Parkinson’s disease (PD) is a common neurodegenerative disorder affecting about 1.5% of people aged 65 or older (de Rijk et al, 1997). PD is defined pathologically as cell loss in the pigmented dopaminergic cells of the pars compacta, of the substantia nigra and synuclein pathology (Lewy neurites and Lewy bodies) in the surviving cells. In addition, cholinergic forebrain nuclei and other brainstem nuclei, including the serotonergic raphe nuclei and the noradrenergic locus ceruleus, are usually affected. From these brainstem changes, the topographical progression subsequently involves the anteromedial temporal mesocortex, including the transentorhinal region, and reaches into adjoining high-order sensory association areas and important limbic structures such as amygdala and hippocampus (Braak et al, 2003; Jellinger, 2003). In addition, amyloid plaques and even neurofibrillary tangles are found in most patients at autopsy ((Mattila et al, 1999; Jellinger et al, 2002). The cardinal clinical features of PD are resting tremor, bradykinesia, rigidity and postural abnormalities (Gelb et al, 1999). However, due to the wide distribution of neurodegeneration, it is not surprising that a wide range of nonmotor symptoms also occur, including neuropsychiatric symptoms and autonomic dysfunction.
CITATION STYLE
Aarsland, D. (2005). Dementia in parkinson’s disease. In Dementia with Lewy Bodies: and Parkinson’s Disease Dementia (pp. 221–240). CRC Press. https://doi.org/10.5005/jp/books/10538_14
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