Connectomics and molecular imaging in neurodegeneration
| Autor: | James B. Rowe, Merle C Hoenig, Ece Kocagoncu, Michael Ewers, Minc faculty, Nicolai Franzmeier, Julia Neitzel, Michel J. Grothe, Alexander Drzezga, Antonio P. Strafella, Thilo van Eimeren, Gérard N. Bischof |
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| Přispěvatelé: | Kocagoncu, Ece [0000-0002-6292-7472], Rowe, James [0000-0001-7216-8679], Apollo - University of Cambridge Repository |
| Rok vydání: | 2019 |
| Předmět: |
Connectomics
diagnostic imaging [Neurodegenerative Diseases] Disease Neuropathology Selective Vulnerability Biology Multimodal Imaging Article Functional Connectivity 030218 nuclear medicine & medical imaging 03 medical and health sciences methods [Connectome] Pathophysiological Spreading 0302 clinical medicine Neuroimaging methods [Molecular Imaging] Connectome medicine Animals Humans Radiology Nuclear Medicine and imaging ddc:610 Proteinpathology Mechanism (biology) Neurodegeneration Neurodegenerative Diseases General Medicine medicine.disease Molecular Imaging 030220 oncology & carcinogenesis Molecular imaging Neuroscience |
| Zdroj: | Eur J Nucl Med Mol Imaging European journal of nuclear medicine and molecular imaging 46(13), 2819-2830 (2019). doi:10.1007/s00259-019-04394-5 |
| ISSN: | 1619-7089 1619-7070 |
| DOI: | 10.1007/s00259-019-04394-5 |
| Popis: | Our understanding on human neurodegenerative disease was previously limited to clinical data and inferences about the underlying pathology based on histopathological examination. Animal models and in vitro experiments have provided evidence for a cell-autonomous and a non-cell autonomous mechanism for the accumulation of neuropathology. Combining modern neuroimaging tools to identify distinct neural networks (Connectomics) with target-specific Positron Emission Tomography (PET) tracers is an emerging and vibrant field of research with the potential to examine the contributions of cell-autonomous and non-cell autonomous mechanisms to the spread of pathology. The evidence provided here suggests that both cell-autonomous and non-cell autonomous processes relate to the observed in vivo characteristics of protein pathology and neurodegeneration across the disease spectrum. We propose a synergistic model of cell- autonomous and non-cell autonomous accounts that integrates the most critical factors (i.e., protein strain, susceptible cell feature and connectome) contributing to the development of neuronal dysfunction and in turn produces the observed clinical phenotypes. We believe that a timely and longitudinal pursuit of such research programs will greatly advance our understanding of the complex mechanisms driving human neurodegenerative diseases. |
| Databáze: | OpenAIRE |
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