Neurodegenerative proteinopathies, including Alzheimer’s disease, Frontotemporal dementia, Parkinson’s disease and Lewy body dementia, represent a tremendous unmet clinical need. A common feature of these diseases is the abnormal accumulation and spreading of pathological protein aggregates that play a central role in affecting selective vulnerable circuits in a disease-specific topographic pattern. Translational research with a combination of molecular imaging modalities such as positron emission tomography (PET) and experimental animal models mimicking disease-specific pathologies provide valuable tools for understanding these disease mechanisms and the development of biomarker and treatment strategies. The rapid advancement in the development of specific imaging probes has enabled early detection of amyloid-beta and tau, while imaging a-synuclein and TDP-43 remains a great challenge in the field.
To better explain the utility of using imaging and living animal models to develop new treatment/drug targets/imaging biomarkers, and to clarify novel disease mechanisms, we need to understand recent advances in preclinical imaging, the difference in imaging human patients with neurodegenerative proteionopathies and animal models. Similarly, comparing the binding characteristics of probes in postmortem brain tissues from human patients and animal models is important for understanding in vivo imaging results. This Research Topic aims to understand the advantages and limitations of imaging modalities (PET/SPECT, optical imaging etc.)/probes, as well as preclinical imaging of neurodegenerative proteinopathies.
Contributions summarizing recent advances in imaging of animal models of neurodegenerative proteinopathies (mainly including amyloid-beta, tau, a-synuclein and TDP-43 aggregates) and imaging modalities/probes for the above-mentioned targets with comparisons of preclinical and clinical results, as well as future perspectives, are welcomed. As well, we welcome contributions that address the close relationship surrounding the process of proteinpathies of non-specific pathologies in neurodegenerative proteinopathies such as neuroinflammation or synaptic damage.
Contributions should provide a clear summary of the advantages and limitations of current animal models in developing imaging tools to detect neurodegenerative proteinopathies and/or imaging modalities and probes, to enable better application in translational research.
Neurodegenerative proteinopathies, including Alzheimer’s disease, Frontotemporal dementia, Parkinson’s disease and Lewy body dementia, represent a tremendous unmet clinical need. A common feature of these diseases is the abnormal accumulation and spreading of pathological protein aggregates that play a central role in affecting selective vulnerable circuits in a disease-specific topographic pattern. Translational research with a combination of molecular imaging modalities such as positron emission tomography (PET) and experimental animal models mimicking disease-specific pathologies provide valuable tools for understanding these disease mechanisms and the development of biomarker and treatment strategies. The rapid advancement in the development of specific imaging probes has enabled early detection of amyloid-beta and tau, while imaging a-synuclein and TDP-43 remains a great challenge in the field.
To better explain the utility of using imaging and living animal models to develop new treatment/drug targets/imaging biomarkers, and to clarify novel disease mechanisms, we need to understand recent advances in preclinical imaging, the difference in imaging human patients with neurodegenerative proteionopathies and animal models. Similarly, comparing the binding characteristics of probes in postmortem brain tissues from human patients and animal models is important for understanding in vivo imaging results. This Research Topic aims to understand the advantages and limitations of imaging modalities (PET/SPECT, optical imaging etc.)/probes, as well as preclinical imaging of neurodegenerative proteinopathies.
Contributions summarizing recent advances in imaging of animal models of neurodegenerative proteinopathies (mainly including amyloid-beta, tau, a-synuclein and TDP-43 aggregates) and imaging modalities/probes for the above-mentioned targets with comparisons of preclinical and clinical results, as well as future perspectives, are welcomed. As well, we welcome contributions that address the close relationship surrounding the process of proteinpathies of non-specific pathologies in neurodegenerative proteinopathies such as neuroinflammation or synaptic damage.
Contributions should provide a clear summary of the advantages and limitations of current animal models in developing imaging tools to detect neurodegenerative proteinopathies and/or imaging modalities and probes, to enable better application in translational research.
