K. Del Tredici

TL;DR: The here hypothesized mechanism offers one possible explanation for the sequential and apparently uninterrupted manner in which vulnerable brain regions, subcortical grays and cortical areas become involved in idiopathic Parkinson's disease.

TL;DR: The data suggest that many patients with 'idiopathic' RBD are actually exhibiting an early clinical manifestation of an evolving neurodegenerative disorder, and may be appropriate for future drug therapies that affect synuclein pathophysiology, in which the development of parkinsonism and/or dementia could be delayed or prevented.

TL;DR: It is concluded that the most parsimonious explanation for the initial events of sporadic Parkinson's disease is pathogenic access to the brain through the stomach and nose – hence the term ‘dual‐hit’.

TL;DR: The decrease in median Mini-Mental State Examination scores between PD stages 3 to 6 indicates that the risk of developing dementia increases with disease progression, and in some individuals, cognitive decline can develop in the presence of mild Parkinson disease–related cortical pathology and, conversely, widespread cortical lesions do not necessarily lead to cognitive decline.

TL;DR: 19 of the 301 cases with PD-related pathology displayed a pathological distribution pattern of Lewy neurites and Lewy bodies that diverged from the staging scheme described above, and most of the divergent cases had advanced concomitant Alzheimer's disease-related neurofibrillary changes.