Core D, the Neuropathology Core (NP Core), is a continuation of the same core that has served the ADRC for the past 4 years. The personnel are the same except for a recently hired histology technician. Because Dr. Bruce Miller and the Clinical Core have recruited patients with FTDs and atypical dementing disorders throughout Northern California and beyond, we have hired Glen Oaks Pathology Services (San Francisco) to remove brains from enrolled patients within a 150 mile radius from UCSF. The chilled brain is transported to Dr. Eric Huang at the San Francisco VA Medical Center where the first of three brain dissection steps is performed: Dr. Huang coronally sections the fresh brain and alternate slabs are either immersion fixed in paraformaldehyde or frozen. Next, the fixed brain slabs are transported to Dr. William Seeley's laboratory at the UCSF Mission Center Building (MCB). Dr. Seeley has been studying selective neuronal vulnerability in FTD in close collaboration with Dr. DeArmond and the NP Core. Dr. Seeley dissects brain regions of interest for his studies and also performs dissections for other ADRC investigators. Finally, the remaining fixed brain samples are sent to Dr. DeArmond's Lab (adjacent to Dr. Seeley's) for removal of ~30 blocks of tissue for diagnostic neuropathological analysis. Dr. DeArmond and his staff perform multiple neurohistological and immunohistochemical stains on the blocks, perform semiquantitiatve analysis of the stained slides, write a detailed neuropathology final report on each case, and complete a NACC form. The NP Core provides quality digital photographs and quantitative morphometric analysis of neuropathological changes as needed for publications. The overall aim of this ADRC is to better understand the clinical heterogeneity of patients with AD, FTD and related disorders, and to tackle the problem of selective vulnerability. Complimentary to the clinical aim, the overall aim of the NP Core is to better understand the overlap of multiple different clinically and neuropathologically defined entities we are finding in many dementia patients. Through a consortium arrangement with Dr. Daniel Geschwind at UCLA, the NP Core will oversee transport of blood samples to his lab for differential genetic analysis of heterogeneity.
This core will provide a unique resource to dementia neuroscience investigators at the UCSF ADRC and beyond by systematically banking brain tissue and genetic materials from patients with AD, FTD, and other dementias. These resources are intended to facilitate modern neuroscientific research studies related to these disorders that will ultimately lead to new treatments.
|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|
|Rabinovici, Gil D (2016) Amyloid biomarkers: pushing the limits of early detection. Brain 139:1008-10|
|Mez, Jesse; Mukherjee, Shubhabrata; Thornton, Timothy et al. (2016) The executive prominent/memory prominent spectrum in Alzheimer's disease is highly heritable. Neurobiol Aging 41:115-21|
|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|
|Yokoyama, Jennifer S; Desikan, Rahul S (2016) Association of Alzheimer Disease Susceptibility Variants and Gene Expression in the Human Brain-Reply. JAMA Neurol 73:1255|
|Voyle, N; Kim, M; Proitsi, P et al. (2016) Blood metabolite markers of neocortical amyloid-Î² burden: discovery and enrichment using candidate proteins. Transl Psychiatry 6:e719|
|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|
|Oh, Hwamee; Madison, Cindee; Baker, Suzanne et al. (2016) Dynamic relationships between age, amyloid-Î² deposition, and glucose metabolism link to the regional vulnerability to Alzheimer's disease. Brain 139:2275-89|
|LoBue, Christian; Denney, David; Hynan, Linda S et al. (2016) Self-Reported Traumatic Brain Injury and Mild Cognitive Impairment: Increased Risk and Earlier Age of Diagnosis. J Alzheimers Dis 51:727-36|
|Jun, G; Ibrahim-Verbaas, C A; Vronskaya, M et al. (2016) A novel Alzheimer disease locus located near the gene encoding tau protein. Mol Psychiatry 21:108-17|
Showing the most recent 10 out of 390 publications