Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review

Cognitive Impairment Models Using Complementary Species

In: Animal Models of Cognitive Impairment. Boca Raton (FL): CRC Press/Taylor & Francis; 2006. Chapter 15.
Affiliations
Free Books & Documents
Review

Cognitive Impairment Models Using Complementary Species

Daniel T. Cerutti et al.
Free Books & Documents

Excerpt

In the development and use of animal models of cognitive dysfunction, it is important to develop complementary models to exploit the unique advantages of the different species. Nonmammalian vertebrates such as fish provide the opportunity to directly observe neurodevelopmental processes and determine the impact of developmental permutations on learning and memory. Zebrafish in particular are valuable because of the availability of morpholine techniques to transiently suppress specific parts of genomic expression. Invertebrate models such as C. elegans and drosophila provide other advantages, particularly the elegant genetic manipulations available. The simple nervous systems in these models are useful in determining mechanisms of cognitive function. The development of new methods for high-throughput tests of cognitive function for fish can provide a means for rapid screening of potential toxic agents as well as promising therapeutic agents. It is equally important to develop specific tests of various aspects of cognitive function, including habituation, associative learning, memory, and attention as well as to be able to differentiate changes in sensorimotor function from cognition. Key in the use of nonmammalian models is the determination of which mechanisms of cognitive function are similar to mammals and which are different. Nonmammalian models can be used in concert with classic mammalian models to determine the neural bases of cognitive function and to aid in the discovery of toxicants and potential therapeutic agents.

PubMed Disclaimer

References

    1. Beal MF. Experimental models of Parkinson’s disease. Nature Reviews Neuroscience. 2001;2:325–332. - PubMed
    1. Arendash GW, Gordon MN, Diamond DM, Austin LA, Hatcher JM, Jantzen P, Dicarlo G, Wilcock D, Morgan D. Behavioral assessment of Alzheimer’s transgenic mice following long-term A beta vaccination: task specificity and correlations between A beta deposition and spatial memory. DNA and Cell Biology. 2001;20:737–744. - PubMed
    1. Bard F, Cannon C, Barbour R, Burke RL, Games D, Grajeda H, Guido T, Hu K, Huang JP, Johnson-Wood K, Khan K, Kholodenko D, Lee M, Lieberburg I, Motter R, Nguyen M, Soriano F, Vasquez N, Weiss K, Welch B, Seubert P, Schenk D, Yednock T. Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease. Nature Medicine. 2000;6:916–919. - PubMed
    1. German DC, Eisch AJ. Mouse models of Alzheimer’s disease: insight into treatment. Reviews in the Neurosciences. 2004;15:353–369. - PubMed
    1. Hsiao K, Chapman P, Nilsen S, Eckman C, Harigaya Y, Younkin S, Yang FS, Cole G. Correlative memory deficits, A beta elevation, and amyloid plaques in transgenic mice. Science. 1996;274:99–102. - PubMed

LinkOut - more resources