If we have to select an animal to study either the effect of some drugs on Alzheimer's disease what would be the best choice ? Mice ? Rats ? Others ?
Why ?
It depends on what you mean by Alzheimer's Disease and what effect you're trying to see. AD is a hugely multifaceted disease, and no small animal model represents it fully. Some questions to consider before seeing if "a drug has any effect on Alzheimer's Disease":
Are you trying to see an effect on pathology? If so, what kind of pathology? Is that pathology an accurate representation of AD pathology? Does that pathology have any correlation to cognitive decline seen in AD? If so, does the animal model display any cognitive decline and can said cognitive decline be attributed to pathology?
Does your model use transgenes or mutations to exacerbate or eradicate proteinopathy? Are there any effects of the transgene or mutation on non-target pathways that may complicate your findings? If you have a model expressing multiple transgenes or mutations, are there any interactions between the transgenes or mutations?
In my opinion, the best animal model is the one you can use to answer the question you are trying to ask.
Best of luck.
Depends on what you want to test on your model. If you want to test human intended devices or experimental neurosurgery. I have found the minipig very useful.
Dear Abdelaziz. I have used the APP/PS1 double transgenic mice for our neuroprotection studies using 2 separate interventions and they both worked pretty well. We established a litter after retrieving breeders from Jackson Labs several years ago, starting the colony from scratch. Take a look at my recent publications for more info.
Generally it has been found that transgenic mice expressing plaques and tangles do not predict outcome in clinical trials. Holmes (2008) showed that immunization against beta-amyloid is effective in reducing plaque load but has no effect on outcome of dementia nor time to death. More than a dozen clinical trials aimed at blocking plaques and tangles have produced negative results. Neuropathology studies (many) show a lack of correlation between plaques and tangles and dementia in AD patients. Plaques and tangles may be a consequence of AD, rather than its cause. In recent years, it has been shown that 81% of confirmed AD brains have a prior mid-life history of insulin resistance and abnormally low insulin-like growth factor levels. This is a huge correlation. Using diabetic rats, it is now shown that insulin and IGF regulate adult brain mass, and replacement doses can prevent the massive loss of brain total proteins and cells (Serbedzija et al., 2008). IGFs are required for learning/memory, and impaired cognition can be prevented by IGF replacement (Lupien et al., 2003). Part of the discovery is the demonstration that insulin and IGFs help regulate brain mass and cognition in a manner independent of unabated hyperglycemia in diabetes. Hence, diabetic rodents are a promising model for the study of pathogenesis of AD.
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