Further, systemic administration of a compound must achieve adequate CNS levels, and inevitably leaves doubts about whether CNS neurons vs. peripheral tissues might be responsible for any improved behavior outcome. By contrast, it has been suggested that the retinal dystrophy in mutant mice might serve as a facile model for therapy in polyglutamine diseases. Here we have demonstrated the feasibility of using retinal physiology as a robust readout of a therapeutic effect in vivo. The retina is one part of the CNS that is readily accessible to chemical and genetic treatment. It is also uniquely amenable to accurately monitor neuronal physiology non-invasively via ERG. Although not used here, fundoscopy and optical coherence tomography can also be employed to image neural anatomy in situ. Because any therapeutic trial can be conducted using the contralateral eye as an internal control, the number of animals needed to observe a statistically significant effect is vastly reduced. In this case, we have used the R6/2 mouse, which overexpresses an N-terminal exon 1 fragment of the Htt protein. Our studies here suggest that it should be possible to model toxicity in vivo for a variety of pathogenic proteins, simply by engineering animals that feature retina-specific expression. The use of the retina also allows modifications to be BW-B 70C carried out on a very defined group of neurons, thus ensuring that specific CNS responses are linked directly to the targeted cells. Future work will help determine the predictive value of this system with other compounds that have demonstrated efficacy in standard transgenic models, and may ultimately speed preclinical testing. Oral biofilms play an important role in periodontal disease, a primary reason for human adult tooth loss. With more than 700 species identified in the oral cavity, this biofilm presents a complex and dynamic ecosystem, whose growth is dictated by microenvironmental factors. As proof of concept, studies in murine models have demonstrated the multiple species biofilms display increased pathogenicity, reflecting the increased alveolar bone loss, which is the hallmark of periodontitis. Within a biofilm, the bacteria exert a significantly increased virulence and resistance to the host immune defences. Therefore, ��traditional�� experimental models that simply study single individual bacterial species might not be CK 869 optimal to acknowledge the role of oral biofilms in periodontal diseases. To understand the role of the oral biofilms in disease, it is necessary to unravel the relationships between their constituent species.