2018
DOI: 10.2174/1567205015666180427122746
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Semantic Intrusions and Failure to Recover From Semantic Interference in Mild Cognitive Impairment: Relationship to Amyloid and Cortical Thickness

Abstract: Background: Accumulating evidence indicates that the failure to recover from the effects of proactive semantic interference [frPSI] represents an early cognitive manifestation of preclinical Alzheimer’s disease. A limitation of this novel paradigm has been a singular focus on the number of targets correctly recalled, without examining co-occurring semantic intrusions [SI] that may highlight specific breakdowns in memory. Objectives: We focused on SI and their relationship to amyloid load and regional cortica… Show more

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Cited by 16 publications
(8 citation statements)
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“…There is increasing evidence that semantic intrusion errors are likely the result of incomplete or faulty storage and consolidation of initial to‐be‐remembered information. When a semantically related list of competing information is presented, deficits in inhibitory systems and elective impairments in source memory occur 17,52–54 . We are aware that correlation does not necessarily imply causation and that the current results should not be taken to imply that amyloid in and of itself is responsible for increased PSI and frPSI errors.…”
Section: Discussionmentioning
confidence: 70%
See 1 more Smart Citation
“…There is increasing evidence that semantic intrusion errors are likely the result of incomplete or faulty storage and consolidation of initial to‐be‐remembered information. When a semantically related list of competing information is presented, deficits in inhibitory systems and elective impairments in source memory occur 17,52–54 . We are aware that correlation does not necessarily imply causation and that the current results should not be taken to imply that amyloid in and of itself is responsible for increased PSI and frPSI errors.…”
Section: Discussionmentioning
confidence: 70%
“…When a semantically related list of competing information is presented, deficits in inhibitory systems and elective impairments in source memory occur. 17,[52][53][54] We are aware that correlation does not necessarily imply causation and that the current results should not be taken to imply that amyloid in and of itself is responsible for increased PSI and frPSI errors. In fact, even in early AD, synaptic dysconnectivity, 32 tau deposition, 17 and other brain-related processes may underlie PSI and frPSI errors.…”
mentioning
confidence: 75%
“…Thus, mean uptake in counts for each of the FreeSurfer defined regions were calculated and global standard uptake value ratio (SUVR) was calculated by averaging cortical uptake in the frontal, parietal, lateral temporal, occipital, and anterior and posterior cingulate regions, normalized to mean gray matter counts in the cerebellum. SUVR values were normalized to the mean cerebellar gray matter, which has minimal amyloid load in AD (Curiel et al, 2018). The typical mean SUVR cut-off for amyloid positivity is 1.42 (Bullich et al, 2017).…”
Section: Methodsmentioning
confidence: 99%
“…It should be noted that the brain regions involved in the significant abnormal connectivity pathways (with over 50 selected frequency times) are located mainly within the default mode network (DMN), including Temporal_Pole_Sup_R, Temporal_Pole_Sup_L, Temporal_Pole_ Mid_R, ParaHippocampal_L, Cingulum_Post_L, Angular_L, Supp_Motor_Area_L, Frontal_ Med_Orb_R, Frontal_Sup_R, Cingulum_Ant_R. These brain regions, listed in Table 4 and displayed in Figure 6C , are reported as highly associated with AD pathology (Rose et al, 2006 ; Matsuda, 2013 ; Salvatore et al, 2015 ; Scheff et al, 2015 ; Xu et al, 2016 ; Loewenstein et al, 2018 ).…”
Section: Resultsmentioning
confidence: 99%