36 In later stages of the disease a clearer pattern of atrophy di

36 In later stages of the disease a clearer pattern of atrophy distinct from AD could be observed, with more pronounced atrophy of click here temporal lobe structures in AD than in LBD.37 The posterior cingulum island sign in the 18FFDG-PET seems to be an exclusive feature of LBD and may help in the distinction from AD if present.38 Clinically, neurological signs of Parkinsonism may be absent in the early stages of the disease. In a community-based longitudinal neuropathological study, as described above, Lewy Inhibitors,research,lifescience,medical bodies were found in 13% of the elderly population,

even without dementia.34 Cognitive decline, including episodic memory decline, was related to cortical Lewy body selleck Z-VAD-FMK pathology independent of coexisting AD pathology in a large neuropathological study.33 Vascular dementia Vascular cognitive impairment, or vascular dementia, due to vascular brain lesions may also lead to an amnestic syndrome resembling AD, and may clinically mimic AD.31 Neuropathologically confirmed vascular lesions have been found to be related to episodic Inhibitors,research,lifescience,medical memory impairment in elderly individuals without dementia.34 In addition to multiple lesions that may be seen in multi-infarct dementia, single strategic lesions, eg, in the hippocampal network or thalamus, Inhibitors,research,lifescience,medical may

lead to specific neuropsychological deficits. Vascular lesions may cause cognitive deficits by themselves or contribute to other neurodegenerative processes. It is under discussion as to whether vascular lesions and white matter hyperintensities may foster AD pathology and accelerate the course of AD.39 Frontotemporal dementia FTD, or frontotemporal lobar degeneration, comprises Inhibitors,research,lifescience,medical a group of degenerative diseases: behavioral variant of FTD (bvFTD), primary progressive aphasia, and semantic dementia. Although behavioral disturbances and personality change are the most prominent features of bvFTD, episodic memory disturbances may also be present that may account for different patterns of impairment of neuronal networks, including the frontal and anterior temporal lobes in FTD Inhibitors,research,lifescience,medical patients.40 The abundance of AD variants2 (eg, frontotemporal

variants) and AD-typical patterns of biomarkers found in one fifth of FTD patients28 makes the differentiation between FTD and AD even more difficult. A recent study showed that hippocampal volume measurement was not a sufficient biomarker to distinguish bvFTD from AD, and found similarly reduced hippocampal volumes in bvFTD and Entinostat AD. Hippocampal volume reduction may be due to hippocampal sclerosis observed in a large proportion of bvFTD patients.12 Hippocampal sclerosis Hippocampal sclerosis is a common neuropathological finding in the elderly, has been shown to be present in one fourth of elderly autopsy cases,41 and is the leading neuropathological diagnosis in nearly 2% of cases previously diagnosed as having AD.31 Hippocampal atrophy is even more pronounced in hippocampal sclerosis than in AD.

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