Mismatch negativity as a potential neurobiological marker of early-stage Alzheimer disease and vascular dementia

Jiang, Shixiang; Chang, Yan; Qiao, Zhengxue; Yao, Haiqian; Jiang, Shuyun; Qiu, Xiaohui; Yang, Xiuxian; Fang, Deyu; Yang, Yanjie; Zhang, Limei; Wang, Lina; Zhang, Liming

doi:10.1016/j.neulet.2017.03.032

Cited by 25 publications

(23 citation statements)

References 37 publications

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“…Although consciousness-related late components of ERPs have been the main focus of investigations in Alzheimer's patients [22,39,40], several studies have shown a correlation between AD pathology and alterations in early components. Compared to that in normal older control subjects, the amplitude of the MMN has been shown to be attenuated in AD [20,41], MCI [21,24] and pre-symptomatic individuals who have mutations in an AD-related gene [42]. In mild AD, the N1 amplitude also been shown to decrease in response to both standard and deviant auditory stimuli [20].…”

Section: Introductionmentioning

confidence: 99%

“…One of the most commonly used paradigms for measuring neural function is the presentation of sensory input, such as the auditory oddball paradigm. Event-related potentials (ERPs) have been investigated as biomarkers of cognitive decline and disease severity in patients with mild cognitive impairment (MCI) and Alzheimer's disease [20][21][22][23][24]. Auditory ERP traces have several positive and negative peaks after sound onset, representing a well-defined brain response to a sensory process.…”

Section: Introductionmentioning

confidence: 99%

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Destruction of ERP responses to deviance in an auditory oddball paradigm in amyloid infusion mice with memory deficits

et al. 2020

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The amyloid-β (Aβ) oligomer is considered one of the major pathogens responsible for neuronal and synaptic loss in Alzheimer's disease (AD) brains. Although the neurotoxic mechanisms of Aβ have been widely investigated, experimental evidence for the direct linkage between neural signaling and cognitive impairments in association with peptide oligomers is lacking. Here, we conducted an auditory oddball paradigm utilizing an Aβ-infused Alzheimer's disease mouse model and interpreted the results based on Y-maze behavioral tests. We acutely injected Aβ oligomers into the intracerebroventricular brain region of normal mice to induce Aβ-associated cognitive impairments. During the auditory oddball paradigm, electroencephalograms (EEG) were recorded from frontal and parietal cortex of Aβ-infused and control mice. The event-related potentials (ERPs) elicited by auditory stimuli showed no significant difference in Aβ-infused mice compared to control mice. On the other hand, the differential ERP signature elicited by oddball sound stimuli was destructed in the Aβ-infused mice group. We noticed that ERP traces to standard and deviant tones were not significantly different in the Aβ group, while the control group showed differences in the amplitude of ERP components. In particular, the difference in the first negative component (N1) between standard and deviant tone, which indexes the sensory memory system, was significantly reduced in the parietal cortex of Aβ-infused mice. These findings demonstrate the direct influence of Aβ oligomers on the functional integrity of cortical areas in vivo. Furthermore, the N1 amplitude difference may provide a potential marker of sensory memory deficits in a mouse model of AD and yield additional targets for drug assessment in AD.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Destruction of ERP responses to deviance in an auditory oddball paradigm in amyloid infusion mice with memory deficits

et al. 2020

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“…Alzheimer’s disease patients show impairments in both sensory and associative memory. They show reduced medial temporal lobe activity to novel scenes parallel to poor performance on explicit memory tests (Düzel et al, 2018; Golby et al, 2005; Rombouts et al, 2000), reduced electrophysiological response to infrequent ‘oddballs’ as measured by the P300 (Daffner et al, 2001; Hedges et al, 2016; Lee et al, 2013) and by mismatch negativity (Engeland et al, 2002; Gaeta et al, 1999; Jiang et al, 2017; Laptinskaya et al, 2018; Mowszowski et al, 2012; Pekkonen et al, 2001; Ruzzoli et al, 2016). Further, they show impairments in multimodal binding, encoding and retrieval of associative memory (Della Sala et al, 2012; Gallo et al, 2004; Parra et al, 2009; Parra et al, 2010; Troyer et al, 2008), reduced hippocampal and entorhinal activity during encoding of novel pairings of stimuli (Dickerson et al, 2005; Sperling, R.A. et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…The novelty deviant is akin to the classic mismatch negativity response, an index of auditory predictive coding. The classic mismatch negativity is not hippocampal dependent, but is abnormal Alzheimer's disease (Jiang et al, 2017;Laptinskaya et al, 2018;Pekkonen et al, 2001;Ruzzoli et al, 2016). Although neurophysiological responses in the hippocampus are difficult to detect with E/MEG, owing to its depth and orientation, a strong mismatch response can be recorded from auditory cortex where sensory predictions are established from cross-model associative learning.…”

Section: Introductionmentioning

confidence: 99%

Neurophysiological and brain structural markers of cognitive frailty differs from Alzheimer’s disease

Kocagöncü

Nesbitt

Emery

et al. 2021

Preprint

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With increasing life span, there is growing importance of understanding the mechanisms of successful cognitive ageing. In contrast, cognitive frailty has been proposed to be a precursor to Alzheimer’s disease. Here we test the hypothesis that cognitively frail adults represent a branch of healthy ageing, distinct from latent dementia. We used electro-magnetoencephalography and magnetic resonance imaging to investigate the structural and neurophysiological features of cognitive frailty in relation to healthy aging, and clinical presentations of mild cognitive impairment and Alzheimer’s disease. Cognitive performance of the cognitively frail group was similar to those with mild cognitive impairment. We used a novel cross-modal oddball task to induce mismatch responses to unexpected stimuli. Both controls and cognitively frail showed stronger mismatch responses and larger temporal grey matter volume, compared to people with mild cognitive impairment and Alzheimer’s disease. Our results suggest that cognitively frail represents a spectrum of normal ageing rather than incipient or undiagnosed Alzheimer’s disease. Lower cognitive reserve, hearing impairment and medical comorbidity might contribute to the aetiology of cognitive impairment.

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“… 16 , 17 , 18 , 19 The generation of the MMN/MMNm has been interpreted as a pre‐attentive cognitive process indexing functional integrity of sensory memory and accuracy in detecting changes. 20 , 21 , 22 Although the existing literature has shown the deficits of MMN/MMNm in patients with AD, 23 , 24 , 25 , 26 the results in aMCI are substantially inconsistent. There are only five studies so far investigating the auditory MMN in patients with aMCI/MCI.…”

Section: Introductionmentioning

confidence: 99%

Altered mismatch response of inferior parietal lobule in amnestic mild cognitive impairment: A magnetoencephalographic study

Chen

Hsu

et al. 2021

CNS Neurosci Ther

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Mismatch negativity as a potential neurobiological marker of early-stage Alzheimer disease and vascular dementia

Cited by 25 publications

References 37 publications

Destruction of ERP responses to deviance in an auditory oddball paradigm in amyloid infusion mice with memory deficits

Destruction of ERP responses to deviance in an auditory oddball paradigm in amyloid infusion mice with memory deficits

Neurophysiological and brain structural markers of cognitive frailty differs from Alzheimer’s disease

Altered mismatch response of inferior parietal lobule in amnestic mild cognitive impairment: A magnetoencephalographic study

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