ADNI data is made available to researchers around the world. As such, there are many active research projects accessing and applying the shared ADNI data. To further encourage Alzheimer’s disease research collaboration, and to help prevent duplicate efforts, the list below shows the specific research focus of the active ADNI investigations. This information is requested annually as a requirement for data access.
| Principal Investigator | |
| Principal Investigator's Name: | Yasmine Said |
| Institution: | Faculty of Medicine, Ain Shams University |
| Department: | Neurology |
| Country: | |
| Proposed Analysis: | The objectives of this study are therefore to determine the correlation between the volumes of the entorhinal cortex(EC), transentorhinal area (TEA), and hippocampus(HP)with cingulum bundle atrophy in controls, amnestic MCI, and AD patients as well as the correlation of those three variables with memory scores using at least 2 main domains from the neuropsychological testing. Then, test the correlation between the cingulum bundle and perforant path (PP) atrophy and the correlation of each with memory scores. Aim I: To determine the correlation between the EC, TEA and Hp volumes and their rates of atrophy with white matter atrophy in the cingulum bundle. The aim of this objective is to assess the relationship between pathology initiation and continuation in the EC, which is a very early process, and white matter changes in the cingulum bundle carrying inputs from different areas of the brain to the EC. Segmentation of the EC will be done manually using protocols made at the IDeA Lab or using already developed and used protocols from Rush University. Aim II: To determine the correlation between Hp volume and rate of atrophy with white matter atrophy in cingulum bundle. Other studies (Villain et al.) have shown that there is a correlation between Hp atrophy and white matter atrophy including the cingulum bundle but has not shown the correlation with the EC. Therefore, the importance of it in this study is to perform a comparison between the correlations with EC and Hp and determine which volume has a stronger one. Aim III: To correlate the Hp, TEA, and EC volumes as well as cingulum bundle changes with memory scores. Other studies have found a stronger correlation between white matter (PP) and Hp with memory scores more than EC. But in this study, memory scores specific for each volume will be used as a function of each area. Therefore, immediate free recall will be used as a function of EC and delayed free recall will be used as a function of Hp. Neuropsychological test scores for the subjects will be used. Aim IV: To correlate between the cingulum bundle changes and those in PP. Since both PP and cingulum bundle are related to the EC and transentorhinal area which undergo marked changes in AD, how do changes among those white matter fibers correlate as a result of EC pathological changes? And how do changes in white matter fibers projecting into and from those affected areas correlate to memory scores? If the results show a positive correlation then the correlations can be compared to determine whether changes in the cingulum bundle can predict future changes in the PP sending inputs to the hippocampus. Voxel based morphometry and MedINRIA will be used. |
| Additional Investigators | |
| Investigator's Name: | Beth Kuczynski |
| Proposed Analysis: | Presuming that AD is a consequence of dissociation of the cortical areas and the medial temporal lobe areas both of which are involved in episodic memory, a question prevails as to whether the memory network is the target of such a degenerative process and whether there is a certain gateway to such a network. The aim of this study is to determine the sequence of changes occurring in amnestic MCI (aMCI), both converters and non-converters, and AD patients as compared to controls using both hippocampal atrophy rates and cortical CMRglu. Methodology: All of the data is provided from the Alzheimer’s disease Neuroinitiative (ADNI) project. A small sample size was used as an initiation with 4 controls, 5 aMCI, and 5 AD. The MCI patients were chosen according to Peterson criteria and remained stable over a period of 2 years. All subjects’ data were taken at both baseline and follow up at 24 months. The hippocampus was manually segmented on a 1.5 Tesla MRI for all subjects and only the hippocampal head was used to determine atrophy rates. A software Midas.1.11 was used for the manual segmentation which was done by one individual then reviewed by another for correction of errors. The CMRglu of each region was normalized to the whole brain. Statistical Analysis used ANOVA and paired testing as well as post-Tukey test. Results and Discussion: Across all 3 groups (controls, MCI, and AD), hippocampal atrophy rates were siginificant. At baseline, the data showed that there was a significant change in CMRglu from normal to AD in both the left hippocampus and the posterior cingulate cortex (PCC) with only a trend for the inferior parietal and no changes in the frontal regions(fig 1). At follow up, decline in CMRglu of the hippocampus was progressive along with reductions in CMRglu of the prefrontal cortex and medial frontal gyrus. Meanwhile, there was positive change for the posterior cingulate cortex with rise in the metabolic rates in both MCI and AD compared to normal controls (fig 2). Previous studies have shown this sequence of progression of reduction in CMRglu in MCI patients including those who did convert to AD but had shown a consistent decrease in the PCC CMRglu. Our data suggests that the disease process in AD primarily targets the medial temporal lobe areas that are important parts of the memory system and that since other cortical areas are also involved, the damage occurs in a sequential process that ends up with damage of the frontal lobes. With change in the metabolic rates of the PCC, it is suggested that the PCC is a sensitive area in the memory network, responding quickly to the process first with decreased metabolic rate. However, it remains poorly understood why it shows an increase after a 24 months follow up in both MCI and AD. Future work will include an increase in the sample size, segmentation of 2 more areas in the medial temporal lobe. Furthermore, to determine the correlation between atrophy rates of the medial temporal grey matter and the cortical CMRglu before they show changes in volumetric measurements in an effort to assess the exact relationship between the Hp, EC damage and changes throughout the cortex. |
| Investigator's Name: | Mony De Leon |
| Proposed Analysis: | Presuming that AD is a consequence of dissociation of the cortical areas and the medial temporal lobe areas both of which are involved in episodic memory, a question prevails as to whether the memory network is the target of such a degenerative process and whether there is a certain gateway to such a network. The aim of this study is to determine the sequence of changes occurring in amnestic MCI (aMCI), both converters and non-converters, and AD patients as compared to controls using both hippocampal atrophy rates and cortical CMRglu. Methodology: All of the data is provided from the Alzheimer’s disease Neuroinitiative (ADNI) project. A small sample size was used as an initiation with 4 controls, 5 aMCI, and 5 AD. The MCI patients were chosen according to Peterson criteria and remained stable over a period of 2 years. All subjects’ data were taken at both baseline and follow up at 24 months. The hippocampus was manually segmented on a 1.5 Tesla MRI for all subjects and only the hippocampal head was used to determine atrophy rates. A software Midas.1.11 was used for the manual segmentation which was done by one individual then reviewed by another for correction of errors. The CMRglu of each region was normalized to the whole brain. Statistical Analysis used ANOVA and paired testing as well as post-Tukey test. Results and Discussion: Across all 3 groups (controls, MCI, and AD), hippocampal atrophy rates were siginificant. At baseline, the data showed that there was a significant change in CMRglu from normal to AD in both the left hippocampus and the posterior cingulate cortex (PCC) with only a trend for the inferior parietal and no changes in the frontal regions(fig 1). At follow up, decline in CMRglu of the hippocampus was progressive along with reductions in CMRglu of the prefrontal cortex and medial frontal gyrus. Meanwhile, there was positive change for the posterior cingulate cortex with rise in the metabolic rates in both MCI and AD compared to normal controls (fig 2). Previous studies have shown this sequence of progression of reduction in CMRglu in MCI patients including those who did convert to AD but had shown a consistent decrease in the PCC CMRglu. Our data suggests that the disease process in AD primarily targets the medial temporal lobe areas that are important parts of the memory system and that since other cortical areas are also involved, the damage occurs in a sequential process that ends up with damage of the frontal lobes. With change in the metabolic rates of the PCC, it is suggested that the PCC is a sensitive area in the memory network, responding quickly to the process first with decreased metabolic rate. However, it remains poorly understood why it shows an increase after a 24 months follow up in both MCI and AD. Future work will include an increase in the sample size, segmentation of 2 more areas in the medial temporal lobe. Furthermore, to determine the correlation between atrophy rates of the medial temporal grey matter and the cortical CMRglu before they show changes in volumetric measurements in an effort to assess the exact relationship between the Hp, EC damage and changes throughout the cortex. |
| Investigator's Name: | Yi Li |
| Proposed Analysis: | Presuming that AD is a consequence of dissociation of the cortical areas and the medial temporal lobe areas both of which are involved in episodic memory, a question prevails as to whether the memory network is the target of such a degenerative process and whether there is a certain gateway to such a network. The aim of this study is to determine the sequence of changes occurring in amnestic MCI (aMCI), both converters and non-converters, and AD patients as compared to controls using both hippocampal atrophy rates and cortical CMRglu. Methodology: All of the data is provided from the Alzheimer’s disease Neuroinitiative (ADNI) project. A small sample size was used as an initiation with 4 controls, 5 aMCI, and 5 AD. The MCI patients were chosen according to Peterson criteria and remained stable over a period of 2 years. All subjects’ data were taken at both baseline and follow up at 24 months. The hippocampus was manually segmented on a 1.5 Tesla MRI for all subjects and only the hippocampal head was used to determine atrophy rates. A software Midas.1.11 was used for the manual segmentation which was done by one individual then reviewed by another for correction of errors. The CMRglu of each region was normalized to the whole brain. Statistical Analysis used ANOVA and paired testing as well as post-Tukey test. Results and Discussion: Across all 3 groups (controls, MCI, and AD), hippocampal atrophy rates were siginificant. At baseline, the data showed that there was a significant change in CMRglu from normal to AD in both the left hippocampus and the posterior cingulate cortex (PCC) with only a trend for the inferior parietal and no changes in the frontal regions(fig 1). At follow up, decline in CMRglu of the hippocampus was progressive along with reductions in CMRglu of the prefrontal cortex and medial frontal gyrus. Meanwhile, there was positive change for the posterior cingulate cortex with rise in the metabolic rates in both MCI and AD compared to normal controls (fig 2). Previous studies have shown this sequence of progression of reduction in CMRglu in MCI patients including those who did convert to AD but had shown a consistent decrease in the PCC CMRglu. Our data suggests that the disease process in AD primarily targets the medial temporal lobe areas that are important parts of the memory system and that since other cortical areas are also involved, the damage occurs in a sequential process that ends up with damage of the frontal lobes. With change in the metabolic rates of the PCC, it is suggested that the PCC is a sensitive area in the memory network, responding quickly to the process first with decreased metabolic rate. However, it remains poorly understood why it shows an increase after a 24 months follow up in both MCI and AD. Future work will include an increase in the sample size, segmentation of 2 more areas in the medial temporal lobe. Furthermore, to determine the correlation between atrophy rates of the medial temporal grey matter and the cortical CMRglu before they show changes in volumetric measurements in an effort to assess the exact relationship between the Hp, EC damage and changes throughout the cortex. |
| Investigator's Name: | Tsui Wai |
| Proposed Analysis: | Presuming that AD is a consequence of dissociation of the cortical areas and the medial temporal lobe areas both of which are involved in episodic memory, a question prevails as to whether the memory network is the target of such a degenerative process and whether there is a certain gateway to such a network. The aim of this study is to determine the sequence of changes occurring in amnestic MCI (aMCI), both converters and non-converters, and AD patients as compared to controls using both hippocampal atrophy rates and cortical CMRglu. Methodology: All of the data is provided from the Alzheimer’s disease Neuroinitiative (ADNI) project. A small sample size was used as an initiation with 4 controls, 5 aMCI, and 5 AD. The MCI patients were chosen according to Peterson criteria and remained stable over a period of 2 years. All subjects’ data were taken at both baseline and follow up at 24 months. The hippocampus was manually segmented on a 1.5 Tesla MRI for all subjects and only the hippocampal head was used to determine atrophy rates. A software Midas.1.11 was used for the manual segmentation which was done by one individual then reviewed by another for correction of errors. The CMRglu of each region was normalized to the whole brain. Statistical Analysis used ANOVA and paired testing as well as post-Tukey test. Results and Discussion: Across all 3 groups (controls, MCI, and AD), hippocampal atrophy rates were siginificant. At baseline, the data showed that there was a significant change in CMRglu from normal to AD in both the left hippocampus and the posterior cingulate cortex (PCC) with only a trend for the inferior parietal and no changes in the frontal regions(fig 1). At follow up, decline in CMRglu of the hippocampus was progressive along with reductions in CMRglu of the prefrontal cortex and medial frontal gyrus. Meanwhile, there was positive change for the posterior cingulate cortex with rise in the metabolic rates in both MCI and AD compared to normal controls (fig 2). Previous studies have shown this sequence of progression of reduction in CMRglu in MCI patients including those who did convert to AD but had shown a consistent decrease in the PCC CMRglu. Our data suggests that the disease process in AD primarily targets the medial temporal lobe areas that are important parts of the memory system and that since other cortical areas are also involved, the damage occurs in a sequential process that ends up with damage of the frontal lobes. With change in the metabolic rates of the PCC, it is suggested that the PCC is a sensitive area in the memory network, responding quickly to the process first with decreased metabolic rate. However, it remains poorly understood why it shows an increase after a 24 months follow up in both MCI and AD. Future work will include an increase in the sample size, segmentation of 2 more areas in the medial temporal lobe. Furthermore, to determine the correlation between atrophy rates of the medial temporal grey matter and the cortical CMRglu before they show changes in volumetric measurements in an effort to assess the exact relationship between the Hp, EC damage and changes throughout the cortex. |
| Investigator's Name: | Elizabeth Pirraglia |
| Proposed Analysis: | Alzheimer’s disease (AD) is a complex disease process in which there is early atrophy of the hippocampus (Hp), entorhinal cortex, and transentorhinal region. Another condition antecedent to AD, Mild Cognitive Impairment (MCI), has been important in understanding AD before extensive damage occurs. The aim of our study is to determine the sequence of changes occurring in amnestic MCI, both converters to AD and non-converters, and AD patients, using Hp atrophy rates as well as cortical cerebral metabolic rate (CMRglu) in a longitudinal study. Methods: Three groups (AD, MCI, and normal (NL)) of 36 subjects were selected from ADNI for which age and education were controlled with 2 years follow up. In MCI, half converted to AD. The hippocampus was manually segmented and only the hippocampal head was used. Results: Significance for Hp atrophy rates; NL vs MCI p<.01, NL vs AD p<.001, MCI vs AD p<.05. Change in L MTL was significantly different for AD from MCI and NL at p<0.1 and p<0.5 respectively. For Posterior cingulate cortex (PCC), significant difference were present at baseline between AD and NL at p<0.5. Parital correlation of atrophy rate with PCC L showed high atrophy associated with high CMRglu (r= .37, p<.05). AD was significantly different from control at p<0.5 for R Hp at both times and change in L Hp was significant in AD compared to control and MCI at p<0.5. In conclusion, there has been significant difference across groups for PCC, MTL, and Hp with difference between the right and left hemispheres. The L PCC showed an unexpected result of increased CMRglu with increased Hp atrophy perhaps as compensation due to its role in episodic memory. There has also been a discrepancy between both sides for the Hp. The MTL changes differentiated between the stable MCI and those who converted to AD. |