Abstract
Current biomarkers used in research and in clinical practice in Alzheimer's Disease (AD) are the analysis of cerebral spinal fluid (CSF) to detect levels of Aβ42 and phosphorylated-tau, amyloid and FDG-PET, and MRI volumetry. Some of these procedures are still invasive for patients or expensive. Electroencephalography (EEG) and Magnetoencephalography (MEG) are two non-invasive techniques able to detect the early synaptic dysfunction and track the course of the disease. However, in spite of its added value they are not part of the standard of care in clinical practice in dementia. In this paper we review what these neurophysiological techniques can add to the early diagnosis of AD, whether results in both modalities are related to each other or not, as well as the need of its validation against current biomarkers. We discuss their potential implications for the better understanding of the pathophysiological mechanisms of the disease as well as the need of performing simultaneous M/EEG recordings to better understand discrepancies between these two techniques. Finally, more studies are needed studying M/EEG with amyloid and Tau biomarkers.
Highlights
Alzheimer’s disease (AD) is the major cause of dementia in the elderly (Qiu et al, 2009)
Current biomarkers used in research and in clinical practice are the analysis of cerebral spinal fluid (CSF) to detect levels of Aβ42 and phosphorylated-tau, amyloid and FDGPET, and MRI volumetry
The results summarized in the column “Result” are described referring to the first group in the corresponding column “comparison.” Subjective Cognitive Decline (SCD), subjective memorry complain; CN, cognitive normal; Mild Cognitive Impairment (MCI), mild cognitive impairment; Aβ, Amyloid beta; XX0,1,2ε4, XX participants with 0, 1, or 2 allele/s of Apoε4; FC, functional connectivity
Summary
Alzheimer’s disease (AD) is the major cause of dementia in the elderly (Qiu et al, 2009). Tau deposition disrupts the axonal microtubule architecture (Taniguchi et al, 2001) and its deposits correlates with cognitive impairment (Nelson et al, 2012; Vos et al, 2013; Albert et al, 2018) and network dysfunction (Schultz et al, 2017) This progressive loss of synapse efficiency and quantity, disrupts inter- and intra-regional communication, leading to the proposal that AD is a disconnection syndrome (Hardy and Selkoe, 2002; Delbeuck et al, 2003). If synaptic dysfunction and network impairment start decades before the main cognitive symptoms appear (Jansen et al, 2015), they could be detected early in time by M/EEG Their non-invasive nature allows the performance of as many recordings as needed.
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