Neuronal cell loss causes cognitive, behavioral and/or motor symptoms in dementia. Several pathological mechanisms can lead to neurodegeneration, such as the deposition of β-amyloid plaques and tau-containing neurofibrillary tangles in Alzheimer’s disease, α synuclein in Parkinson’s disease, or TDP in (part ...
Neuronal cell loss causes cognitive, behavioral and/or motor symptoms in dementia. Several pathological mechanisms can lead to neurodegeneration, such as the deposition of β-amyloid plaques and tau-containing neurofibrillary tangles in Alzheimer’s disease, α synuclein in Parkinson’s disease, or TDP in (part of the) patients with frontotemporal dementia. The common denominator across these neurodegenerative disease is that neurodegeneration usually follows a stereotypical pattern that parallels the worsening of symptoms: these initially emerge in a specific cognitive domain (e.g. memory problems in Alzheimer’s disease) when neurodegeneration is still circumscribed, while other functions decline at later points in time as neurodegeneration spreads. Brain connectivity, as can be measured with neuroimaging techniques such as magnetic resonance imaging (MRI), electroencephalography (EEG) and magnetoencephalography (MEG), may explain this disease specific spread of neurodegeneration. In addition, Positron Emission Tomography (PET) allows probing of the pathological substrates underlying various forms of dementia. Combining these neuroimaging techniques is a powerful approach to study the causes and mechanisms, and may lead to novel insights about the pathogenesis of neurodegenerative disorders.
The aim of this Research Topic is to generate an across disease view understanding of how brain connectivity may serve as general mechanism to explain patterns of neurodegeneration, and to stimulate new cross disciplinary collaborations in neurodegenerative imaging. We call for original research articles, review papers and perspectives for publication in this Research Topic in Frontiers in Neuroscience.
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