Abstract

Alzheimer’s disease (AD) is the most common form of neurodegenerative dementia accounting for 50–80% of all age-related dementia. This pathology is characterized by the progressive and irreversible alteration of cognitive functions, such as memory, leading inexorably to the loss of autonomy for patients with AD. The pathology is linked with aging and occurs most commonly around 65 years old. Its prevalence (5% over 65 years of age and 20% after 80 years) constitutes an economic and social burden for AD patients and their family. At the present, there is still no cure for AD, actual treatments being moderately effective only in early stages of the pathology. A lot of efforts have been deployed with the aim of defining new AD biomarkers. Successful early detection of mild cognitive impairment (MCI) linked to AD requires the identification of biomarkers capable of distinguishing individuals with early stages of AD from other pathologies impacting cognition such as depression. In this article, we will review recent evidence suggesting that electroencephalographic (EEG) recordings, coupled with behavioral assessments, could be a useful approach and easily implementable for a precocious detection of AD.

Highlights

  • Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that starts with mild shortterm memory deficits before progressively culminating in total loss of cognitive and executive functions

  • Many studies showed an increased production of more amyloidogenic Aβ peptides associated with familial AD (FAD)-linked mutations, providing strong support for the amyloid hypothesis (Hardy and Selkoe, 2002)

  • Given the key role played by oscillatory activities on cognitive processes such as memory, numerous studies have closely looked at brain oscillatory alterations in AD patients, as well as in animal models of the pathology

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Summary

INTRODUCTION

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that starts with mild shortterm memory deficits before progressively culminating in total loss of cognitive and executive functions. Many studies showed an increased production of more amyloidogenic Aβ peptides associated with FAD-linked mutations, providing strong support for the amyloid hypothesis (Hardy and Selkoe, 2002). According to this conceptual framework, it would be the early accumulation of soluble Aβ in specific brain areas that elicits abnormal patterns of neuronal activity leading to cognitive decline (Palop and Mucke, 2010). A second hypothesis highlights the fact that treatments were given too late in the time-course of AD, when neuronal damages are already too extensive and irreversible We propose that characterization of cross-frequency coupling (CFC), a specific motif of oscillatory interactions, might represent an extremely sensitive early biomarker

BRAIN OSCILLATORY ACTIVITY
OSCILLATORY ACTIVITY IN ANIMAL MODELS OF AD
Findings
CONCLUSION
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