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: | Pradeep Nathan |
| Institution: | GlaxoSmithKline and University of Cambridge |
| Department: | Clinical Unit Cambridge |
| Country: | |
| Proposed Analysis: | BDNF is a synaptogenic molecule that modulates Atoxicity. A polymorphism (rs6265, Val66Met) that affects secretion of mature BDNF has been implicated in learning and memory in healthy humans, where carriage of the Met allele is associated with poor memory, reduced hippocampal volume, and lower hippocampal activation on functional imaging. While previous studies have implicated this polymorphism in Alzheimer’s disease (AD)-related cognitive impairment, it is unclear how this polymorphism affects cognitive decline, and in particular, the decline associated with Aβ toxicity. We aimed to determine whether the BDNF Val66Met polymorphism modulates Aβ amyloid-related cognitive decline, reduction in hippocampal volume, Aβ accumulation and changes in CSF Tau, Aβ1-42, and P-tau181P in normal healthy(NL) and MCI subjects. We hypothesized that Aβ amyloid-related memory decline and reduction in hippocampal volulme in normal controls and MCI subjects will be larger in carriers on the Met allele. |
| Additional Investigators | |
| Investigator's Name: | Paul Maruff |
| Proposed Analysis: | BDNF is a synaptogenic molecule that modulates Atoxicity. A polymorphism (rs6265, Val66Met) that affects secretion of mature BDNF has been implicated in learning and memory in healthy humans, where carriage of the Met allele is associated with poor memory, reduced hippocampal volume, and lower hippocampal activation on functional imaging. While previous studies have implicated this polymorphism in Alzheimer’s disease (AD)-related cognitive impairment, it is unclear how this polymorphism affects cognitive decline, and in particular, the decline associated with A toxicity. We aimed to determine whether the BDNF Val66Met polymorphism modulates Aβ amyloid-related cognitive decline, reduction in hippocampal volume, Aβ accumulation and changes in CSF Tau, Aβ 1-42, and P-tau181P in healthy normal (NL) and MCI subjects. We hypothesized that Aβ amyloid-related memory decline and reduction in hippocampal volulme in normal controls and MCI subjects will be larger in carriers on the Met allele. |
| Investigator's Name: | Fruzsina Soltesz |
| Proposed Analysis: | BDNF is a synaptogenic molecule that modulates Atoxicity. A polymorphism (rs6265, Val66Met) that affects secretion of mature BDNF has been implicated in learning and memory in healthy humans, where carriage of the Met allele is associated with poor memory, reduced hippocampal volume, and lower hippocampal activation on functional imaging. While previous studies have implicated this polymorphism in Alzheimer’s disease (AD)-related cognitive impairment, it is unclear how this polymorphism affects cognitive decline, and in particular, the decline associated with A toxicity. We aimed to determine whether the BDNF Val66Met polymorphism modulates Aβ amyloid-related cognitive decline, reduction in hippocampal volume, Aβ accumulation and changes in CSF Tau, Aβ 1-42, and P-tau181P in healthy normal (NL) and MCI subjects. We hypothesized that Aβ amyloid-related memory decline and reduction in hippocampal volulme in normal controls and MCI subjects will be larger in carriers on the Met allele. |
| Investigator's Name: | Chris Dodds |
| Proposed Analysis: | BDNF is a synaptogenic molecule that modulates Atoxicity. A polymorphism (rs6265, Val66Met) that affects secretion of mature BDNF has been implicated in learning and memory in healthy humans, where carriage of the Met allele is associated with poor memory, reduced hippocampal volume, and lower hippocampal activation on functional imaging. While previous studies have implicated this polymorphism in Alzheimer’s disease (AD)-related cognitive impairment, it is unclear how this polymorphism affects cognitive decline, and in particular, the decline associated with A toxicity. We aimed to determine whether the BDNF Val66Met polymorphism modulates Aβ amyloid-related cognitive decline, reduction in hippocampal volume, Aβ accumulation and changes in CSF Tau, Aβ 1-42, and P-tau181P in healthy normal (NL) and MCI subjects. We hypothesized that Aβ amyloid-related memory decline and reduction in hippocampal volulme in normal controls and MCI subjects will be larger in carriers on the Met allele. |