actually show the main pathological events of Alzheimer’s disease for high-throughput drug screening.7
  • Biochemical assays with isolated cells to discover disease mechanisms.8
  • Computer modelling can be used to predict drug reactionsand to learn more about disease mechanisms.10
  • Human cells or spinal fluids obtained ethically from brain biopsies, in vitro cell lines and post-mortems can be used to study disease mechanisms,11 for therapy development12 and to study genes associated with Alzheimer’s.13
  • Brain-on-chip or microfluidic systems can be used in many ways! Researchers have even developed a 3D human triculture model for Alzheimer’s disease.14

And more!


It is very clear that animal models don’t work in finding a cure for Alzheimer’s Disease and that change is needed. Can you imagine the progress that we could make for human health and for animals if only a portion of the funding for animal experiments was diverted to use and develop superior human-relevant methods?

Our Striking at the Source campaign is looking to implement these solutions on a massive scale. We are calling on the government to implement changes across the sector, including changes to funding and the ways that we make decisions around research.


Take action

  • Help spread the word and share this article with friends and whānau.
  • Learn more about our Striking at the Source campaign – our most important campaign of the year! 
  • Make a donation today to help change the paradigm to human-relevant, evidence-based research for a cure for Alzheimer’s, rather than sinking more Kiwi dollars into a flawed and fraudulent system. 





  1. https://alzheimers.org.nz/explore/facts-and-figures/ 
  2. https://doi.org/10.1186/alzrt269
  3. https://doi.org/10.1007%2Fs40266-013-0108-6
  4. https://doi.org/10.1007/s00401-007-0312-8
  5. https://www.reuters.com/article/us-pfizer-alzheimers/pfizer-ends-research-for-new-alzheimers-parkinsons-drugs-idUSKBN1EW0TN  
  6. https://doi.org/10.1186/s13041-021-00889-1  
  7. http://dx.doi.org/10.1038/s41598-018-20436-8
  8. http://dx.doi.org/10.1073/pnas.1421182112
  9. http://dx.doi.org/10.1021/acschemneuro.7b00107
  10. http://dx.doi.org/10.1016/j.jalz.2014.06.007
  11. http://dx.doi.org/10.1038/s41598-018-20117-6
  12. https://doi.org/10.1007/s12640-014-9485-9 
  13. http://dx.doi.org/10.1186/s13024-018-0277-1
  14. http://dx.doi.org/10.1038/s41593-018-0175-4