The neuropathology of PDD is similar to dementia with Lewy bodies (DLB), which is thought to fall within the same spectrum of disease as Lewy body dementia (LBD). As a result, the Movement Disorder Society Task Force established consensus criteria for the diagnosis of PDD and PD with mild cognitive impairment (PD-MCI) to distinguish these entities from other types of cognitive impairment.ĭespite extensive clinicopathological studies conducted over the last few decades, the exact neuropathological substrate contributing to cognitive decline in PD remains unclear. In terms of the memory domain, retrieval memory is more affected in PDD whereas encoding and storage memory decline in AD. Clinically, PDD patients present with more severe attention deficits and impairment in executive function and visuospatial function as compared with Alzheimer’s disease (AD), with relative sparing of language functions. In particular, cognitive impairment is prevalent among PD patients and progression to dementia is common in the later stages of disease. It has been increasingly recognised that non-motor symptoms produce a significant impact on the quality of life of both patients and their carers. The clinical presentation of Parkinson’s disease (PD) displays a high degree of heterogeneity, not limited to the classical quartet of motor signs. ![]() Such specific Lewy pathology targeting the cholinergic system within the CA2 subfield may contribute to the unique memory retrieval deficit seen in patients with Lewy body disorders, as distinct from the memory storage deficit seen in Alzheimer’s disease. In addition, multiple antigen immunofluorescence demonstrated colocalisation between cholinergic fibres and alpha-synuclein but not tau pathology. We found that only cases with dementia have a significantly greater Lewy pathology, whereas cholinergic fibre depletion was evident in cases with mild cognitive impairment and this was significantly correlated with loss of cholinergic neurons in Ch2. In a subset of cases, the degree of CA2 cholinergic depletion was quantified using confocal microscopy and correlated with cholinergic neuronal loss in Ch2. ![]() Hippocampal sections from 67 PD, 34 PD with mild cognitive impairment and 96 PDD cases were immunostained for tau and alpha-synuclein, and the respective pathology burden was assessed semi-quantitatively. ![]() Therefore, in this study, we investigated the burden of pathology in the CA2 subsector of PD cases with varying degrees of cognitive impairment and correlated this with the extent of septohippocampal cholinergic deficit. However, the relationship between Lewy pathology of the CA2 subfield and cholinergic fibres has not been explored. Early non-human primate tracer studies demonstrated connections from the nucleus of the vertical limb of the diagonal band of Broca (nvlDBB, Ch2) to the hippocampus. Although the precise neuropathological substrates of cognitive decline in Parkinson’s disease (PD) remain elusive, it has long been regarded that pathology in the CA2 hippocampal subfield is characteristic of Lewy body dementias, including dementia in PD (PDD).
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