This possibility is ruled out by the experiment presented in Fig. 2, which shows that the stability of the M-transcripts is not affect by the ybeY deletion. In contranst, it should be mentioned that the stability of the short transcripts is affected by the ybeY mutation, but in the opposite directions. Thus, in the absence of YbeY the short transcripts are more stable. This result could be explained by the recent findings of Jacob et al that attributed RNase activity to YbeY. This RNase may be more active on short transcripts, as these are not yet covered by the binding of various protein factors. Further support for the effect of YbeY on the transcription antitermination of rRNA transcripts is obtained by the findings that the ybeY deletion mutation can be partially complemented by over-expression of the NUS factors involved in transcription antitermination. The overexpression of these NUS factors has virtually no effect on the wild type. Although there is no trivial explanation for these 
findings – that are highly significant and reproducible – we assume that these transcriptional factors affect the rate of transcription in the mutant by supporting the correct folding of the rRNA and thus improving rRNA maturation even in the absence of YbeY. The results presented here show the importance of YbeY for ongoing rRNA transcription elongation. They are also compatible with the findings that immature 16S RNA accumulates in ybeY deletion mutants, as a correct transcription antitermination process is required for accurate maturation of rRNA. The maintenance of an optimal transcription elongation rate which allows the proper maturation and folding of the rRNA becomes difficult when the temperature is increased, as at the higher temperatures the rate of transcription increases. Therefore, the suggested involvement of YbeY in the transcription antitermination process and in assuring proper RNA maturation implies that its importance may increase with temperature. This assumption is compatible with the finding that the ybeY deletion has a stronger phenotype at high temperatures – the deletion mutant is temperature sensitive. Moreover, YbeY is a conserved heat shock protein which is induced upon temperature shift-up, probably ensuring sufficient levels of this protein to satisfy the AbMole Aristolochic-acid-A increased requirement upon shift to higher temperatures. Passive immunization with appropriate amyloid beta antibodies has been shown to reduce extracellular amyloid deposition in hAPP transgenic mice, and numerous humanized monoclonal antibodies to various A? epitopes are making their way into clinical trials. The last few years has seen major developments in the tau field that seem likely to have a significant impact on the development of strategies to target insoluble tau aggregates. The idea that tau pathology can diffuse from cell to cell in a prion-like fashion has been shown by different laboratories. Additional publications seem to confirm the spreading of pathological tau in certain transgenic mouse models, again implying the existence of an extracellular tau species that is important in the development of the disease. These studies together with more recent data showing that tau is actively released from cultured cells suggest that, even under normal conditions, a significant amount of tau is present in the extracellular space. In this context, assuming that tau is at least in part an extracellular protein, efforts to target tau pathology with antibodies appear to be a reasonable exercise. Recent studies from different laboratories have strongly suggested that immunotherapy can be an effective means of preventing the development of tau accumulation. Our initial approach to passive immunotherapy was to attempt to classify the available tau monoclonal antibodies into groups, based on specificity for tau pathology relative to reactivity with normal tau.