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: | Thomas kandris |
| Institution: | Hoag Memorial Hospital Presbyterian |
| Department: | Pickup Family neurosciences |
| Country: | |
| Proposed Analysis: | What effect does long term alcohol use and severity of depression have on the development of AD/ dementia? Recent empirical findings suggest that dementia is the leading cause of cognitive decline among older adults, and that approximately 40% of dementia cases are influenced by preventable environmental or lifestyle factors (Beresford TP, Arciniegas DB, Alfers J, Clapp L, Martin B, Du Y, Liu D, Shen D, Davatzikos, 2006; Prince M, Wimo AGM, Ali G, Wu Y, Prina M., 2019; Livingston G, Huntley J, Sommerlad A et al., 2020). Major Depressive disorder and substance use disorders are increasingly more prominent causes of disability in younger adults (Center for Behavioral Health Statistics and Quality, 2015). As two of the most modifiable risk factors, it is pertinent to continue to examine lifestyle risk factors, such as mental health symptoms and alcohol use, and their relationships to diseases that occur later in life. Previous research reflects Alzheimer’s disease dementia-related hippocampal atrophy is well-established (Jack et. al., 2000). Additionally, chronic and severe alcohol use has been linked with a number of cognitive impairments in learning and memory, executive functioning, mood, and motor coordination (Hoffman, J. L., Faccidomo, S., Kim, M., Taylor, S. M., Agoglia, A. E., May, A. M., et al., 2019). Additionally, alcohol use has demonstrated links to hippocampal atrophy, limbic structures, and white matter changes in the premotor corpus callosum (Kapogiannis, D., Kisser, J., Davatzikos, C., Ferrucci, L., Metter, J., and Resnick, S. M., 2012; Kryger, R., and Wilce, P. A., 2010). However, these findings are inconsistent with some studies limited in their findings without associated psychiatric co-morbidities (Fein G, Greenstein D, Cardenas VA, Cuzen NL, Fouche JP, Ferrett H, Thomas K, Stein, 2013). There is also variable evidence of depression’s relationship to hippocampal atrophy and associated cognitive deficits (Bremner JD, Narayan M, Anderson ER, Staib LH, Miller HL, Charney DS., 2000; Campbell S, Marriott M, Nahmias C, MacQueen GM, 2004; Sawyer et. al., 2012; Brinkley TE, Berger M, Callahan KE et al, 2018). The proposed mechanism between alcoholism and Alzheimer’s disease (AD) dementia is that and chronic alcohol consumption decreased glutathione (GSH) level in the brain and prolonged oxidative stress in the brain causes neuronal dysfunction and cell death, which could lead to neurodegeneration, particularly in the hippocampus (Guerri and Grisola, 1980; Bhat et al., 2015). The mechanistic link between alcohol use and Alzheimer’s dementia is still however inconclusive whether it is due to the oxidative stress or co-morbid psychiatric and lifestyle choices. It is hypothesized that it is not the alcohol use associated with the severity of AD, but the associated psychiatric implications of alcoholism and depression. Therefore, the present study wishes to examine the compared relationship between individuals diagnosed with both AD and depression without history of alcohol use disorder against those with AD and depression with an alcohol use disorder. The present study seeks to examine the relationship between hippocampal volume and self-endorsed depressive symptoms in individuals diagnosed Alzheimer’s disease, while controlling for dementia severity (operationalized as Clinical Dementia Rating scale total score at baseline) and history of chronic alcohol misuse (self-endorsed history). |
| Additional Investigators |
