Cristina M. Alberini - US grants
Affiliations: | New York University, New York, NY, United States |
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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.
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High-probability grants
According to our matching algorithm, Cristina M. Alberini is the likely recipient of the following grants.Years | Recipients | Code | Title / Keywords | Matching score |
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2002 — 2021 | Alberini, Cristina M | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. R37Activity Code Description: To provide long-term grant support to investigators whose research competence and productivity are distinctly superior and who are highly likely to continue to perform in an outstanding manner. Investigators may not apply for a MERIT award. Program staff and/or members of the cognizant National Advisory Council/Board will identify candidates for the MERIT award during the course of review of competing research grant applications prepared and submitted in accordance with regular PHS requirements. |
Gene Expression in Long-Term Memory @ Mount Sinai School of Medicine of Nyu DESCRIPTION (provided by applicant): Long-term memory formation consists of multiple phases. A new memory is initially labile. To become stable this new memory undergoes a process known as consolidation that, in the case of declarative memories, occurs within the medial temporal lobes and requires gene expression. When recalled, memories reenter a new phase of vulnerability and seem to require a "reconsolidation" process in order to be maintained. The goal of this project is to characterize, particularly in the temporal lobe regions hippocampus and amygdala, the gene expression regulation underlying different phases of long-term memory formation. It has been shown that members of the transcription factor family cAMP response element binding protein (CREB) play an essential role in the consolidation of long-term memory. However, the cascade of events activated downstream of CREB is still poorly understood. In Inhibitory Avoidance (IA) learning, a significant and persistent activation (phosphorylation) of CREB and CREB-dependent gene expression occur in the hippocampus. We have recently found that a CREB-downstream evolutionarily conserved molecular event essential for IA long-term memory consolidation is the induction of another transcription factor, a member of the CCAAT enhancer binding protein (C/EBPBeta). Preliminary data suggest that, together with C/EBPBeta, another member of the C/EBP family C/EBPdelta, may play a role in memory consolidation. We have also identified a number of putative CREB-C/EBPdownstream genes. Two of these, Insulin-like growth factor-Il (IGF-II) and cyclin-dependent kinase 5 (CDK5), may have a critical role as modulators of the synaptic morphological changes that underlie memory storage. In contrast, the molecular mechanisms of "reconsolidation" are not yet known. In this project we propose to continue our characterization of the gene cascade underlying memory formation, and specifically to: 1- Characterize the anatomical and temporal profiles of CREB-C/EBPBeta activation and asses the contribution of this molecular pathway to the storage of medial temporal lobe-dependent memories; 2- Determine whether C/EBPdelta plays an essential role as a memory activator or repressor. 3- Determine the role of the target genes CDK5 and IGF-II. 4. Characterize the molecular basis of the memory "reconsolidation" process. The proposed experiments will provide significant insight into the molecular mechanisms of memory consolidation. An understanding of the molecular changes underlying memory formation may indicate new strategies for the treatment of memory disorders. |
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2003 — 2004 | Alberini, Cristina M | 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.) |
Molecular Bases of Addictive Memories @ Mount Sinai School of Medicine of Nyu [unreadable] DESCRIPTION (provided by applicant): [unreadable] [unreadable] Drugs of abuse, such as morphine, cause long-lasting changes that underlie behaviors associated with drug addiction. It has been proposed that these changes are similar to those underlying memory formation. In agreement, many compounds that impair memory formation and inhibit memory-associated molecular pathway also attenuate drug tolerance and dependence. Newly formed memories are initially labile and require protein synthesis in order to be consolidated into a long-term memory. Furthermore, when a consolidated memory is recalled, it again becomes labile and requires protein synthesis in order to be maintained. The requirement for protein synthesis of addictive memories is virtually unknown. Here we propose to address several fundamental questions that will target the protein synthesis-dependent processes of addictive memory and other addictive behaviors. The results of these experiments will lay a foundation for further studies, which will examine molecules, pathways and pharmacological intervention in addiction. These investigations may produce significant breakthroughs that could help in the development of new therapies for drug addiction. The Aims of this project are: 1) To determine the temporal and anatomical specificity of protein synthesis requirement in addictive contextual associations. 2) To determine the behavioral specificity of the requirement for protein synthesis in addiction. 3) To determine whether the requirement for protein synthesis is a general mechanism underlying addictive memories. [unreadable] [unreadable] |
0.901 |
2007 — 2011 | Alberini, Cristina M | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Mechanisms Underlying Memory Stabilization @ Mount Sinai School of Medicine of Nyu [unreadable] DESCRIPTION (provided by applicant): A new memory is stabilized through a process of consolidation, which is known to depend on a critical phase of protein synthesis. Consolidated memories are widely believed to be stable and resilient to disruption. This belief, however, has been recently challenged by studies showing that established memories become labile when reactivated and, furthermore, require another phase of protein synthesis to be maintained. Although this process has been termed "re-consolidation", it is not known whether it is, in fact, a true recapitulation of consolidation. Very little is known about the underlying mechanisms and the specific functions of memory reconsolidation. This knowledge is not only essential for the understanding of how memory works, but it will also contribute to the development of novel strategies for treating psychiatric conditions based on traumatic memories (i.e. post-traumatic stress disorders, phobias and depression) and novel approaches for increasing memory strength. In this project, we propose to use a fear-conditioned-based task (inhibitory avoidance, IA) and molecular investigations to carry out a comparative multiple level analysis of the anatomical and temporal molecular requirements of memory consolidation and reconsolidation. Our Aims are to determine to what extent both consolidation and reconsolidation involve the same molecules and brain areas (circuits) with similar temporal dynamics and to test the functional roles and the contribution of modulation on memory reconsolidation. The results of this project should provide important information for developing new strategies for the pharmacotherapeutic intervention of cognitive disorders caused by traumatic memories (i.e. PTSD, phobias, addiction and depression) and debilitating conditions of memory loss such as those occurring in aging and Alzheimer's Disease. [unreadable] [unreadable] [unreadable] |
0.901 |
2010 — 2012 | Alberini, Cristina M | R13Activity Code Description: To support recipient sponsored and directed international, national or regional meetings, conferences and workshops. |
Molecular and Cellular Cognition Meeting @ New York University We are requesting partial support for the next three Molecular and Cellular Cognition (MCC) Meetings. The next Conference will be held in the San Diego Convention Center on November 11th and 12th, 2010, right before the annual meeting of the Society for Neuroscience. The MCC meeting brings together junior and senior scientists that combine molecular (pharmacology, genetics, transgenics, viral approaches, etc) and physiological (electrophysiology, optical physiology) and other cellular approaches to study behavior, including learning and memory. The general goal of these studies is to derive explanations of cognitive processes that integrate molecular, cellular, and behavioral mechanisms, as well as to use this information and related animal models in the search for treatments for cognitive, psychiatric and neurological disorders in children, adults and the elderly. These meetings have been organized under the sponsorship and leadership of the Molecular and Cellular Cognition Society (MCCS) (www.molcellcog.org), a society that started in 2002 and whose main function is to organize meetings and promote interaction and collaborations among laboratories working in this general area. Although there are a few learning and memory meetings in the USA and abroad, the Molecular and Cellular Cognition meeting is unique because it brings together individuals that integrate molecular, physiological and behavioral approaches in studies of cognition, memory and learning related disorders. Although the molecular and cellular cognition field is relatively new, it has already had a profound impact on neuroscience research. Currently, this is the only periodic meeting in the field, an invaluable opportunity to exchange information, and develop this young field. The 2007-2009 meetings were highly successful, attracting each year a diverse group of approximately 500 participants from North America, Europe, and Asia, and we have every reason to believe that the 2010-2012 meetings will be equally successful. (Summaries at http://www.molcellcog.org/meetings.htm). |
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2012 — 2016 | Alberini, Cristina M | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Mechanism Underlying Memory Stabilization @ New York University DESCRIPTION (provided by applicant): Maintaining healthy cognitive functions, of which memory is a most important one, is one of the major goals of mental health research. Aging, diseases, stress and injury can lead to cognitive and memory impairments. It is estimated that up to one third of adults will experience a gradual decline in cognitive function known as mild cognitive impairment as they age. Furthermore, risk for Alzheimer's disease, memory loss and dementia increases with increasing age. Thus, minimizing or preventing cognitive and memory loss is very important as the average life span continues to lengthen. It is therefore imperative to understand the physiology of memory formation, persistence and storage and identify molecular mechanisms and targets that are associated with memory impairments in order to develop strategies that will prevent or reverse them. Newly learned information is in a labile state for a limited time and becomes a long-term memory through a process of stabilization that is known as memory consolidation. Once stable, memory can become labile again if retrieved and re-stabilizes through another process known as memory reconsolidation. Using contextual fear conditioning types of memory in rats, we have recently found that the growth factor insulin like growth factor II (IGF-II) acts as a potent memory enhancer when administered during the consolidation or reconsolidation phases. Furthermore, using inhibitory avoidance (IA), we have found that retrieval-dependent reconsolidation promotes memory strengthening and prevents forgetting. These findings suggest that it is possible to identify post-retrieval mechanisms that can be used as targets to develop new therapies that promote cognition and alleviate age-related memory decline. Using IA and social transmission of food preference in rats, this proposal will test the molecular mechanisms and brain circuitry of the retrieval-dependent IGF-II-induced memory enhancement. It will investigate circuitry and molecular mechanisms of retrieval-induced memory strengthening and prevention of forgetting. Finally, it will investigate how memory retrieval and IGF-II can be used in aging to delay or reverse memory impairments. Results from these studies will advance our knowledge of neural mechanisms underlying memory enhancement and aging-related cognitive impairment in rats. |
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2013 — 2017 | Alberini, Cristina M | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Astrocytic-Neuronal Mechanisms in Memory Formation and Cognitive Impairments @ New York University DESCRIPTION (provided by applicant): Maintaining and promoting healthy cognitive functions, of which memory is a most important one, is one of the major goals of mental health research. Identifying mechanisms of long-term memory formation and targets that help in preventing or treating memory impairments is an important goal in mental health. Thus far, the studies of mechanisms underlying cognitive functions including memory have mainly focused on elucidating the contribution of neurons and neuronal networks. However, findings of the last few decades indicate that astrocytes actively participate in the regulation of synaptic functions including long-term plasticity and memory. Very little is known about the nature and functions of these astrocytic mechanisms. Furthermore, very little is known also about possible involvement of astrocytic functions in memory and cognitive impairments. Using a contextual fear conditioning memory task in rats we have recently identified a critical role of astrocytes- dependent metabolic coupling with neurons in long-term memory formation in rats. These findings show, for the first time to our knowledge, that, in a mammalian brain, astrocytes play a necessary and active role in long-term memory formation. This proposal aims at further investigating the biological mechanisms of astrocytes and their interactions with neurons in long-term memory formation and in memory impairments that accompany stress-related cognitive impairments. Importantly, mechanisms underlying memory formation during early development and in adulthood will be investigated to determine similarities and differences. Results from these studies should advance our knowledge of the biological mechanisms underlying memory formation and should lead to novel hypotheses and tools for understanding cognitive functions and preventing or reversing cognitive impairments linked to stress-related cognitive disorders. |
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2021 | Alberini, Cristina M | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Molecular Mechanisms of Infantile Learning and Memory @ New York University Project Summary Behavioral studies have shown that early life experience significantly shapes the development of brain abilities. Accordingly, if early experiences are highly unbalanced, e.g. if they occur under the influence of chronic challenges or stresses, the individual's personality will develop specific traits, including some that are associated with severe psychopathologies. Despite these extensive behavioral characterizations, very little is known about the biological mechanisms underlying learning and memory in early life, with the exception of the effects of trauma and stress. Understanding the mechanisms underlying learning and memory in early development is key for comprehending how the learning and memory systems are built and function throughout life, as well as to better elucidate the deficits associated to neurodevelopmental disabilities. One of the most important systems operating in the brain is the medial temporal lobe-dependent memory system, which processes information about episodic, spatial, contextual and social experiences. Until recently it was believed that this memory system does not function in infancy because it is developmentally immature, and only begins to be involved late in development. However, recent studies in rodent models, including our own, showed that episodic and spatial forms of learning require the function of biological mechanisms in the dorsal hippocampus (dHC), a main region, together with the medial prefrontal cortex (mPFC), of the medial temporal lobe memory system. Despite this recent progress, knowledge of the biological and system-level mechanisms of infantile, hippocampus-dependent learning and memory is lacking. To fill this knowledge gap we propose to employ rodent models of episodic and spatial learning, genetically engineered mouse models, molecular imaging technology, spatial transcriptomics and RiboTag mouse technology combined with omic analyses to pursue the following specific aims: (1) To map the distribution at a system level (dHC and mPFC) of the cellular networks activated in response to episodic learning in infancy and in memory recovery following reminders at later ages, and to test the malleability and roles of recovered infantile memories in adult behavior. (2) To comprehensively profile in situ dHC and mPFC gene expression at the level of the whole transcriptome, as well as obtain a comprehensive translatome specifically regulated in excitatory and inhibitory neurons, in response to learning in both infant and adult brains. These experiments will provide an unprecedented amount of novel information regarding the biological and system-level mechanisms underlying infantile learning and memory, as well as an invaluable source of knowledge for generating novel hypotheses regarding neurodevelopmental and adult cognitive disorders. |
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