There are many active research projects accessing and applying shared ADNI data. Use the search above to find specific research focuses on the active ADNI investigations. This information is requested annually as a requirement for data access.
| Principal Investigator | |
| Principal Investigator's Name: | Juliana Nery Souza-Talarico |
| Institution: | University of Iowa |
| Department: | College of Nursing |
| Country: | |
| Proposed Analysis: | The overall objective of this proposal is to identify allostatic states that predict the pathological changes that feature the AD preclinical stage. An allostatic state indicates a subclinical condition caused by cumulative effects of neuroendocrine, inflammatory, and metabolic stress mediators on target body systems, including the central nervous system (CNS). Our central hypothesis is that combinations of neuroendocrine, immunological, and metabolic allostatic states at mid-life predict Aβ deposition, hippocampus atrophy, and cognitive decline in late life. Sustained cortisol levels, proinflammatory cytokines, and glucose, which are the primary stress mediators, induce neuroinflammation, which triggers Aβ accumulation, brain atrophy, and consequently, cognitive decline. We propose demonstrating that sustained allostatic states at mid-life contribute to Aβ deposition, hippocampal volume decrease, and cognitive performance decline. These findings will provide the foundation for subsequent studies to identify protective factors and explore preventive strategies capable of shaping cognitive functioning towards a healthy trajectory. To attain the overall objective, the following specific aims will be pursued: Specific aim #1: determine the association between high chronic stress and cognitive functioning changes in middle adults between 50 and 64. Specific aim #2: identify patterns of hyper or hypo allostatic states associated with chronic stress. Specific aim # 3: determine the allostatic states that predict Aβ deposition, hippocampus volume decrease, and memory decline from middle-age to aging. Upon completing this project, we expect that we will have demonstrated that allostatic load states represent one of the pathways through incubated effects of chronic stress leads to the same set of brain changes that feature the preclinical stage of AD. We also expect to identify sociodemographic and psychological moderators of the negative consequences of stress on cognitive functioning from mid-life to aging. This accomplishment would set the basis for new therapeutic and preventive avenues to screen vulnerable individuals and test effective interventions to delay or transform deleterious cognitive trajectories into promisor aging. |
| Additional Investigators | |
| Investigator's Name: | Maria Hein |
| Proposed Analysis: | Data manager |
| Investigator's Name: | Bradley Aouizerat |
| Proposed Analysis: | Dr. Aouizerat will be responsible for performing Aim 4. Aim 4: Determine the role of aging clocks in mediating the relationship between Allostatic load profiles and Aβ deposition, hippocampus volume decrease, and memory decline from middle age to aging. Aging clocks will be determined using DNA methylation data from ADNI1/GO/2 cohorts. Upon completing this project, we expect to propose a potential mechanism linking allostatic load states and epigenetic factors to the same brain changes that feature the preclinical stage of AD. |
