Are tau and alpha synuclein filamentous inclusions in neurons and glia analogous to accumulation of myosin/actin filaments in myofiber hypertrophy?
Degenerative disruption of neuronal networks would appear to constitute a pathogenetic series of mechanisms that would adequately account for the effects of neurodegeneration in its full complexity clinically and pathologically beyond any consideration of the neuron as the basic unit of involvement. In this sense, neurodegeneration as reflected in terms of neurofibrillary tangles and Lewy bodies might actually be a process of integral tau opathy and synucleinopathy that in probably multiple different ways in the individual patient contributes to a disruption of neuronal interactions as an integral neuronal network. In terms therefore of aggregation of neurofilaments or of synuclein filaments it might be valid to consider simple biophysical phenomena of inclusion body formation in neurons directly analogous to myosin/actin accumulation in myofibers in an overall common system of neuronal and myofiber biology and pathobiology.
Agius
Lawrence M
LM
St. Luke's Hospital, University of Malta, MSIDA, Europe. lawrence.agius@um.edu.mt
D000199:Actins / Q000378:metabolism*; D006801:Humans; D006984:Hypertrophy / Q000378:metabolism*; D008962:Models, Theoretical; D009210:Myofibrils / Q000473:pathology; D009218:Myosins / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D009457:Neuroglia / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D051843:Synucleins; D051844:alpha-Synuclein; D016875:tau Proteins / Q000378:metabolism*
D000199:Actins; D009419:Nerve Tissue Proteins; C497604:SNCA protein, human; D051843:Synucleins; D051844:alpha-Synuclein; D016875:tau Proteins; D009218:Myosins