The chief goals of the Neuropathology Core (Core C) are to arrange and perform autopsies and provide neuropathological diagnoses in subjects enrolled by the Clinical Core for prospective autopsy, and to maintain a repository (Brain Resource Center) of well-characterized postmortem human brain tissue for investigations of the etiology and basic mechanisms of Parkinson's disease (PD) and Lewy body diseases (LBD). These tissues will be essential to validate the hypotheses and observations generated by the cell biology and biochemical studies of genetically engineered mice proposed in Projects 1-4. Core C will also maintain and staff histology/immunocytochemistry and stereology laboratories to support and facilitate the morphological assessment of human and experimental mouse models relevant to the studies of PD delineated in Projects 1-4. Finally, the staff of Core will train basic investigators and clinical neuroscientists in clinical and neuropathology issues relevant to PD. The staff of Core C has experience with the arrangement and conduction of autopsies, dissection and preparation of human brain tissues for research protocols, neuropathological diagnoses, morphological studies, and quantitative morphometry of neurodegenerative disorders. To accomplish its goals, Core C will staff and maintain the Brain Resource Center (BRC), a histology/immunocytochemistry (ICC) laboratory, and a quantitative morphometry/stereology facility. The BRC serves as a repository of fixed and frozen brain tissues prepared for research including cases of PD, other LBD, and normal and diseased controls. Through its many functions and facilities, Core C will support and coordinate the accession of human postmortem brain tissue material critical for studies of the basic mechanisms underlying Parkinson's disease and facilitate the morphological assessments of experimental animals from Projects 1-4.
| Hinkle, Jared Thomas; Perepezko, Kate; Bakker, Catherine C et al. (2018) Onset and Remission of Psychosis in Parkinson's Disease: Pharmacologic and Motoric Markers. Mov Disord Clin Pract 5:31-38 |
| Kam, Tae-In; Mao, Xiaobo; Park, Hyejin et al. (2018) Poly(ADP-ribose) drives pathologic ?-synuclein neurodegeneration in Parkinson's disease. Science 362: |
| Sathe, Gajanan; Na, Chan Hyun; Renuse, Santosh et al. (2018) Phosphotyrosine profiling of human cerebrospinal fluid. Clin Proteomics 15:29 |
| Guerreiro, Rita; Ross, Owen A; Kun-Rodrigues, Celia et al. (2018) Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study. Lancet Neurol 17:64-74 |
| Hinkle, Jared T; Perepezko, Kate; Bakker, Catherine C et al. (2018) Domain-specific cognitive impairment in non-demented Parkinson's disease psychosis. Int J Geriatr Psychiatry 33:e131-e139 |
| Hinkle, Jared T; Perepezko, Kate; Mills, Kelly A et al. (2018) Dopamine transporter availability reflects gastrointestinal dysautonomia in early Parkinson disease. Parkinsonism Relat Disord 55:8-14 |
| Kim, Donghoon; Hwang, Heehong; Choi, Seulah et al. (2018) D409H GBA1 mutation accelerates the progression of pathology in A53T ?-synuclein transgenic mouse model. Acta Neuropathol Commun 6:32 |
| Kim, Sangjune; Yun, Seung Pil; Lee, Saebom et al. (2018) GBA1 deficiency negatively affects physiological ?-synuclein tetramers and related multimers. Proc Natl Acad Sci U S A 115:798-803 |
| Kim, Donghoon; Yoo, Je Min; Hwang, Heehong et al. (2018) Graphene quantum dots prevent ?-synucleinopathy in Parkinson's disease. Nat Nanotechnol : |
| Hinkle, Jared T; Perepezko, Kate; Mari, Zoltan et al. (2018) Perceived Treatment Status of Fluctuations in Parkinson Disease Impacts Suicidality. Am J Geriatr Psychiatry 26:700-710 |
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