Books are simply books. Remember that, and that they follow a pre-designed agenda. There is no correct answer to your question simply because only humans develop true AD. And even that is hard to distinguish early from FTD's and other forms of aging-related dementia. Mouse people will argue mice are the best model and so on and so forth. All models are the best when used appropriately and in a complementary manner...from Dictyostelium to flies to zebrafish to mice. Some will have you believe that iPS and NPCs are the way to go without telling you the intrinsic difficulty and lack of reproduciblity in these cellular systems. So, to answer the question, there cannot be a "best" model for AD or we would have figured out a way to prevent or treat it after 2 decades.

Hi,

Have a look at Chin J 2011 (PMID:20967591), this review gives you a broad background about AD models. Good luck :)

Hi,

Please go through following book and one recent publication.

1. HANDBOOK OF ANIMAL MODELS IN ALZHEIMER’S DISEASE by Gemma Casadesus, Ph.D.

2. F. Fang et al. /Aging and Neurodegeneration, Vol. 1 (1): 15-19, September 2013 

I feel it will help you.

All d best.

Regards

Ramanatha

Books are simply books. Remember that, and that they follow a pre-designed agenda. There is no correct answer to your question simply because only humans develop true AD. And even that is hard to distinguish early from FTD's and other forms of aging-related dementia. Mouse people will argue mice are the best model and so on and so forth. All models are the best when used appropriately and in a complementary manner...from Dictyostelium to flies to zebrafish to mice. Some will have you believe that iPS and NPCs are the way to go without telling you the intrinsic difficulty and lack of reproduciblity in these cellular systems. So, to answer the question, there cannot be a "best" model for AD or we would have figured out a way to prevent or treat it after 2 decades.

I think The best Alzheimer's disease model mouse is 5XFAD(TG6799). This mouse show behavior like AD just 5~6month. It is faster then TG2576. 

I would like to thank you all for your valuable answers. It sure helped me getting started with my studies.

I do agree with Mr. Myre on the debate about models. It remembers me of this SMBC comic, in which a man holds a piece of cheese and say something like "This object is running a perfect simulation of this particular piece of cheese". I mean, of course, any model has its limitations and these limitations relate to what is being investigated and to other factors (such as viability).

In the other hand, models have obvious value in the investigation of diseases, including neuropathies such as AD. My question, thus, relate to a hypothetical consensus on a good animal mimetic of the human condition, one that does allow the development of therapies and the broadening of knowledge.

It is the same case of models in Epileptology. There are some models that mimic seizures (i.e. the symptoms), while others relate better to the disease itself (with neurobiological hallmarks of the human condition). In other terms, they are all limited, yet they have been proven useful for the development of therapies and knowledge.

In my case, we want a good (or a putatively best) model for drug screening. Thus, I believe, a good model would reflect well symptoms, while also displaying to some extent the neurobiology of AD in humans, particularly, the amyloid plaque aggregation.

Mr. Myre, would you please help me with the acrnoyms in your answer? I'm completly new to these models.

Sure Vinicius,

AD = Alzheimer's disease

FTD = frontal temporal dementia

NPCs = neural progenitor cells

iPS = induced pluripotent  stem cells

Alzforum.org has a great resource for comparing AD models - you can see the characteristics of the different models side by side.

http://www.alzforum.org/research-models

If you are looking for a model of drug screening it depends on the mechanisms of your drug/compounds and what it is they target. Models like the Tg2576, PDAPP etc have specific site mutations of APP. Others overexpress APP, which increase amyloid levels. The 3xTg gives the closest of the pathological hallmarks, but obviously uses an FTD mutation, which does not occure in AD. Essentially there is a range of models you could choose based on the drug mechanisms you wish the screen. If you are looking at behavioural differences a great review paper is: Behavioral phenotypes of amyloid-based genetically modified mouse models of Alzheimer's disease.

Kobayashi DT1, Chen KS. PMID:

15810905

Please read carefully this article (https://www.ncbi.nlm.nih.gov/pubmed/28880417) "Neuropathology and behavioural features of transgenic murine models of Alzheimer's disease". Actually, this article describes most of the transgenic mice animal model. Here the author tried to find out the advantages and disadvantages of these animal model by comparing one another. Moreover, authors provided a critical assessment of the behavioural tests used with AD mice to assess cognitive changes and decline and discuss how successfully they correlate with cognitive impairments in humans with AD. I think this is the best way to choose the better animal model in AD.