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Articles by Michael Gold
Total Records ( 4 ) for Michael Gold
  Roberto Gomeni , Monica Simeoni , Marina Zvartau- Hind , Michael C. Irizarry , Daren Austin and Michael Gold
  A novel mechanistic model based on a disease system analysis paradigm was developed to explore the role of homeostatic mechanisms involved in Alzheimer‘s disease (AD) progression. We used longitudinal AD Assessment Scale-cognitive subscale (ADAS-cog) scores from 926 subjects with AD on stable acetylcholinesterase inhibitor therapy randomized to placebo treatment in two 54-week clinical trials. Alternative mechanistic models were evaluated by assuming that the rate of change of ADAS-cog over time was jointly regulated by a process characterizing the deterioration of ADAS-cog and by a process associated with a compensatory regulatory response. The model based on a time-varying deterioration rate of ADAS-cog performed better than the model based on a time-varying homeostatic control. The covariate analysis indicated that baseline Mini-Mental State Examination score, education, age, and apolipoprotein ɛ4 genotype had a significant effect on the level and shape of the trajectories of the mean model predicted ADAS-cog change from baseline.
  Barry D. Greenberg , Maria C. Carrillo , J. Michael Ryan , Michael Gold , Kim Gallagher , Michael Grundman , Robert M. Berman , Timothy Ashwood and Eric R. Siemers
  Over the past 30 years, many drugs have been studied as possible treatments for Alzheimer‘s disease, but only four have demonstrated sufficient efficacy to be approved as treatments, of which three are in the same class. This lack of success has raised questions both in the pharmaceutical industry and academia about the future of Alzheimer‘s disease therapy. The high cost and low success rate of drug development across many disease areas can be attributed, in large part, to late-stage clinical failures (Schachter and Ramoni, Nat Rev Drug Discov 2007;6:107–8). Thus, identifying in phase II, or preferably phase I, drugs that are likely to fail would have a dramatic impact on the costs associated with developing new drugs. With this in mind, the Alzheimer‘s Association convened a Research Roundtable on June 23 and 24, 2011, in Washington, DC, bringing together scientists from academia, industry, and government regulatory agencies to discuss strategies for improving the probability of phase II trial results predicting success when considering the go/no-go decision-making process leading to the initiation of phase III.
  Adam L. Boxer , Michael Gold , Edward Huey , Fen-Biao Gao , Edward A. Burton , Tiffany Chow , Aimee Kao , Blair R. Leavitt , Bruce Lamb , Megan Grether , David Knopman , Nigel J. Cairns , Ian R. Mackenzie , Laura Mitic , Erik D. Roberson , Daniel Van Kammen , Marc Cantillon , Kathleen Zahs , Stephen Salloway , John Morris , Gary Tong , Howard Feldman , Howard Fillit , Susan Dickinson , Zaven Khachaturian , Margaret Sutherland , Robert Farese , Bruce L. Miller and Jeffrey Cummings
  Frontotemporal degeneration (FTD) is a common cause of dementia for which there are currently no approved therapies. Over the past decade, there has been an explosion of knowledge about the biology and clinical features of FTD that has identified a number of promising therapeutic targets as well as animal models in which to develop drugs. The close association of some forms of FTD with neuropathological accumulation of tau protein or increased neuroinflammation due to progranulin protein deficiency suggests that a drug's success in treating FTD may predict efficacy in more common diseases such as Alzheimer's disease. A variety of regulatory incentives, clinical features of FTD such as rapid disease progression, and relatively pure molecular pathology suggest that there are advantages to developing drugs for FTD as compared with other more common neurodegenerative diseases such as Alzheimer's disease. In March 2011, the Frontotemporal Degeneration Treatment Study Group sponsored a conference entitled ”FTD, the Next Therapeutic Frontier,“ which focused on preclinical aspects of FTD drug development. The goal of the meeting was to promote collaborations between academic researchers and biotechnology and pharmaceutical researchers to accelerate the development of new treatments for FTD. Here we report the key findings from the conference, including the rationale for FTD drug development; epidemiological, genetic, and neuropathological features of FTD; FTD animal models and how best to use them; and examples of successful drug development collaborations in other neurodegenerative diseases.
  Adam L. Boxer , Michael Gold , Edward Huey , William T. Hu , Howard Rosen , Joel Kramer , Fen-Biao Gao , Edward A. Burton , Tiffany Chow , Aimee Kao , Blair R. Leavitt , Bruce Lamb , Megan Grether , David Knopman , David Knopman , Ian R. Mackenzie , Laura Mitic , Erik D. Roberson , Daniel Van Kammen , Marc Cantillon , Kathleen Zahs , George Jackson , Stephen Salloway , John Morris , Gary Tong , Howard Feldman , Howard Fillit , Susan Dickinson , Zaven S. Khachaturian , Margaret Sutherland , Susan Abushakra , Joseph Lewcock , Robert Farese , Robert O. Kenet , Frank LaFerla , Steve Perrin , Steve Whitaker , Lawrence Honig , Marsel M. Mesulam , Brad Boeve , Murray Grossman , Bruce L. Miller and Jeffrey L. Cummings
  Frontotemporal degeneration (FTD) encompasses a spectrum of related neurodegenerative disorders with behavioral, language, and motor phenotypes for which there are currently no effective therapies. This is the second of two articles that summarize the presentations and discussions that occurred at two symposia in 2011 sponsored by the Frontotemporal Degeneration Treatment Study Group, a collaborative group of academic and industry researchers that is devoted to developing treatments for FTD. This article discusses the current status of FTD clinical research that is relevant to the conduct of clinical trials, and why FTD research may be an attractive pathway for developing therapies for neurodegenerative disorders. The clinical and molecular features of FTD, including rapid disease progression and relatively pure molecular pathology, suggest that there are advantages to developing drugs for FTD as compared with other dementias. FTD qualifies as orphan indication, providing additional advantages for drug development. Two recent sets of consensus diagnostic criteria will facilitate the identification of patients with FTD, and a variety of neuropsychological, functional, and behavioral scales have been shown to be sensitive to disease progression. Moreover, quantitative neuroimaging measurements demonstrate progressive brain atrophy in FTD at rates that may surpass Alzheimer's disease. Finally, the similarities between FTD and other neurodegenerative diseases with drug development efforts already underway suggest that FTD researchers will be able to draw on this experience to create a road map for FTD drug development. We conclude that FTD research has reached sufficient maturity to pursue clinical development of specific FTD therapies.
 
 
 
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