Robert Beech - US grants
Affiliations: | Yale University, New Haven, CT |
We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the NIH Research Portfolio Online Reporting Tools and the NSF Award Database.The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please sign in and mark grants as correct or incorrect matches.
High-probability grants
According to our matching algorithm, Robert Beech is the likely recipient of the following grants.Years | Recipients | Code | Title / Keywords | Matching score |
---|---|---|---|---|
2006 | Beech, Robert David | R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Genetic Model Role Neurogenesis Antidepressant Response @ Yale University [unreadable] DESCRIPTION (provided by applicant): Patients with major depression, bipolar disorder and schizophrenia have all been found to have decreased hippocampal volumes, suggesting that decreased hippocampal cell number may be a common endophenotype in multiple mental illnesses. Several classes of psychotropic medications including antidepressants, mood stabilizers and atypical antipsychotics have also been shown to increase neurogenesis in the adult hippocampus. The relationship between adult neurogenesis and the behavioral response to psychotropic medications remains unclear, however recent evidence suggests that generation of new neurons may be critical for antidepressant action. To investigate the role of hippocampal neurogenesis in antidepressant-response we will make use of a novel genetic model for deficits in adult neurogenesis: BF- 1/FoxG1 heterozygous mice. BF-1/FoxG1 is a transcriptional represser that inhibits signaling through the Smad/TGF-beta pathway, and is required for the normal development of the cerebral hemispheres. Mice lacking both copies of the BF-1/FoxG1 gene die shortly before birth (E18.5). Heterozygous BF-1/FoxG1 mice survive, but do not produce new neurons as adults. Thus, these mice offer a genetic model for an endophenotype common to several metal illnesses. To explore the hypothesis that increasing adult neurogenesis is critical for response to antidepressant medications we will treat BF-1/FoxG1 heterozygous mice with different classes of antidepressant medications including tricyclic antidepressants (amitriptyline), serotonin-specific reuptake inhibitors (fluoxetine) and norepinephrine-specific reuptake inhibitors (reboxetine), either subchronically or chronically and characterize both the behavioral response and the effects (if any) on neurogenesis. Preliminary results from these studies should lead to an RO1 proposal aimed at extending these findings. Briefly, follow up studies will extend these studies to other classes of medications including atypical antipsychotics, which may similarly be dependent on adult neurogenesis for their clinical effects. These studies should lead to a better understanding of the mechanism of action of existing antidepressant medications. This, in turn, should allow for a more rational search for new medications for the treatment of depression, and potentially other mental illnesses as well. [unreadable] [unreadable] [unreadable] |
0.958 |
2007 | Beech, Robert David | R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Genetic Model For the Role of Neurogenesis in Antidepressant Response @ Yale University [unreadable] DESCRIPTION (provided by applicant): Patients with major depression, bipolar disorder and schizophrenia have all been found to have decreased hippocampal volumes, suggesting that decreased hippocampal cell number may be a common endophenotype in multiple mental illnesses. Several classes of psychotropic medications including antidepressants, mood stabilizers and atypical antipsychotics have also been shown to increase neurogenesis in the adult hippocampus. The relationship between adult neurogenesis and the behavioral response to psychotropic medications remains unclear, however recent evidence suggests that generation of new neurons may be critical for antidepressant action. To investigate the role of hippocampal neurogenesis in antidepressant-response we will make use of a novel genetic model for deficits in adult neurogenesis: BF- 1/FoxG1 heterozygous mice. BF-1/FoxG1 is a transcriptional represser that inhibits signaling through the Smad/TGF-beta pathway, and is required for the normal development of the cerebral hemispheres. Mice lacking both copies of the BF-1/FoxG1 gene die shortly before birth (E18.5). Heterozygous BF-1/FoxG1 mice survive, but do not produce new neurons as adults. Thus, these mice offer a genetic model for an endophenotype common to several metal illnesses. To explore the hypothesis that increasing adult neurogenesis is critical for response to antidepressant medications we will treat BF-1/FoxG1 heterozygous mice with different classes of antidepressant medications including tricyclic antidepressants (amitriptyline), serotonin-specific reuptake inhibitors (fluoxetine) and norepinephrine-specific reuptake inhibitors (reboxetine), either subchronically or chronically and characterize both the behavioral response and the effects (if any) on neurogenesis. Preliminary results from these studies should lead to an RO1 proposal aimed at extending these findings. Briefly, follow up studies will extend these studies to other classes of medications including atypical antipsychotics, which may similarly be dependent on adult neurogenesis for their clinical effects. These studies should lead to a better understanding of the mechanism of action of existing antidepressant medications. This, in turn, should allow for a more rational search for new medications for the treatment of depression, and potentially other mental illnesses as well. [unreadable] [unreadable] [unreadable] |
0.958 |
2009 — 2010 | Beech, Robert David Sinha, Rajita (co-PI) [⬀] |
R03Activity Code Description: To provide research support specifically limited in time and amount for studies in categorical program areas. Small grants provide flexibility for initiating studies which are generally for preliminary short-term projects and are non-renewable. |
Progesterone-Induced Gene Expression Changes and Risk of Relapse to Cocaine Use @ Yale University DESCRIPTION (provided by applicant): This preliminary study, which will be of 2 years duration, will assess the relationship between changes in gene-expression induced by treatment with progesterone and laboratory measures of stress-induced craving, negative emotion, and physiology previously shown to predict risk for early relapse in cocaine addicted subjects. The long-term goal of this project is to develop novel molecular tools that can be used to predict and monitor the response to specific treatments for cocaine dependence. Preliminary studies have shown that men and women differ in their subjective and physiological responses to cocaine, as well as stress or drug-cue related stimuli associated with risk for relapse. Men and women also differ in their clinical response to various proposed pharmacological treatments for cocaine addiction. Differences in the level of gonadal steroids may underlie some or all of these differences. Recently, a number of small scale laboratory investigations and clinical trials have investigated progesterone as a possible treatment for cocaine addiction. Studies in animal models have shown that progesterone receptors are widely expressed in the brain and regulate the expression of a large number of genes in the brains of both female and male animals. In addition, progesterone has been shown to activate both the ERK/CREB/bcl-2 and Akt second messenger signaling pathways in neurons. These effects have been proposed to underlie the neuroprotective actions of progesterone in several experimental models. Activation of these pathways may oppose the actions of stress-induced patterns of gene expression, which could mediate increased risk for relapse in cocaine dependent individuals. In this study, we will recruit (n=60;30 male and 30 female) treatment-seeking cocaine-dependent subjects who are currently being recruited to take part in a NIDA-funded study of progesterone effects on stress and cue- induced cocaine craving and relapse susceptibility. In that study, subjects are randomly assigned to receive either progesterone (400mg/day) or placebo for a period of five days and undergo brief guided imagery sessions involving personalized stressful, drug-cue or neutral-relaxing situations (one imagery condition per session). In the proposed study, we will isolate RNA from blood collected prior to treatment and on day 5 of treatment with either progesterone or placebo. Gene-expression levels will be assessed by microarray hybridization using Illumina Sentrix Beadchip (Human-6v2) arrays (the same platform used in our preliminary studies). Gene-expression levels will be correlated with drug craving, anxiety and emotion ratings, as well as behavioral distress responses, heart rate, blood pressure, and salivary cortisol measures assessed during each session. Differential expression of selected genes of interested will be confirmed using Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Specific aims include: (1) comparing progesterone-induced changes in peripheral blood gene-expression in cocaine-dependent men and women;and (2) identifying specific progesterone-regulated transcripts whose expression is correlated with the subjective response to stress or drug-cue related stimuli. PUBLIC HEALTH RELEVANCE: These studies will allow us to better understand the molecular basis for individual differences in the response to progesterone in cocaine dependent men and women. Better understanding of these differences will allow us to identify those individuals (both men and women) most likely to benefit from treatment with progesterone. In addition, better understanding of the mechanism of action of progesterone at the genomic level may help to guide the development of novel hormonally based pharmacotherapies for the treatment of cocaine dependence. |
0.958 |
2009 — 2010 | Beech, Robert David | R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Stress-Related Changes in Gene Expression as Biomarkers of Relapse Vulnerability @ Yale University DESCRIPTION (provided by applicant): The proposed study, which will be of 2 years duration, will assess the relationship between changes in gene-expression and laboratory measures of stress-induced craving, negative emotion, and physiology previously shown to predict risk for early relapse after treatment. The long-term goal of this project is to develop novel molecular tools that can be used to predict and monitor the response to specific treatments for alcohol dependence. Preliminary studies conducted by our group have identified peripheral blood gene-expression differences between alcohol dependent subjects and social drinkers. Biological processes associated with these genes include apoptosis (programmed cell death), cell cycle regulation, and intracellular signaling cascades. Key transcription factors implicated by these gene- expression differences include HNF4-alpha, c-myc, ESR1, AR, and NF-:B. Abnormal expression of gene- networks involving these transcription factors may underlie the heightened response to stress observed in alcohol dependent subjects as well as differences in response to treatment, risk for relapse, and co-morbid disorders (e.g. depression). In the proposed study, we will recruit (n=25) treatment-seeking alcohol-dependent subjects, and (n=25) social drinkers and isolate RNA from blood collected before, immediately after, and one hour after brief guided imagery sessions involving personalized stressful or neutral-relaxing situations (one imagery condition per session) as previously described (Sinha et al., 2008). Imagery sessions will be conducted after a period of prolonged (28-day) abstinence. Gene-expression levels will be assed by microarray hybridization using Illumina Sentrix Beadchip (Human-6v2) arrays (the same platform used in our preliminary studies). Differential expression of selected genes of interested will be confirmed using Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Alcohol craving, anxiety and emotion ratings, behavioral distress responses, heart rate, blood pressure, and salivary cortisol measures will be assessed during each session. Alcoholic subjects will also be followed for 90 days after completion of the laboratory sessions to assess alcohol relapse. Specific aims include: (1) assessing whether stress imagery as compared to neutral-relaxing imagery results in differential changes in peripheral blood gene-expression;(2) assessing whether alcohol-dependent subjects and healthy controls differ in their reactivity to stress imagery as measured by induction of specific stress-related genes;and (3) determining the relationship between stress-related changes in gene-expression and physiologic and emotional responses previously shown to predict risk for relapse. As an exploratory aim we will also assess the relationship between stress-related changes in gene-expression identified in specific aims 1-3 and risk for relapse among alcohol-dependent subjects during the 90 days after testing. PUBLIC HEALTH RELEVANCE: Stress is a well known risk factor for relapse in alcohol-dependence. The goal of this project is to identify specific stress-related genes that may predict the risk for relapse in alcohol dependent subjects and allow individuals at higher-risk to be directed to more intensive treatment interventions. Better understanding of the molecular and genetic pathways mediating the effects of stress on the risk for relapse will also aid in the development of more effective treatments for dependence on alcohol and other drugs of abuse. |
0.958 |