Alpha-Synuclein Pathology in Human Diseases

Dear Colleagues,

Alpha-synuclein insoluble protein aggregates are among the key neuropathological characteristics of several neurodegenerative disorders. In particular, the protein is known as the main component of Lewy bodies (LB), intra-neuronal/parenchymal inclusions found in the post-mortem brains of patients affected by Parkinson’s disease (PD), LB dementia (DLB), or the LB variant of Alzheimer’s disease (LBVAD) as well as of glial cytoplasmic inclusions (GCI), which are instead oligodendrocyte inclusions typical of multiple system atrophy (MSA). Neurodegeneration with brain iron accumulation (NBIA) and pure autonomic failure (PAF) are other less diffuse disorders characterized by central and peripheral alpha-synuclein pathological deposits, respectively.

The gradual spreading and diffusion of alpha-synuclein pathological aggregates in and between the central and peripheral nervous system is believed to underlie the progression of disease symptoms in several of the above-cited disorders. In addition, in PD, the selective vulnerability of diverse neuronal populations to pathological alpha-synuclein accumulation could account for the differential severity of motor/non-motor symptoms. This notwithstanding, whether alpha-synuclein fibrils or oligomers are the most toxic pathological species is still matter of debate. Likewise, we still ignore the mechanisms through which the deposition of alpha-synuclein aggregates impact on central or peripheral neurons, glia, or other cellular populations such as immune cells.

This Special Issue aims at providing an up-to-date in depth overview on the impact of alpha-synuclein pathology deposition and spreading on neurodegenerative disorders.

Prof. Dr. Arianna Bellucci
Guest Editor
Dr. Francesca Longhena
Assistant Guest Editor

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• alpha-synuclein pathology
• alpha-synuclein spreading
• Lewy bodies
• glial cytoplasmic inclusions
• Parkinson’s disease
• Alzheimer’s disease Lewy body variant
• dementia with Lewy bodies
• multiple system atrophy
• pure autonomic failure
• neurodegeneration with brain iron accumulation