The proposed project is a plan to add an imaging core to the UCSF Program Project Grant, entitled: Frontotemporal Dementia: Genes, Images and Emotions. This new core for this PPG is a response to the increasing complexity of imaging and increased use of imaging to answer questions related to FTD. Since the inception of this PPG, the number of techniques for brain imaging has expanded significantly. Our group began using structural imaging as the mainstay for anatomical assessment of FTD, and has moved on to embrace diffusion tensor imaging (DTI), arterial spin labelled perfusion (ASL) and intrinsic connectivity functional MRI (ICN fMRI), as well as FDG-PET and PIB-PET. A major goal for the next cycle of the PPG will be to investigate the relative utility of these various techniques, alone or in combination, for diagnosis and for delineating brain-behavior relatioships in FTD. Many of the cores and projects will make use of these various types of imaging modalities. While two other projects will investigate sophisticated new anaytic approaches for multimodality imaging (Project 2) and ICN fMRI (Project 6), this imaging core will facilitate use of images by these projects and the rest of the PPG by ensuring acquistion and archiving of high quality images, performing basic pre-processing, and providing basic imaging data and images. Specifically, Core E will: 1) collect and manage the following MRI sequences at 3Tesla in patients with bvFTD, nfvPPA, svPPA, IvPPA, CBS, PSPS, ALS, memory-predominant cognitive deficits (MEM), asymptomatic carriers of FTLD-causing mutations (MUT) and controls: MP-RAGE, FLAIR, T2-weighted, DTI, ASL perfusion, and ICN fMRI. We will also acquire [18FJFDG and [1 ICjPIB PET scans, 2) preprocess MR images including RF field bias and geometrical distortion corrections and coregistration of all images to each subject's "native space", 3) process Tl-weighted images with FreeSurfer (FS) and derive cortical thickness and volumes, regional perfusion, FDG-metabolism, and normalized amyloid tracer binding values for standard ROIs in FS space, 4) consult with Pis and staff serving the other PPG projects and cores on incorporating imaging data into their analyses.
This core will be an important resource for this PPG as well as for the field of FTD in general, because it will establish a large archive of structural and functional images of various types in a very well characterized clinical sample. The images acquired will be compatible with images collected for other large-scale imaging projects, in particular ADNI, significantly increasing their usefulness for other reasearchers.
|Naasan, Georges; Rabinovici, Gil D; Ghosh, Pia et al. (2016) Amyloid in dementia associated with familial FTLD: not an innocent bystander. Neurocase 22:76-83|
|Barton, Cynthia; Ketelle, Robin; Merrilees, Jennifer et al. (2016) Non-pharmacological Management of Behavioral Symptoms in Frontotemporal and Other Dementias. Curr Neurol Neurosci Rep 16:14|
|Ranasinghe, Kamalini G; Rankin, Katherine P; Pressman, Peter S et al. (2016) Distinct Subtypes of Behavioral Variant Frontotemporal Dementia Based on Patterns of Network Degeneration. JAMA Neurol 73:1078-88|
|Yokoyama, Jennifer S; Marx, Gabe; Brown, Jesse A et al. (2016) Systemic klotho is associated with KLOTHO variation and predicts intrinsic cortical connectivity in healthy human aging. Brain Imaging Behav :|
|Vatsavayai, Sarat C; Yoon, Soo Jin; Gardner, Raquel C et al. (2016) Timing and significance of pathological features in C9orf72 expansion-associated frontotemporal dementia. Brain 139:3202-3216|
|Schott, Jonathan M; Crutch, Sebastian J; Carrasquillo, Minerva M et al. (2016) Genetic risk factors for the posterior cortical atrophy variant of Alzheimer's disease. Alzheimers Dement 12:862-71|
|ChÃ©telat, GaÃ«l; Ossenkoppele, Rik; Villemagne, Victor L et al. (2016) Atrophy, hypometabolism and clinical trajectories in patients with amyloid-negative Alzheimer's disease. Brain 139:2528-39|
|Mair, Waltraud; Muntel, Jan; Tepper, Katharina et al. (2016) FLEXITau: Quantifying Post-translational Modifications of Tau Protein in Vitro and in Human Disease. Anal Chem 88:3704-14|
|Silva, M Catarina; Cheng, Chialin; Mair, Waltraud et al. (2016) Human iPSC-Derived Neuronal Model of Tau-A152T Frontotemporal Dementia Reveals Tau-Mediated Mechanisms of Neuronal Vulnerability. Stem Cell Reports 7:325-40|
|Nascimento, Camila; Suemoto, Claudia K; Rodriguez, Roberta D et al. (2016) Higher Prevalence of TDP-43 Proteinopathy in Cognitively Normal Asians: A Clinicopathological Study on a Multiethnic Sample. Brain Pathol 26:177-85|
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