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Dementia with Lewy bodies (DLB) is characterized clinically by fluctuating cognitive impairment, visual hallucinations, and parkinsonism.1 It is the second most common neurodegenerative disease that causes dementia after AD. The pathologic hallmark of the disease is the presence of Lewy bodies in the cerebral cortex as well as in the brainstem.1 In most cases, numerous senile plaques are also observed in the cerebral cortex, similar to those in the AD brain; neocortical neurofibrillary tangles (NFTs) are rare or absent.2,3 In AD, levels of CSF amyloid β42 (Aβ42) are decreased and levels of CSF tau are increased.4 CSF Aβ42 and tau are thought to be linked with plaques and tangles in the AD brain. Thus, we hypothesized that levels of CSF Aβ42 would be decreased and levels of CSF tau would be normal in DLB. To test this hypothesis we measured levels of CSF Aβ42 …
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Kanemaru et al. (2000) studied this question.
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