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Co-existing neuropathological comorbidities have been repeatedly reported to be extremely common in subjects dying with dementia due to Alzheimer disease. As these are likely to be additive to cognitive impairment, and may not be affected by molecularly-specific AD therapeutics, they may cause significant inter-individual response heterogeneity amongst subjects in AD clinical trials. Furthermore, while originally noted for the oldest old, recent reports have now documented high neuropathological comorbidity prevalences in younger old AD subjects, who are more likely to be included in clinical trials.

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Background: Degeneration of the basal forebrain cholinergic system is a hallmark feature shared by Alzheimer's disease (AD) and Lewy body disease (LBD) whereas hippocampus atrophy is more specifically related to AD. We aimed to investigate the relationship between basal forebrain and hippocampus atrophy, cognitive decline, and neuropathology in a large autopsy sample.

Methods: Data were obtained from the National Alzheimer's Coordinating Center (NACC).

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The EIF4G1 gene has been considered an autosomal dominant cause of Parkinson disease (PD), even if its role is still debated. The objective of this study was to describe the phenotype and α-synuclein distribution in peripheral tissues in 2 related PD patients (mother and daughter), who are carriers of the same variant in exon 10 of EIF4G1 (c.1216G>A, p.

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Resting state electroencephalography (EEG) has proved useful in studying electrophysiological changes in neurodegenerative diseases. In many neuropathologies, microstate analysis of the eyes-closed (EC) scalp EEG is a robust and highly reproducible technique for assessing topological changes with high temporal resolution. However, scalp EEG microstate maps tend to underestimate the non-occipital or non-alpha-band networks, which can also be used to detect neuropathological changes.

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Endoplasmic reticulum (ER) is a crucial organelle associated with cellular homeostasis. Accumulation of improperly folded proteins results in ER stress, accompanied by the reaction involving triggering unfolded protein response (UPR). The UPR is mediated through ER membrane-associated sensors, such as protein kinase-like ER kinase (PERK), inositol-requiring transmembrane kinase/endoribonuclease 1α, and activating transcription factor 6 (ATF6).

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