Animal Models of Disease

Animals can be used to model disease in the laboratory.

For a long time, using animals posed the best possible way to investigate human diseases. Although animals aren’t humans, they share a lot of the same processes and types of cells that us humans have. As a result, it is possible to emulate lots of different human diseases in these animals and study what is happening and test out different potential therapies.  

Different animals can be used to model disease – from mice and rats to pigs and dogs. They are specially bred for this purpose and their genetics can be manipulated to emulate different diseases if there is not an animal equivalent available. 

Advantages of animal models: 

  • Readily available – particularly for rare diseases. Animals can be bred on demand to create animal models with enough of them available to study.
  • Known diseases – the animals used have a known disease or emulation of disease. 

Disadvantages of animal models: 

  • Animals are not humans – not all diseases that humans suffer from have an animal equivalent. If they do then these may not work in the same way as the human version of the disease. 
  • Many animals use to model macular disease, such as mice and rats don’t have a macula 
  • Although animals can be bred there are still a finite number of animals that can be bred and stored. 
  • Animals don’t always react in the same was as humans – something that improves the animal's disease won’t always improve the human version of the disease. 
  • Inhumane – although all is done to protect the animal’s welfare, animal models do come at the expense of the animals used. 

With the advancement of cell model technologies there has been a decrease in the use of animal models. This is because cell models don’t have many of the negatives of animal models. 

Some animal models have provided useful insights into bestrophinopathies and potential treatments, Guziewicz et al, have used dogs with  “Canine Multifocal Retinopathy”, a canine form of Autosomal Recessive Bestrophinopathy to examine disease progression and test a gene therapy, which provides healthy copies of BEST1 to treat the disease  

References:

GUZIEWICZ, K. E., SLAVIK, J., LINDAUER, S. J., AGUIRRE, G. D. & ZANGERL, B. 2011. Molecular consequences of BEST1 gene mutations in canine multifocal retinopathy predict functional implications for human bestrophinopathies. Invest Ophthalmol Vis Sci, 52, 4497-505.
https://www.pnas.org/content/115/12/E2839

Useful Links: