Subjective Cognitive Decline and APOE ɛ4: A Systematic Review

Ali, Jordan I.; Smart, Colette M.; Gawryluk, Jodie R.

doi:10.3233/jad-180248

Cited by 38 publications

(40 citation statements)

References 89 publications

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“…Regarding SCD and APOE ε4, population‐based studies as well as studies with memory‐clinic patients have shown higher rates of cognitive decline and worse cognitive performance in APOE ε4 carriers with SCD compared with noncarriers either with or without SCD [12,27]. A current systematic review incorporating cross‐sectional and two longitudinal studies examined the association of SCD and APOE ε4 [28]. The authors reported an additional risk of APOE ε4 in participants with SCD for objective cognitive impairment, which coincides with the results of our female but not our male participants.…”

Section: Discussionmentioning

confidence: 99%

Subjective cognitive decline, APOE ε4, and incident mild cognitive impairment in men and women

Müller-Gerards

Weimar

Abramowski

et al. 2019

Alz & Dem Diag Ass & Dis Mo

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Introduction Possible joint effects of subjective cognitive decline (SCD) and apolipoprotein E ( APOE ) ε4 genotype on incident mild cognitive impairment (MCI) were examined for men and women separately. Methods Cognitively normal participants with and without SCD were included from the first follow-up examination of the population-based Heinz Nixdorf Recall study. Sex-stratified logistic regression models estimated main effects and interactions (additive, multiplicative) of SCD at the first follow-up (yes+/no−) and APOE ε4 (positive+/negative−) groups for MCI 5 years later. Results Odds for MCI 5 years later were higher in SCD/ APOE ε4 group +/+ than the sum of groups +/− and −/+ in women, with a trend for positive interaction. Odds for incident MCI in men was highest in group +/−, with no interaction effect. Discussion Our findings indicate that APOE ε4 may play an important role in the association of SCD and incident MCI, especially considering sex. Further studies need to examine these associations with larger sample sizes.

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Section: Discussionmentioning

confidence: 99%

Subjective cognitive decline, APOE ε4, and incident mild cognitive impairment in men and women

Müller-Gerards

Weimar

Abramowski

et al. 2019

Alz & Dem Diag Ass & Dis Mo

View full text Add to dashboard Cite

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“…Consequently, we included incongruent, unrelated, nonassociated, mismatched and unpredictable target stimuli in the weak association condition. We also included the sample size as a weight variable in the ANOVAs, as previously done by Ali et al [ 31 ]. In case of a significant interaction, we performed simple effects tests.…”

Section: Methodsmentioning

confidence: 99%

Semantic Processing in Healthy Aging and Alzheimer’s Disease: A Systematic Review of the N400 Differences

et al. 2020

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Semantic deficits are common in individuals with Alzheimer’s disease (AD). These deficits notably impact the ability to understand words. In healthy aging, semantic knowledge increases but semantic processing (i.e., the ability to use this knowledge) may be impaired. This systematic review aimed to investigate semantic processing in healthy aging and AD through behavioral responses and the N400 brain event-related potential. The results of the quantitative and qualitative analyses suggested an overall decrease in accuracy and increase in response times in healthy elderly as compared to young adults, as well as in individuals with AD as compared to age-matched controls. The influence of semantic association, as measured by N400 effect amplitudes, appears smaller in healthy aging and even more so in AD patients. Thus, semantic processing differences may occur in both healthy and pathological aging. The establishment of norms of healthy aging for these outcomes that vary between normal and pathological aging could eventually help early detection of AD.

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“…ApoE4 is associated with greater memory decline rate and cognitive dysfunction in MCI patients [16], as well as with increased risk of progression from MCI to AD [17]. However, the relationship between apoE and SCD remains unclear [18].…”

Section: Introductionmentioning

confidence: 99%

Quantification of total apolipoprotein E and its isoforms in cerebrospinal fluid from patients with neurodegenerative diseases

et al. 2020

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Background: The human APOE gene, which codes for apolipoprotein E (apoE), has three major polymorphic alleles: ε2, ε3, and ε4 that give rise to amino acid substitutions. APOE-ε4 is a strong risk factor of sporadic Alzheimer's disease (AD) but the reason why is still unknown despite intense research for more than 20 years. The aim of the study was to investigate if the concentrations of total apoE and the specific apoE isoforms in cerebrospinal fluid (CSF) differ between various neurodegenerative diseases and control individuals, as well as among the APOE genotypes. Methods: Quantification of total apoE and specific apoE isoforms (E2, E3, and E4) in CSF was performed using highresolution parallel reaction monitoring mass spectrometry. In total, 1820 individuals were involved in the study including clinically diagnosed AD patients (n = 228), cognitively unimpaired (CU) patients (n = 896), and patients with other neurodegenerative disorders (n = 696). Follow-up data was available for 100 individuals, assessed at two time points. Subjects were dichotomized based on an Aβ 42/40 CSF concentration ratio cutoff into Aβ positive (Aβ+, < 0.091) and Aβ negative (Aβ−, > 0.091) groups. Results: Even though there was a significant increase of total apoE in the amyloid β-positive (Aβ+) group compared with amyloid β-negative (Aβ−) individuals (p < 0.001), the magnitude of the effect was very small (AUC = 0.55). Moreover, CSF total apoE concentrations did not differ between Aβ− CU controls and clinically diagnosed AD patients. There was a difference in concentration between isoforms in heterozygous individuals in an isoform-dependent manner (E2 < E3 < E4) (p < 0.001, AUC = 0.64-0.69), and these associations remained when dichotomizing the samples into Aβ+ and Aβ− groups (p < 0.01, AUC = 0.63-0.74). In the cohort with follow-up samples, neither total apoE nor isoform-specific apoE concentrations differed between the two time points (p > 0.05). Conclusions: The results indicate that neither the concentrations of total apoE nor the different apoE isoforms in CSF are associated with APOE-ε4 carrier status, Aβ status, or clinical dementia diagnoses.

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Subjective Cognitive Decline and APOE ɛ4: A Systematic Review

Cited by 38 publications

References 89 publications

Subjective cognitive decline, APOE ε4, and incident mild cognitive impairment in men and women

Subjective cognitive decline, APOE ε4, and incident mild cognitive impairment in men and women

Semantic Processing in Healthy Aging and Alzheimer’s Disease: A Systematic Review of the N400 Differences

Quantification of total apolipoprotein E and its isoforms in cerebrospinal fluid from patients with neurodegenerative diseases

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