Area:
synaptic transmission
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High-probability grants
According to our matching algorithm, Geraldine J. Kress is the likely recipient of the following grants.
| Years |
Recipients |
Code |
Title / Keywords |
Matching
score |
| 2016 — 2018 |
Kress, Geraldine J. |
K01Activity Code Description:
For support of a scientist, committed to research, in need of both advanced research training and additional experience. |
Circadian Regulation of Memory
Project Summary An NIA funded K01 Mentored Research Scientist Development Award will provide valuable training in the fields of aging and Alzheimer?s disease to facilitate my career as an independent research investigator. This grant mechanism will not only allow for critical scientific training, but also valuable career development under the mentorship of Dr. David Holtzman. During this award period, I propose to investigate the association between cognitive function and circadian rhythms during the aging process and Alzheimer?s disease (AD) progression. Cognitive decline is associated with aging and is the defining feature of AD. Circadian rhythms, which are 24-hour oscillations in behavior and physiological functions decline with age and are severely blunted with AD progression. In fact, recent studies suggest disruptions to the circadian system may occur prior to the clinical onset of memory deficits in AD. Yet, mechanisms by which the circadian system impacts cognitive processes during aging and AD pathogenesis are relatively unknown. The goal of this project is to test the hypothesis that the decay in circadian rhythmicity as observed in aging and to a greater extent in AD, causes pathological disturbances in brain regions associated with memory processing. The following aims will test this hypothesis: (1) Examine the circadian oscillation of transcriptional, biochemical, and electrophysiological processes in brain regions which support memory function in mouse models of aging and AD. (2) Examine the effects of altering circadian function on behavioral, physiological, and molecular rhythms, and if this intervention influences AD pathogenesis. The concepts and methods in this proposal are innovative and have the potential for substantially impacting our understanding for the role of circadian function on memory in aging and AD progression. Our long-term goal is to identify possible strategies to ameliorate cognitive impairments and disease progression.
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1 |
| 2019 — 2020 |
Kress, Geraldine J. |
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. |
Circadian Regulation of Memory During Alzheimer's Disease Pathogenesis
Project Summary We propose to investigate the association between circadian system dysfunction, cognition, and Alzheimer?s disease (AD) pathogenesis. Originally, most circadian system changes were thought to be driven by the disease process. Recently, however, there is a growing realization that long-term circadian dysfunction has serious health consequences and may even precede the clinical onset of memory deficits in AD. This field is embarking on a paradigm shift that the circadian system may directly influence AD pathogenesis. Specifically, disruption of the circadian system central pacemaker, the suprachiasmatic nucleus (SCN), may contribute to the observed fragmented circadian system dysregulation in preclinical AD. The goal of this project is to test the hypothesis that poor circadian rhythms mediated by a dysfunctional central clock directly influence AD pathogenesis. The following aims will test this hypothesis: (1) examine the effects of altered SCN function on downstream hippocampal-dependent behavioral, physiological, and molecular rhythms; (2) examine the effects of chronic aberrant SCN signaling on amyloidogenic processes; (3) examine the effects of a circadian intervention on AD pathogenesis. We will combine cutting-edge in vivo optogenetic techniques with sophisticated neurophysiological measures to examine the dynamic regulation of learning and memory processes by the circadian system. Circuit-specific optogenetic manipulation of circadian system function while assaying cognitive functions represents a highly novel and methodologically unique approach. We will decipher a mechanistic link between circadian system dysregulation and cognitive decline in AD. With this project, we are well-poised to uncover new insights into the complex biological mechanisms associated with AD. Because sleep-wake and circadian disruptions are major causes of morbidity and institutionalization among AD patients, we hope that these studies may lead to effective interventions to forestall disease progression, which would also lessen caregiver burden and decrease financial care costs associated with progressing dementia.
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1 |