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First, it would enable early diagnosis, which also relates to early detection of pathophysiology. Rabbit Polyclonal to 5-HT-2B This is particularly important for disease modification and early intervention in a condition that progresses for 5 to 8 years prior to awareness of cognitive loss. Secondly, the biomarker would enable assessment of objective treatment benefit so that the therapeutic regimen could be adjusted according to patient response. Those biomarkers could also serve as objective end points in clinical trials assessing the efficacy of new compounds. Table I. Potential disease-modifying and amyloid-targeting brokers in development. Sources: a, www.clinicaltrials.gov; b, www.neurochem.com; c, www.lilly.com; d, www.cornell.edu; e, www.phrma.org; f, www.regentherapeutics.com; g, www.affiris.com 1998;19:109C116. [PubMed] [Google Scholar] 2. Frank RA., Galasko D., Hampel H., et al. Biological markers for therapeutic trials in Alzheimer’s disease. 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Accordingly, new guideline documents from regulatory authorities, such as the FDA and EMEA, will most likely strongly recommend thorough validation of biological, as well as imaging, candidate SCH00013 markers as primary end points in upcoming phase II and III treatment trials of compounds claiming disease-modifying properties. In this context, the ideal biomarker would serve at least two purposes. First, it would enable early diagnosis, which also relates to early detection of pathophysiology. This is particularly important for disease modification and early intervention in a condition that progresses for 5 to 8 years prior to awareness of cognitive loss. Secondly, the biomarker would enable assessment of objective treatment benefit so that the therapeutic regimen could be adjusted according to patient response. Those biomarkers could also serve as objective end points in clinical trials assessing the efficacy of new compounds. Table I. Potential disease-modifying and amyloid-targeting agents in development. Sources: a, www.clinicaltrials.gov; b, www.neurochem.com; c, www.lilly.com; d, www.cornell.edu; e, www.phrma.org; f, www.regentherapeutics.com; g, www.affiris.com 1998;19:109C116. [PubMed] [Google Scholar] 2. Frank RA., Galasko D., Hampel H., et al. Biological markers for therapeutic trials in Alzheimer’s disease. Proceedings of the biological markers working group; NIA initiative on neuroimaging in Alzheimer’s disease. 2003;24:521C536. [PubMed] [Google Scholar] 3. Morris JC., Price AL. Pathologic correlates of nondemented aging, mild cognitive impairment, and early-stage Alzheimer’s disease. 2001;17:101C118. [PubMed] [Google Scholar] 4. Jack CR Jr., Petersen RC., Xu YC., et al. Prediction of AD with MRI-based hippocampal volume in mild cognitive impairment. 1999;52:1397C1403. [PMC free article] [PubMed] [Google Scholar] 5. Wang PN., Lirng JF., Lin KN., Chang FC., Liu HC. 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Accordingly, new guideline paperwork from regulatory government bodies, such as the FDA and EMEA, will most likely strongly recommend thorough validation of biological, as well as imaging, candidate markers as main end points in upcoming phase II and III treatment tests of compounds claiming disease-modifying properties. With this context, the ideal biomarker would serve at least two purposes. First, it would enable early analysis, which also relates to early detection of pathophysiology. This is particularly important for disease changes and early treatment inside a condition that progresses for 5 to 8 years prior to awareness of cognitive loss. Second of all, the biomarker would enable assessment of objective treatment benefit so that the restorative regimen could be modified according to patient response. Those biomarkers could also serve as objective end points in clinical tests assessing the effectiveness of new compounds. Table I. 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PI 3-Kinase