The Pathology Core provides tissue diagnoses of Alzheimer's disease (AD), cerebrovascular disease (CVD) and related dementias and links the clinical studies with basic and translational research by project-driven, tissue procurement and allocation. During the current funding period, the Core served a total of funded 53 projects yielding 44 publications in peer review journals.
In AIM 1, the diagnostic protocol integrates the NIA-Reagan Institute Workshop Group protocol, components of the CERAD program, Braak and Braak parameters and the Aging Brain Program Project protocol, and global indicators of dementia.
AIM 2 : In the renewal, there are proposed projects of 19 investigators located at 9 academic centers. Relationship of aging, sex hormones, the retina and cerebral vasculature to dementia are areas of emphasis. Postmortem tissues are obtained from patients enrolled in the USC Clinical Core Brain Research Study and are all clinically defined by the UDS database. A twenty-four hour autopsy service minimizes postmortem delay insuring high-fidelity preparations for biochemistry and molecular biology, including mRNA expression profiling, and viable tissue for endothelial cell cultures. Following the ADC Biospecimen Best Practice Guidelines, tissue preparations are tailored to special protocols with reliable neuroanatomical dissections performed at autopsy. Postmortem tissues will be available for synaptoneurosome preparations to evaluate molecular pathology and plasticity changes of the synapse for four projects.
AIM 3 : Neuropathology summary reports are entered with the National Alzheimer's Coordinating Center (NACC).
AIM 4 : The Core will coordinate genotyping for risk factors, such as ApoE, from postmortem tissues and clinical blood samples.
AIM 5 : Training in the neuropathology of AD is extended to neuropathology fellows, neurology and pathology residents, and graduate students in neuroscience and pathobiology programs, both diagnostically and translational, emphasizing the neurobiology of dementia.
The Neuropathology Core confirms the presence of AD, vascular, and other types of neurodegenerative pathology will is essential to achieve most accurate etiological diagnosis. The Core is central for distributing human tissues for basic research into the cause and treatment of neurodegeneration disorders. The Core also provide a source of DNA for genomic wide association studies.
|Kammen, Alexandra; Law, Meng; Tjan, Bosco S et al. (2016) Automated retinofugal visual pathway reconstruction with multi-shell HARDI and FOD-based analysis. Neuroimage 125:767-79|
|Soosman, Steffan K; Joseph-Mathurin, Nelly; Braskie, Meredith N et al. (2016) Widespread white matter and conduction defects in PSEN1-related spastic paraparesis. Neurobiol Aging 47:201-209|
|Barnes, Samuel R; Ng, Thomas S C; Montagne, Axel et al. (2016) Optimal acquisition and modeling parameters for accurate assessment of low Ktrans blood-brain barrier permeability using dynamic contrast-enhanced MRI. Magn Reson Med 75:1967-77|
|Forrester, Sarah N; Gallo, Joseph J; Smith, Gwenn S et al. (2016) Patterns of Neuropsychiatric Symptoms in Mild Cognitive Impairment and Risk of Dementia. Am J Geriatr Psychiatry 24:117-25|
|Ebbert, Mark T W; Boehme, Kevin L; Wadsworth, Mark E et al. (2016) Interaction between variants in CLU and MS4A4E modulates Alzheimer's disease risk. Alzheimers Dement 12:121-9|
|Kennedy, Richard E; Cutter, Gary R; Wang, Guoqiao et al. (2016) Post Hoc Analyses of ApoE Genotype-Defined Subgroups in ClinicalÂ Trials. J Alzheimers Dis 50:1205-15|
|Crawford, Karen L; Neu, Scott C; Toga, Arthur W (2016) The Image and Data Archive at the Laboratory of Neuro Imaging. Neuroimage 124:1080-3|
|Finch, Caleb E; Shams, Sara (2016) Apolipoprotein E and Sex Bias in Cerebrovascular Aging of Men and Mice. Trends Neurosci 39:625-37|
|Halliday, Matthew R; Rege, Sanket V; Ma, Qingyi et al. (2016) Accelerated pericyte degeneration and blood-brain barrier breakdown in apolipoprotein E4 carriers with Alzheimer's disease. J Cereb Blood Flow Metab 36:216-27|
|Bilousova, Tina; Miller, Carol A; Poon, Wayne W et al. (2016) Synaptic Amyloid-Î² Oligomers Precede p-Tau and Differentiate High Pathology Control Cases. Am J Pathol 186:185-98|
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