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Cognitive frailty: A pre‐dementia syndrome or a branch of healthy ageing?
Author(s) -
Kocagoncu Ece,
Nesbitt David,
Hughes Laura,
Henson Richard N,
Can Cam,
Rowe James B
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.043129
Subject(s) - novelty , dementia , audiology , psychology , cognition , neuropsychology , cognitive reserve , cognitive decline , hippocampus , magnetoencephalography , neuroscience , disease , cognitive impairment , medicine , electroencephalography , social psychology
Background There is a pressing need for new therapeutic strategies to arrest Alzheimer’s disease (AD) at its prodromal stage. MTL pathology at this stage causes widespread synaptic dysfunction, before any cognitive decline and atrophy. We propose that neurophysiological biomarkers sensitive to this early synaptic dysfunction could be recorded using electro‐magnetoencephalography (E/MEG). Cam‐CAN Frail study, investigates neurophysiological changes that occur in cognitively frail individuals, who show cognitive decline in the absence of a clinical diagnosis. Method We collected E/MEG data from healthy controls, cognitively frail, MCI and early AD patients (N=90). Frail and MCI groups performed similarly on MMSE or ACER. Frail group had lower education levels than the other groups. Participants were presented fractals followed by sounds. The stimuli consisted of standard and deviant pairs. Deviants were pairs with shuffled sounds (associative deviants) or novel sounds (novelty deviants). We extracted the signal from inferior frontal (IFG), superior temporal (STG) and Heschl’s gyri (HG). We tested the relationship between the mismatch response, hippocampal grey matter volumes (GMV), neuropsychological scores and education. Result Novelty response was found in control and frail groups, with larger clusters in bilateral IFG. MCI and AD groups showed weaker novelty effects only in the RHG and RSTG respectively. The associative deviant response was observed only in the bilateral IFG across the groups. Novelty deviant response in LHG negatively correlated with MMSE and ACER. Education level was not significant correlated with mismatch responses. Hippocampal and entorhinal GMVs of the controls and the cognitively frail were significantly higher than the MCI/AD groups. The difference in GMVs between controls and the frail was not significant. Hippocampal, entorhinal GMV and education levels positively correlated with MMSE and ACER scores. Conclusion Cognitively frail do not show the neurophysiological or structural profile, characteristic of AD. Cognitive frailty might be reflecting an extreme of the normal spectrum of cognition, but not AD. The underperformance could instead be explained by lower education levels. Secondly, we showed that E/MEG identifies the loss of response to novelty deviance in MCI and AD; and E/MEG tasks that are automatic, easy and require minimal training can be used to develop biomarkers in AD.