By Lauretta Ihonor
Amyloid beta (Aβ) protein accumulation without neocortical tau deposition is a common pathologic feature of Parkinson's disease (PD) with dementia, according to study findings.
By contrast, neocortical tau accumulation is a known defining feature of Alzheimer's disease (AD), say the authors.
This, say Paul Kotzbauer (Washington University School of Medicine, St Louis, Missouri, USA) and team, suggests that the pathologic processes that occur in PD with dementia are distinct from those seen in AD.
They add: "Definition of subgroups based on individual pathologic protein deposits, as done in this study, may provide a less ambiguous classification scheme than the application of terms such as AD-like pathology."
In the study, 32 deceased individuals with a confirmed diagnosis of PD and dementia underwent autopsy. Each autopsy involved the assessment of the presence of the proteins α-synuclein, Aβ, and tau via immunohistochemical analysis.
The findings, reported in the Archives of Neurology, revealed three different protein-related pathologic subtypes of PD with dementia. The commonest subtype was predominant synucleinopathy with Aβ accumulation and minimal/no cortical tau deposition (n=19), followed by predominant synucleinopathy alone (n=12).
Only one patient had a third subtype that featured synucleinopathy with Aβ deposition plus moderate neocortical tauopathy.
Patient length of survival after PD diagnosis and also after onset of dementia was found to be significantly shorter among patients with synucleinopathy and Aβ deposits versus those with synucleinopathy only.
Indeed, the hazard ratios for survival after PD diagnosis and survival after dementia onset in patients with synucleinopathy plus Aβ deposition were 0.51 and 0.52, respectively, compared with synucleinopathy-only patients.
This finding persisted even after adjustment for the timing of dementia onset relative to the onset of PD motor symptoms.
Kotzbauer et al say that larger, prospective studies "are needed to clarify the association between Aβ accumulation and clinical features of PD."
They conclude: "Further support for the role of Aβ accumulation in promoting disease progression for PD would provide rationale for testing the therapeutic effects of one or more evolving approaches for reducing Aβ accumulation that, so far, have focused on AD."
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