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However, more recent neuropathological studies have challenged this view. These differences in neuropathological changes should lead to an increasing difference in cognitive impairments during the progression of the two diseases. In PD, neurodegeneration starts in the brain stem, extends into the midbrain, affecting the substantia nigra, and subsequently into cortical areas. For instance, according to the Braak stages in AD, the development of neurofibrillary tangles starts in the entorhinal cortex, extends into the hippocampus and then spreads to secondary association cortices. įrom a neuropathological point of view and against the background of disease-specific pathogenetic processes, it can be argued that AD and PD patients should show different patterns of cognitive deficits. Nonetheless, these conclusions are mainly based on an indirect comparison of patients suffering from each of these disorders with healthy control groups, and the number of studies directly comparing these two patient groups is rather small. There is now a fair consensus that AD is characterized by a severe decline in episodic memory, whereas PD is typically associated with executive and visuoconstructive deficits in combination with psychomotor slowing. Several neuropsychological studies have investigated whether the pattern of cognitive deficits in AD can be distinguished from that in PD.

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However, also the majority of PD patients develops dementia in the course of the disease, and a considerable number of patients already shows cognitive deficits in the early stage, which are severe enough to be diagnosed as dementia. AD is characterized by a progressive cognitive decline. Alzheimer's disease (AD) and Parkinson's disease (PD) are the most frequent neurodegenerative disorders.













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