The UCSF ADRC will integrate basic science and clinical resources to investigate the clinical, imaging, molecular, and neuropathological features of early Alzheimer's disease (AD), non-AD dementias, mild cognitive impairment (MCI) and healthy aging. The Data Management and Statistics (DMS) core will support this mission with a research design, biostatistics, and data management infrastructure that ensures 1) the measurement of behavioral, cognitive, neurological, imaging and genetic information is supported by scientifically and clinically sound techniques that result in a consistent classification of information (i.e., inter- rater reliability);2) that the observed phenomena are accurately recorded;3) that the recorded measurements are accurately reflected in the database;4) that the database is secure, preventing unauthorized changes;5) that analytical data sets are accessible to investigators;and 6) that meaningful patterns in the data are identified using appropriate research design and biostatistical methods.
Our specific aims are 1) Provide high-quality research design and biostatistical consultation for ADRC- related cores, projects, and pilots and promote collaborative research projects utilizing ADRC data, specimens, and subjects;2) Develop and maintain centralized, integrated, data management systems and procedures to ensure the accuracy, availability, and confidentiality of administrative, clinical and research data from ADRC cores, projects, and pilots;3) Develop and maintain appropriate data management and quality assurance processes to ensure the timely and accurate collection, verification, and submission of all datasets to the NACC.
The UCSF ADRC studies of Alzheimer's disease, atypical dementias, mild cognitive impairment, and normal aging depend upon comprehensive and available databases that accurately capture diagnosis, natural history, interactions between genotype and phenotype, clinico-pathological relationships, interactions between structural and functional brain changes and neurobehavioral disturbance, and other clinical characteristics.
|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|
|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|
|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|
|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|
|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|
|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|
|Guo, Christine C; Sturm, Virginia E; Zhou, Juan et al. (2016) Dominant hemisphere lateralization of cortical parasympathetic control as revealed by frontotemporal dementia. Proc Natl Acad Sci U S A 113:E2430-9|
Showing the most recent 10 out of 390 publications