The underlying philosophy of the Core remains a belief that validation of diagnosis is critical to clinical research into neurodegenerative diseases and that tissue-based studies are a critical complement to in vitro studies of the biologic process that underlying these diseases. By providing these two pillars to the clinical and scientific community, the Neuropathology Core is able to make a contribution to the amelioration of suffering associated with AD and related disorders.
The Specific Aims of the Neuropathology Coreare: 1. To establish an accurate neuropathological diagnosis on all brains submitted with standardized reporting, including clinicopathological correlation and interpretation of findings, to the Clinical Core, other treating physicians andfamilies; 2. To maintain a source of brain tissue and other samples for investigators studying AD and related disorders, through preparation of tissue in a standardized manner, including determination of RNAquality, with special consideration of investigators within the Massachusetts ADRC; 3. To work with the Clinical Core to develop, store and distribute DNA, cell lines, plasma and serum collected under the Clinical Core's Biomarkers Initiative; 4. To train diagnostic and experimental neuropathologists in the neuropathology of dementing disorders; and 5. To participate in cooperative ventures with other groups studying neurodegenerative diseases, both human and animal models, including other Alzheimer Centers (ADRCs &ADCs), NACC, NINDS- supported Udall Center, as well as other consortia and individual investigators. These broad goals, which are in continuity with the historical activities of the Neuropathology Core, will enhance the value of the collected brain tissue to individual investigators whose specific research projects depend upon receiving carefully prepared and examined tissue.
Brain tissue is a critical resource for many important experiments that are defining the underlying pathology of Alzheimer disease and other neurodegenerative diseases. The ability to use the collect tissue in experiments is essential as new therapies and disease markers are developed.
|Wang, Tingyan; Qiu, Robin G; Yu, Ming (2018) Predictive Modeling of the Progression of Alzheimer's Disease with Recurrent Neural Networks. Sci Rep 8:9161|
|DeVos, Sarah L; Corjuc, Bianca T; Commins, Caitlin et al. (2018) Tau reduction in the presence of amyloid-? prevents tau pathology and neuronal death in vivo. Brain 141:2194-2212|
|Lee, Christopher M; Jacobs, Heidi I L; Marquié, Marta et al. (2018) 18F-Flortaucipir Binding in Choroid Plexus: Related to Race and Hippocampus Signal. J Alzheimers Dis 62:1691-1702|
|Agogo, George O; Ramsey, Christine M; Gnjidic, Danijela et al. (2018) Longitudinal associations between different dementia diagnoses and medication use jointly accounting for dropout. Int Psychogeriatr 30:1477-1487|
|Eftekharzadeh, Bahareh; Daigle, J Gavin; Kapinos, Larisa E et al. (2018) Tau Protein Disrupts Nucleocytoplasmic Transport in Alzheimer's Disease. Neuron 99:925-940.e7|
|Emerson, Sarah C; Waikar, Sushrut S; Fuentes, Claudio et al. (2018) Biomarker validation with an imperfect reference: Issues and bounds. Stat Methods Med Res 27:2933-2945|
|Crum, Jana; Wilson, Jeffrey; Sabbagh, Marwan (2018) Does taking statins affect the pathological burden in autopsy-confirmed Alzheimer's dementia? Alzheimers Res Ther 10:104|
|Pasi, Marco; Marini, Sandro; Morotti, Andrea et al. (2018) Cerebellar Hematoma Location: Implications for the Underlying Microangiopathy. Stroke 49:207-210|
|Petyuk, Vladislav A; Chang, Rui; Ramirez-Restrepo, Manuel et al. (2018) The human brainome: network analysis identifies HSPA2 as a novel Alzheimer’s disease target. Brain 141:2721-2739|
|Xiong, Li; van Veluw, Susanne J; Bounemia, Narimene et al. (2018) Cerebral Cortical Microinfarcts on Magnetic Resonance Imaging and Their Association With Cognition in Cerebral Amyloid Angiopathy. Stroke 49:2330-2336|
Showing the most recent 10 out of 966 publications