According to the Braak model, it is this apparent selective vulnerability of specific neuronal types that accounts for the predictable regional spread of Lewy pathology observed in PD.
Interestingly, with regard to α-synuclein (αS) pathology, the alteration in the predictable progressions of pathology has been proposed to be due to concomitant AD pathology (16, 22).
Whether the pattern and progression of pathology can be generalized to the predictable, sequential involvement of vulnerable sites as Braak describes, however, remains controversial.
In Parkinson's disease (PD) and dementia with Lewy bodies (DLB) α-synuclein (αS) pathology is seen that displays a predictable topographic distribution.
Neuropathological studies report that AD pathology spreads through the brain in a relatively predictable fashion [ 3].
Neuropathological studies suggest that Alzheimer's pathology spreads throughout the brain in a relatively predictable fashion and starts well before clinical onset of disease [ 3].
In AD, Tau-pathology is known to progress according to stereotypical and predictable patterns reflected in its incorporation in criteria for the neuropathological diagnosis of AD [ 6, 34].
However, the spatial topography of AD and PD pathology supports the notion that inclusions form and progressively spread in a predictable neuroanatomic sequence.
We propose that pathologies in the FTLD spectrum target distributed brain networks in a predictable manner.
