Thus, selective enrollment of individuals with the targeted pathology for either anti-amyloid or anti-tau compounds would offer the additional advantage of increasing trial power. For trials aimed at other putative disease targets, where selective 
enrollment based on amyloid or tau pathology may not be desired, analyses may be stratified by these biomarkers to enhance power for detecting effects in subgroups and to more finely monitor response to therapy by disease stage. CDR-SB is the most sensitive clinical outcome measure used in clinical trials, and its power is strongly enhanced by enrichment. However, several subregional ROIs, particularly the entorhinal cortex, amygdala, and hippocampus, are significantly more powerful than CDR-SB or whole brain volume, the MRI measure currently used as a secondary outcome variable in clinical trials. The power of subregional MRI outcome measures is also enhanced by enrichment. MRI outcome measures have yet to be validated as surrogates for clinical outcome measures, a process that will require successful clinical trials, but they provide strong evidence for disease-modifying �C and not just symptomatic �C claims for therapies. The sensitivity of these measures, as demonstrated here, suggests that detecting efficacy of candidate therapies in MCI participants is unlikely to be a Pimozide limiting factor in AD therapeutics research. Discerning the distribution of these viral proteins in and around the viroplasms was possible using monospecific antisera. In this manner, it is possible to subdivide the viroplasm in an interior and an exterior domain, based on their antibody-accessible protein content. MTs dynamics and function are modulated by interactions with other proteins, molecular motors and non-motor microtubule-associated proteins. Up to date, two major families of molecular motors, dyneins and kinesins are known to generate the force, upon interaction with MTs, required for various intracellular functions including intracellular transport. As molecular motors, these enzymes convert the chemical energy of ATP hydrolysis into mechanical energy and force production. MAPs are a heterogeneous group that includes stabilizing-MT proteins, such as tau, MAP1 and MAP2, as well as destabilizing proteins like spatin and katanin, and the MT plus-end tracking proteins. Despite the importance of the MT-network in many cellular processes, its role in viroplasms dynamics, has been poorly addressed. The lack of a robust reverse genetic system for rotavirus as well as a method for viroplasms purification, hamper the study of viroplasms formation, dynamics, composition or interaction with host components. In this report, we address some fundamental questions on the rotavirus life cycle using alternative methodologies. We present evidence for viroplasm-viroplasm fusion and perinuclear condensation, demonstrating that they are dynamic structures. We show that both the temporal transition as well as the maintenance of viroplasms require the MT-network and a kinesin motor from the Eg5 family. Additionally, in a simplified model for viroplasm interaction with MT-network, using VLS we show that NSP2 is necessary for viroplasm fusion while VP2 is necessary for their perinuclear localization. As part of their infective strategy, some viruses have the ability to subvert the MT transport system of the cell in order to facilitate their replication and to enhance their spread into surrounding cells and tissues. There are numerous examples in the current literature linking the MT-network with trafficking of viral particles, considered as cargoes, which move to opposite ends of MTs to their replication sites immediately after cell entry or to move the newly assembled viral progeny to the plasma membrane. The two most common molecular motors Lomitapide Mesylate involved in viral trafficking are dyneins and kinesins.