Abstract

Progressive declines in memory function accompany normal aging, mild cognitive impairment (MCI), and Alzheimer's disease (AD). Neuropathological studies suggest that damage to neurons providing connections between cortical areas may contribute to memory impairments in AD. Because AD develops slowly, similar neuropathological changes, to a lesser degree, may be present in MCI and some asymptomatic elderly subjects. In this study we tested the hypothesis that corticocortical interactions between sensory regions are impaired in aging, MCI, and AD, as compared with young subjects. When sensory cortical evoked potentials are elicited by pairs of stimuli the amplitudes of potentials to the second stimulus are attenuated. Corticocortical interactions were assessed by presenting stimulus pairs in different modalities (auditory/visual). There were significant group differences in the degree that a visual stimulus attenuated subsequent auditory potentials (young > healthy elderly > MCI > AD). Control experiments indicated equivalent amplitude reductions for all groups to the second stimulus for stimulus pairs having the same modality. These findings are compatible with progressive declines in corticocortical processing in aging, MCI, and AD.

Highlights

  • The ability to retain information for short timeperiods in working memory, or longer timeperiods using episodic memory, involves numerous cortical regions [7,25]

  • In all groups there was a significant reduction in the amplitudes of the P50, negative peak at ϳ100 ms (N100), and peak at ϳ200 ms (P200) components for the second tone relative to the first tone

  • There was a significant effect for vP200 amplitude across stimulus position (Flash 1st Ͼ Flash 2nd) in young vs. elderly, elderly vs. Mild cognitive impairment (MCI), and MCI vs. Alzheimer’s disease (AD)(Fig. 2D)

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Summary

Introduction

The ability to retain information for short timeperiods in working memory, or longer timeperiods using episodic memory, involves numerous cortical regions [7,25]. In addition to memory impairments, AD is characterized by deficits in other cognitive domains including language, attention, and reasoning. Mild cognitive impairment (MCI) is a clinical diagnosis that characterizes elderly individuals with an isolated memory impairment that is more severe than in healthy aging, while other cognitive functions are normal [26,31,33]. Ations in healthy aging, greater memory impairment in MCI, and severe memory and other cognitive deficiencies in AD. The cognitive deficits in AD may be related to a possible disconnection between cortical areas due to pathology affecting neurons that provide long corticocortical connections [13,17,19,22,23]. MCI is considered a risk factor for the development of AD [26], which suggests that less extensive cortical disconnection, relative to AD, may contribute to the memory dysfunction in MCI

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