While many studies have investigated electroencephalographic (EEG) features of dementia, few have analysed
the relationship between EEG and cerebrospinal fluid biomarkers in cognitive impairment. Seizures are frequently
observed at the end stage of Alzheimer disease, and experimental animal studies support the view that epileptiform
activity may contribute to the cognitive decline. In this paper, after reviewing literature findings concerning the role of
EEG in dementia, we show the preliminary results of our study aimed to correlate the presence of epileptiform EEG
patterns with cerebrospinal fluid biomarkers in order to better define the prognosis of dementia. Our study shows a clear
relationship between phospho-tau protein levels and epileptiform EEG pattern. This finding seems to suggest in humans
the observation made in animal models that not only β-amyloid protein, but also tau and phospho-tau proteins, are
involved in the aberrant regulation of neural transmission possibly contributing to EEG deterioration, cognitive decline
and worse prognosis. On the basis of the relationship between phospho-tau protein, cognitive decline and epileptogenicity
we suspect that high liquoral phospho-tau levels and epileptiform EEG pattern may provide an early identification of
patients with dementia and/or represent an aggressive phenotype of dementia. We propose that qualitative EEG analysis
integrated with cerebrospinal biomarkers may be extensively used to better define dementia.
Keywords: Alzheimer’s disease, frailty, electroencephalography, phospho-tau, amyloid β-peptide42.
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