Thursday, August 29, 2013
Despite genetic advances in schizophrenia
research, a lack of predictive preclinical models has hampered the development
of new therapeutics. Now, a team at The Johns Hopkins University
has created a transgenic mouse model of prefrontal dysfunction involving
disrupted networks of neurons that cause behavioral changes similar to those
seen in patients with schizophrenia or mood disorders.1
A failure to communicate
Gallagher's homozygous Dn-Disc1
model reflects a shift in the CNS field toward the view that schizophrenia and
some other CNS disorders are diseases of connectivity, in which a breakdown in
communication occurs between neurons and between regions of the brain.
A low throughput tool
Fishburn, C.S. SciBX 6(33); doi:10.1038/scibx.2013.882 Published online Aug.
1. Johnson, A.W. et al.
Proc. Natl. Acad. Sci. USA; published online July 9, 2013; doi:10.1073/pnas.1307925110
Contact: Michela Gallagher, The Johns Hopkins University, Baltimore, Md.
Contact: Akira Sawa, same affiliation as above e-mail: email@example.com
2. Tong, C. et al. Nat.
Protoc. 6, 827-844 (2011)
3. Millar, J.K. et al.
Hum. Mol. Genet. 9, 1415-1423 (2000)
4. Brandon, N.J. &
Sawa, A. Nat. Rev. Neurosci. 12, 707-722 (2011)
5. Hikida, T. et al.
Proc. Natl. Acad. Sci. USA 104, 14501-14506 (2007)
The Johns Hopkins University, Baltimore, Md.
PsychoGenics Inc., Tarrytown, N.Y.
University of Cambridge, Cambridge, U.K.