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Cited by 4Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsMedicinal Plants and Neuroprotection

The DOI matches its Crossref record; 97 of the 97 references it cites were found in a registry or an index; 2 of the 51 sources its claims cite were checked for support.

Association of APOC1 with cortical atrophy during conversion to Alzheimer’s disease

Open access
Oh, Sewook, Kim, Sunghun, Kim, Jun Pyo, Seo, Sang Won, Park, Bo-yong, Park, Hyunjin·2025·GeroScience
DOI 10.1007/s11357-025-01695-6PMC PMC12638608
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Abstract

Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder, with its progression influenced by aberrant gene expression and alterations in the brain network topology. Although APOE has been extensively studied in relation to AD, the role of APOC1 remains relatively underexplored. This study investigated the impact of APOC1 on changes in cortical thickness (CTh) during conversion to AD in a longitudinal setting. Using a normative modeling approach, we examined changes in CTh in patients with mild cognitive impairment (MCI). The spatial patterns of CTh changes were then correlated with APOC1 mRNA expression levels. We estimated the time to conversion to AD and compared progression rates between the low and high APOC1 expression groups. Finally, mediation analysis was performed to assess the indirect effects of APOC1 expression on memory function via CTh changes. In patients with MCI and AD, reduced CTh was observed in the limbic and default mode regions, with a notable impact on the entorhinal cortex, parahippocampus, and fusiform gyrus when comparing baseline and follow-up measurements. The degree of change in CTh was significantly associated with APOC1 expression, with the paralimbic regions identified as particularly vulnerable. Furthermore, the high APOC1 expression group demonstrated more rapid conversion to AD than that observed in the low expression group. Mediation analysis indicated a trend suggesting that APOC1 expression indirectly affected memory and cognitive function through its influence on CTh. These results highlight the potential of APOC1 as an additional focus of AD research, offering insights into the genetic influences on AD pathology.

Overview

AI snapshot

Written from the paper’s full text.

TL;DR

In ADNI participants with MCI, cortical thinning during conversion to AD was spatially associated with APOC1 mRNA expression, and high APOC1 expression was linked to faster conversion. Mediation analyses suggested a marginal indirect effect of APOC1 on memory/cognitive decline via cortical thickness.

Key findings

  • Among 170 individuals with MCI at risk of conversion, 111 (65.3%) converted; CTh declined significantly in limbic/default mode regions, especially entorhinal cortex, parahippocampus, and fusiform gyrus, with 194 significant vertices (pFWE < 0.05, cluster p = 0.001).
  • APOC1 expression correlated with the CTh change map (r = −0.31, pspin = 0.004), stronger than APOE mRNA expression (r = −0.20, pspin = 0.046).
  • High APOC1 expression was associated with faster conversion (log-rank p = 0.044; HR = 1.77), especially in APOE ε4-positive individuals (p = 0.02; APOE ε4-negative p = 0.714); several APOC1 SNPs were significant (pFDR < 0.05; mean HR = 1.97 ± 0.64), with only rs12691088 independent of APOE ε4 (r² = 0.024).
  • Mediation analysis showed a marginal indirect effect (p < 0.1) of baseline CTh percentile scores on annual ADNI-MEM change; left hippocampal volume showed similar non-significant trends (ADNI-MEM p = 0.127; CDRSB p = 0.114), while right hippocampal effects were not significant.

Methods

  • Longitudinal ADNI study of 170 individuals with MCI at risk of AD conversion, plus 636 cognitively normal reference participants; APOC1 blood expression data were available for 95 of the 170, and mean follow-up was 2.62 ± 1.44 years.
  • T1-weighted MRI was processed with FreeSurfer to estimate cortical thickness; GAMLSS normative modeling in CN participants generated vertex-wise centile scores, followed by surface-based linear mixed-effects models, Cox proportional hazards models, and spatial correlation with Allen Human Brain Atlas APOC1 expression.
  • Additional analyses included gene ontology/cell-type enrichment, Kaplan–Meier survival and SNP/LD analyses, and mediation models using bootstrapping with 5000 iterations, controlling for APOE expression and APOE ε4 status.

Limitations

  • Stated by the paper: relatively small sample size; only baseline gene expression measurements; only CTh and hippocampal volume as atrophy measures; inability to control for systemic metabolic factors such as cholesterol; GO analysis cannot directly attribute mechanisms to APOC1; no direct sex-difference investigation; peripheral blood only, without CSF markers; and no machine-learning prediction analysis.
  • Evident from the text: mediation effects were marginal (p < 0.1) and hippocampal mediation was not statistically significant, so causal mediation and clinical utility claims remain preliminary; APOC1 expression was available for only 95 of 170 MCI participants, limiting power for expression-based analyses.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1007/s11357-025-01695-6

Cites

97 of 97 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Verification

Claims the paper makes

2 of 51 cited sources checked · 1 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    APOC1 may exert independent effects on AD pathogenesis.

    “emerging evidence suggests that APOC1 may exert independent effects on AD pathogenesis [12].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [12] Zhou X, et al. Non-coding variability at the APOE locus contributes to the Alzheimer’s risk. Nature communications. 2019;10(1):3310. source
  • Findingown data

    In patients with MCI and AD, reduced cortical thickness was observed in the limbic and default mode regions, with notable impact on the entorhinal cortex, parahippocampus, and fusiform gyrus when comparing baseline and follow-up measurements.

    “In patients with MCI and AD, reduced CTh was observed in the limbic and default mode regions, with a notable impact on the entorhinal cortex, parahippocampus, and fusiform gyrus when comparing baseline and follow-up measurements.”
    • Also stated in: § Change in CTh during AD conversion · plain
      “The medial and lateral temporal regions, notably the entorhinal cortex, parahippocampus, and fusiform gyrus, exhibited significant reductions in CTh.”
    Quote in the paperSubstantial claim
  • Findingown data

    The 100 genes that exhibited the highest correlation with cortical thickness changes exhibited pathways involving synaptic signaling under chemical synaptic transmission as the predominant processes (pFDR < 0.05).

    “The 100 genes that exhibited the highest correlation with CTh changes exhibited pathways involving synaptic signaling under chemical synaptic transmission, emerging as the predominant processes (pFDR < 0.05; Fig. 3A), consistent with the findings of a previous study [72].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [72] Cai S, et al. Cortical thickness differences are associated with chemical synaptic transmission upregulated genes in degeneration of mild cognitive impairment. Frontiers in aging neuroscience. 2021;13: 745381. source
    • Rests on an assumption: The AHBA post-mortem gene expression data from six donors without psychiatric or neuropathological disorders are representative of cortical APOC1 expression in the study population.
  • Findingown data

    When APOE ε4 status was considered, individuals with high APOC1 expression showed a significantly faster conversion trajectory compared to low APOC1 expression individuals for positive APOE ε4 status only (p = 0.02).

    “When APOE ε4 status was additionally considered, individuals with high APOC1 expression showed a significantly faster conversion trajectory compared to low APOC1 expression individuals for positive APOE ε4 status only (p = 0.02; Fig. S3).”
    Quote in the paperSubstantial claim
    • Rests on an assumption: APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognitive decline.
  • Findingown data

    Mediation analysis indicated a trend suggesting that APOC1 expression indirectly affected memory and cognitive function through its influence on cortical thickness.

    “Mediation analysis indicated a trend suggesting that APOC1 expression indirectly affected memory and cognitive function through its influence on CTh.”
    • Also stated in: § Cortical atrophy mediates the effects of APOC1 on cognitive impairment · hedged
      “We identified a marginal indirect effect (p < 0.1) of baseline CTh percentile scores on annual changes in ADNI-MEM (Fig. 4C).”
    Quote in the paperSubstantial claim
    • Rests on an assumption: APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognitive decline.
    • Rests on an assumption: The mediation model’s assumed causal ordering (baseline APOC1 expression → cortical thickness change → cognitive decline) is correct.
  • Probably not a substantial claim. 36
  • It may state two separate claims as one. 35

  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Premisecitation

    AD patients carrying the APOC1 risk allele have been reported to experience faster cognitive decline and an earlier conversion from MCI to AD when they also carry the APOE ε4.

    “AD patients carrying the APOC1 risk allele have been reported to experience faster cognitive decline and an earlier conversion from MCI to AD when they also carry the APOE ε4 [95].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [95] Zhou Q, et al. APOE and APOC1 gene polymorphisms are associated with cognitive impairment progression in Chinese patients with late-onset Alzheimer’s disease. Neural regeneration research. 2014;9(6):653–60. source

      The Discussion (Synergistic effect; page unavailable) suggests that APOC1 H2 may act with APOE ε4 in cognitive impairment progression among patients already diagnosed with late-onset AD. The study did not follow patients from MCI to AD, so it does not support earlier conversion for carriers of both variants. The Results (Cognitive impairment progress after 30 months; page unavailable) found a significant progression difference for APOE ε4, but not for APOC1 H2 alone. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • It may state two separate claims as one.

    Findingown data

    Individuals with cognitive impairment exhibited greater overall atrophy than normative trajectories, with the extent of atrophy aggravating at follow-up.

    “We identified that individuals with cognitive impairment exhibited greater overall atrophy (extensive blue regions) than normative trajectories, with the extent of atrophy aggravating at follow-up (Fig. 1B).”
    Quote in the paperSubstantial claim

  • It may state two separate claims as one.

    Findingown data

    The most pronounced atrophy in the cortical thickness change map was observed in the limbic region, followed by the default mode and attention networks.

    “we observed the most pronounced atrophy in the limbic region, followed by the default mode and attention networks (Fig. 1D).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Findingown data

    Decoding the cognitive correlates of the cortical thickness change map corroborates a strong association with terms like AD, MCI, morphometry, and memory.

    “Decoding the cognitive correlates of the CTh change map further corroborates the strong association with terms like “AD,” “MCI,” “morphometry,” and “memory,” confirming the relevance of these CTh change patterns to AD conversion (Fig. 1E).”
    Quote in the paperNot a substantial claim

  • It may state two separate claims as one.

    Findingown data

    The degree of change in cortical thickness was significantly associated with APOC1 expression, with the paralimbic regions identified as particularly vulnerable.

    “The degree of change in CTh was significantly associated with APOC1 expression, with the paralimbic regions identified as particularly vulnerable.”
    • Also stated in: § APOC1 expressions are spatially associated with CTh thinning · plain
      “We associated the spatial patterns between the CTh change map and APOC1 expression within the cortex (Fig. 2A–B) and observed a significant correlation (r = −0.31, pspin = 0.004) with regions of high APOC1 expression displaying thin CTh (Fig. 2C).”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The AHBA post-mortem gene expression data from six donors without psychiatric or neuropathological disorders are representative of cortical APOC1 expression in the study population.

  • It may state two separate claims as one.

    Findingown data

    APOC1 expression in peripheral blood and specific SNPs within the APOC1 locus significantly predicted conversion risk.

    “Additionally, APOC1 expression in the peripheral blood and specific SNPs within the APOC1 locus significantly predicted conversion risk”
    Quote in the paperSubstantial claim
    • Rests on an assumption: APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognition.
    • Rests on an assumption: The APOC1 SNPs identified are functional or affect APOC1 expression.

  • It may state two separate claims as one.

    Findingown data

    Although no statistically significant mediation effects were detected, hippocampal volume marginally mediated the relationship between APOC1 expression and cognitive outcomes (ADNI-MEM, CDRSB), whereas no such effect was observed for APOE.

    “Although no statistically significant mediation effects were detected, HV marginally mediated the relationship between APOC1 expression and cognitive outcomes (ADNI-MEM, CDRSB), whereas no such effect was observed for APOE.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognition.
    • Rests on an assumption: The mediation analyses assume no unmeasured confounding between APOC1 expression, cortical atrophy, and cognitive outcomes.

  • It may state two separate claims as one.

    Findingown data

    Our study confirmed a significant role of APOC1 expression in accelerating cortical thickness changes during the conversion from MCI to AD, which was further related to memory loss and cognitive decline.

    “Our study confirmed a significant role of APOC1 expression in accelerating CTh changes during the conversion from MCI to AD, which was further related to memory loss and cognitive decline.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognition.
    • Rests on an assumption: The mediation analyses assume no unmeasured confounding between APOC1 expression, cortical atrophy, and cognitive outcomes.

  • It may state two separate claims as one.

    Findingown data

    Our findings indicated that APOC1 mRNA expression shows a stronger association with brain atrophy and plays a more prominent mediating role in memory decline compared to APOE.

    “Our findings indicated that APOC1 mRNA expression shows a stronger association with brain atrophy and plays a more prominent mediating role in memory decline compared to APOE.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognition.
    • Rests on an assumption: The mediation analyses assume no unmeasured confounding between APOC1 expression, cortical atrophy, and cognitive outcomes.

  • It may state two separate claims as one.

    Findingown data

    Gene enrichment in molecular function and cellular component categories highlighted the importance of synaptic transmission, with cell-type-specific analyses indicating that these gene sets are predominantly expressed in cortical and striatal spiny neurons.

    “Additionally, gene enrichment in the molecular function and cellular component categories further highlighted the importance of synaptic transmission, with cell-type-specific analyses indicating that these gene sets are predominantly expressed in cortical and striatal spiny neurons.”
    Quote in the paperNot a substantial claim

  • It may state two separate claims as one.

    Findingown data

    Both left and right hippocampal volume showed a decreasing trajectory with age in cognitively normal participants.

    “Both left and right HV showed a decreasing trajectory with age (Fig. S6).”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: The sample of 636 cognitively normal participants is representative of normal aging for normative modeling.

  • It may state two separate claims as one.

    Findingown data

    The spatial correlation between the cortical thickness change map and APOE mRNA expression from AHBA was significant but weaker than that of APOC1 (APOE: r = −0.20, pspin = 0.046; APOC1: r = −0.31, pspin = 0.004).

    “We discovered that the spatial correlation between the CTh change map and APOE mRNA expression from AHBA was significant, but weaker than that of APOC1 (APOE: r = −0.20, pspin = 0.046, APOC1: r = −0.31, pspin = 0.004; Fig. S8).”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Spatial correlation between post-mortem AHBA gene expression and in vivo cortical thickness change maps reflects regionally specific gene expression effects relevant to AD progression.

  • It may state two separate claims as one.

    Findingown data

    Baseline cortical thickness percentile scoring within the CPH model confirmed that atrophy patterns are significant predictors of conversion risk and serve as sensitive biomarkers for assessing individuals at elevated risk of conversion to AD.

    “The clinical relevance of these atrophy patterns, evaluated using baseline CTh percentile scoring within the CPH model, confirmed that these patterns are significant predictors of conversion risk and serve as sensitive biomarkers for assessing individuals at an elevated risk of conversion to AD.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The GAMLSS normative model derived from healthy aging individuals is appropriate for identifying deviations in cortical atrophy in those at risk of conversion to AD.

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    APOE ε4 is a well-established factor central to AD progression and risk prediction.

    “Among the genetic factors, APOE ε4 is a well-established factor central to AD progression and risk prediction [2, 3].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [2] Serrano-Pozo A, Das S, Hyman BT. APOE and Alzheimer’s disease: advances in genetics, pathophysiology, and therapeutic approaches. The Lancet Neurology. 2021;20(1):68–80. source
    • cites [3] Kim J, Basak JM, Holtzman DM. The role of apolipoprotein E in Alzheimer’s disease. Neuron. 2009;63(3):287–303. source

  • It may state two separate claims as one.

    Interpretationown data

    APOC1 may further accelerate disease progression in the presence of APOE ε4, suggesting a possible interaction between APOC1 and APOE ε4 on AD conversion.

    “The findings indicate that APOC1 may further accelerate disease progression in the presence of APOE ε4, suggesting a possible interaction between APOC1 and APOE ε4 on AD conversion.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognitive decline.

  • It may state two separate claims as one.

    Premisecitation

    APOC1 insertion allele (H2) is significantly associated with an increased risk of late-onset AD, especially when interacting with APOE ε4.

    “Furthermore, APOC1 insertion allele (H2) is significantly associated with an increased risk of late-onset AD, especially when interacting with APOE ε4, indicating that APOC1 could be considered as a target for AD pathology [15].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [15] Ki C-S, et al. Genetic association of an apolipoprotein CI (APOC1) gene polymorphism with late-onset Alzheimer’s disease. Neuroscience letters. 2002;319(2):75–8. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    APOC1 SNPs perform similar functions as APOE, including roles in signal transduction, plasma lipoprotein regulation, and the transport of small molecules.

    “APOC1 SNPs perform similar functions as APOE, including roles in signal transduction, plasma lipoprotein regulation, and the transport of small molecules [35].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [35] Chelala C, Khan A, Lemoine NR. SNPnexus: a web database for functional annotation of newly discovered and public domain single nucleotide polymorphisms. Bioinformatics. 2009;25(5):655–61. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    Patients with AD exhibit markedly accelerated hippocampal volume loss compared to age-matched older adults.

    “Patients with AD exhibit markedly accelerated HV loss compared to age-matched older adults [89, 90]”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [89] Fraser MA, Shaw ME, Cherbuin N. A systematic review and meta-analysis of longitudinal hippocampal atrophy in healthy human ageing. Neuroimage. 2015;112:364–74. source
    • cites [90] Nobis L, et al. Hippocampal volume across age: nomograms derived from over 19,700 people in UK Biobank. NeuroImage Clin. 2019;23:101904. source

  • Probably not a substantial claim. It may state two separate claims as one.

    Premisecitation

    Cortical thickness is key to assessing brain atrophy in AD, with age-related decreases closely linked to cognitive and memory impairments as well as AD conversion.

    “Specifically, cortical thickness (CTh) is key to assessing brain atrophy in AD, with age-related decreases closely linked to cognitive and memory impairments [18] as well as AD conversion [21, 22].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [18] Dickerson BC, et al. The cortical signature of Alzheimer’s disease: regionally specific cortical thinning relates to symptom severity in very mild to mild AD dementia and is detectable in asymptomatic amyloid-positive individuals. Cerebral cortex. 2009;19(3):497–510. source
    • cites [21] Gross AL, et al. Cortical signatures of cognition and their relationship to Alzheimer’s disease. Brain imaging and behavior. 2012;6:584–98. source
    • cites [22] Tabatabaei-Jafari H, et al. Regional brain atrophy predicts time to conversion to Alzheimer’s disease, dependent on baseline volume. Neurobiology of aging. 2019;83:86–94. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductown data

    We used only baseline gene expression measurements, which may not have fully captured the trajectory of gene expression dynamics throughout the disease progression.

    “Second, we used only baseline gene expression measurements, which may not have fully captured the trajectory of gene expression dynamics throughout the disease progression.”
    Quote in the paperNot a substantial claim

  • It may state two separate claims as one.

    Premisecitation

    APOC1 has been shown to exacerbate soluble Aβ oligomer-induced neuronal cell death in vitro, which may help explain the pronounced hippocampal and cortical atrophy observed in cognitively impaired patients.

    “Additionally, APOC1 has been shown to exacerbate soluble Aβ oligomer-induced neuronal cell death in vitro [94], which may help explain the pronounced hippocampal and cortical atrophy observed in cognitively impaired patients.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [94] Abildayeva K, et al. Human apolipoprotein CI expression in mice impairs learning and memory functions. Journal of lipid research. 2008;49(4):856–69. source

  • Probably not a substantial claim.

    Study design and conductnone given

    Gene expression data from ADNI were log2-scaled and adjusted for biological and technical covariates (age, sex, RNA integrity value, and batch) to mitigate confounding.

    “Gene expression data from ADNI (i.e., APOC1 in peripheral blood) were log2-scaled and adjusted for biological and technical covariates (i.e., age, sex, RNA integrity value, and batch) to mitigate the potential influence of confounding factors on the relationship between APOC1 expression and CTh changes.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    The relatively small sample size limits the generalizability of our findings.

    “First, the relatively small sample size limits the generalizability of our findings.”
    Quote in the paperNot a substantial claim

  • It may state two separate claims as one.

    Interpretationreasoning

    Our results suggest that APOC1 may serve as both a potential biomarker and therapeutic target.

    “Collectively, our results suggest that APOC1 may serve as both a potential biomarker and therapeutic target”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognition.
    • Rests on an assumption: The mediation analyses assume no unmeasured confounding between APOC1 expression, cortical atrophy, and cognitive outcomes.

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Interpretationnone given

    Potential additive or synergistic interactions between APOC1 and APOE cannot be ruled out.

    “However, potential additive or synergistic interactions between APOC1 and APOE cannot be ruled out.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    Other studies have shown that APOC1 may exert an independent effect on both the risk and the pathology of AD, separate from the impact of APOE ε4.

    “Conversely, other studies have shown that APOC1 may exert an independent effect on both the risk and the pathology of AD, separate from the impact of APOE ε4.”
    Quote in the paperNot a substantial claim

  • It may state two separate claims as one.

    Premisecitation

    In a study involving elderly individuals with memory impairment, those carrying the APOC1 risk genotype exhibited smaller hippocampal volume compared to non-carriers, suggesting that APOC1 variants may contribute to AD-like neurodegeneration.

    “In a study involving elderly individuals with memory impairment, those carrying the APOC1 risk genotype exhibited smaller HV compared to non-carriers, suggesting that APOC1 variants may contribute to AD-like neurodegeneration [25].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [25] Serra-Grabulosa J, et al. Apolipoproteins E and C1 and brain morphology in memory impaired elders. Neurogenetics. 2003;4:141–6. source

  • Probably not a substantial claim.

    Study design and conductcitation

    The significance and robustness of the mediation findings were assessed using bootstrapping analysis with 5000 iterations, with all regression weights standardized.

    “The significance and robustness of the findings were assessed using the bootstrapping analysis with 5000 iterations, conducted with the lavaan package in R, with all regression weights standardized [70].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [70] Rosseel Y. lavaan: an R package for structural equation modeling. Journal of statistical software. 2012;48:1–36. source

  • It may state two separate claims as one.

    Premisecitation

    APOC1 polymorphism influences hippocampal volume, which may have a significant effect on brain atrophy compared to APOE.

    “Moreover, APOC1 polymorphism influences HV, which may have a significant effect on brain atrophy compared to that of APOE [25].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [25] Serra-Grabulosa J, et al. Apolipoproteins E and C1 and brain morphology in memory impaired elders. Neurogenetics. 2003;4:141–6. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    We evaluated clinical potential solely based on gene expression levels in peripheral blood.

    “Lastly, we evaluated clinical potential solely based on gene expression levels in peripheral blood.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim.

    Study design and conductnone given

    Confounding effects of APOE were modeled by including APOE gene expression and APOE ε4 status as additional covariates.

    “Confounding effects of APOE were modeled by including APOE gene expression and APOE ε4 status as additional covariates.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Study design and conductown data

    The GO analysis provided functional annotations that hint at processes potentially related to synaptic function, but these results do not directly attribute such roles solely to APOC1.

    “Although this analysis provided functional annotations that hint at processes potentially related to synaptic function, these results do not directly attribute such roles solely to APOC1.”
    Quote in the paperNot a substantial claim

  • It may state two separate claims as one.

    Premisecitation

    GWAS meta-analysis has revealed rs12691088's potential association with AD risk, and it appears to be a variant concurrently implicated in both epigenetic aging and AD risk.

    “However, GWAS meta-analysis has revealed its potential association with AD risk, and it appears to be a variant concurrently implicated in both epigenetic aging and AD risk [81, 82].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [81] Guo Y, et al. Causal associations and shared genetic etiology of neurodegenerative diseases with epigenetic aging and human longevity. Aging cell. 2024;23(11): e14271. source
    • cites [82] Schwartzentruber J, et al. Genome-wide meta-analysis, fine-mapping and integrative prioritization implicate new Alzheimer’s disease risk genes. Nature genetics. 2021;53(3):392–402. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Premisecitation

    A transgenic mouse study revealed that overexpression of human APOC1 protein impaired learning and memory, regardless of APOE expression, indicating a modulatory role for APOC1 in AD development.

    “Additionally, a transgenic mouse study revealed that overexpression of human APOC1 protein impaired learning and memory, regardless of APOE expression, indicating a modulatory role for APOC1 in AD development [94].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [94] Abildayeva K, et al. Human apolipoprotein CI expression in mice impairs learning and memory functions. Journal of lipid research. 2008;49(4):856–69. source

  • Probably not a substantial claim.

    Premisecitation

    Brain atrophy is a validated marker for identifying the risk of developing AD.

    “Brain atrophy is a validated marker for identifying the risk of developing AD [16–19], assisting clinicians in making decisions regarding diagnosis and prognosis [20].”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [16] Pini L, et al. Brain atrophy in Alzheimer’s disease and aging. Ageing research reviews. 2016;30:25–48. source
    • cites [17] Sabuncu MR, et al. The dynamics of cortical and hippocampal atrophy in Alzheimer disease. Archives of neurology. 2011;68(8):1040–8. source
    • cites [18] Dickerson BC, et al. The cortical signature of Alzheimer’s disease: regionally specific cortical thinning relates to symptom severity in very mild to mild AD dementia and is detectable in asymptomatic amyloid-positive individuals. Cerebral cortex. 2009;19(3):497–510. source
    • cites [19] Whitwell JL, et al. Neuroimaging correlates of pathologically defined subtypes of Alzheimer’s disease: a case-control study. The Lancet Neurology. 2012;11(10):868–77. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Premisecitation

    APOC1 regulates lipid levels and cognitive functions.

    “In this family, apolipoprotein C1 (APOC1) regulates lipid levels and cognitive functions [11].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [11] Fuior EV, Gafencu AV. Apolipoprotein C1: its pleiotropic effects in lipid metabolism and beyond. International journal of molecular sciences. 2019;20(23):5939. source

  • Probably not a substantial claim. It may state two separate claims as one.

    Study design and conductcitation

    The association between APOC1 expression and cortical thickness changes was assessed using Pearson's correlation, and statistical significance was evaluated using 1000 nonparametric spin permutation tests.

    “The association between APOC1 expression and CTh changes was assessed using Pearson’s correlation, and the statistical significance of the correlations was evaluated using 1000 nonparametric spin permutation tests [56, 57].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [56] Alexander-Bloch AF, et al. On testing for spatial correspondence between maps of human brain structure and function. Neuroimage. 2018;178:540–51. source
    • cites [57] Larivière S, et al. The ENIGMA Toolbox: multiscale neural contextualization of multisite neuroimaging datasets. Nature methods. 2021;18(7):698–700. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    These variants have been reported in previous studies to exhibit strong associations with AD risk.

    “and have been reported in previous studies to exhibit strong associations with AD risk [4, 12, 77–80].”
    Quote in the paperNot a substantial claim0 of 6 sources checked
    • cites [4] Zhou Q, et al. Association between APOC1 polymorphism and Alzheimer’s disease: a case-control study and meta-analysis. PloS one. 2014;9(1): e87017. source
    • cites [12] Zhou X, et al. Non-coding variability at the APOE locus contributes to the Alzheimer’s risk. Nature communications. 2019;10(1):3310. source
    • cites [77] Kulminski AM, et al. Haplotype architecture of the Alzheimer’s risk in the APOE region via co-skewness. Alzheimer’s & dementia: diagnosis, assessment & disease monitoring. 2020;12(1): e12129. source
    • cites [78] Yan Q, et al. Genome-wide association study of brain amyloid deposition as measured by Pittsburgh compound-B (PiB)-PET imaging. Molecular psychiatry. 2021;26(1):309–21. source
    • cites [79] Ali M, et al. Large multi-ethnic genetic analyses of amyloid imaging identify new genes for Alzheimer disease. Acta neuropathologica communications. 2023;11(1):68. source
    • cites [80] Cervantes S, et al. Genetic variation in APOE cluster region and Alzheimer’s disease risk. Neurobiol Aging. 2011;32(11):2107. e7-2107. e17. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Premisecitation

    Atrophy in the entorhinal cortex intensifies with disease progression and is correlated with cognitive dysfunction.

    “Atrophy in the entorhinal cortex intensifies with disease progression and is correlated with cognitive dysfunction [73]”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [73] Desikan RS, et al. Temporoparietal MR imaging measures of atrophy in subjects with mild cognitive impairment that predict subsequent diagnosis of Alzheimer disease. American Journal of Neuroradiology. 2009;30(3):532–8. source

  • It may state two separate claims as one.

    Interpretationown data

    In this study, we elucidated the role of cortical thickness changes in the conversion of MCI to AD and highlighted APOC1 as a potential gene that may accelerate this process.

    “In this study, we elucidated the role of CTh changes in the conversion of MCI to AD and highlighted APOC1 as a potential gene that may accelerate this process.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognition.
    • Rests on an assumption: The mediation analyses assume no unmeasured confounding between APOC1 expression, cortical atrophy, and cognitive outcomes.

  • Probably not a substantial claim.

    Study design and conductnone given

    Surface-based findings were corrected for multiple comparisons to control for family-wise error rate (pFWE < 0.05), with a cluster threshold of p = 0.001.

    “Surface-based findings were corrected for multiple comparisons to control for family-wise error rate (i.e., pFWE < 0.05), with a cluster threshold of p = 0.001.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    The FDR was employed to adjust for multiple comparisons.

    “The FDR was employed to adjust for multiple comparisons.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    We did not directly investigate sex-related differences in cortical thickness changes.

    “Eighth, we did not directly investigate sex-related differences in CTh changes.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    Previous study revealed that neurodegeneration-related alterations in cortical thickness were associated with genes upregulating these pathways, underscoring the critical role of synaptic regulation in AD progression.

    “A previous study revealed that neurodegeneration-related alterations in CTh were associated with genes upregulating these pathways, underscoring the critical role of synaptic regulation in AD progression [72].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [72] Cai S, et al. Cortical thickness differences are associated with chemical synaptic transmission upregulated genes in degeneration of mild cognitive impairment. Frontiers in aging neuroscience. 2021;13: 745381. source

  • Probably not a substantial claim. It may state two separate claims as one.

    Premisenone given

    AD is a genetically heterogeneous disorder, necessitating the investigation of additional genetic contributors beyond APOE ε4.

    “Although APOE ε4 has been identified as a key genetic risk factor for AD, it is evident that AD is a genetically heterogeneous disorder, necessitating the investigation of additional genetic contributors beyond APOE ε4.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: AD is a genetically heterogeneous disorder necessitating investigation of additional genetic contributors beyond APOE ε4.

  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Premisecitation

    The co-presence of APOE ε4 and APOC1 risk alleles has been reported to be more strongly associated with AD than APOE ε4 alone, indicating that the interaction between these two genes may contribute to the development of AD and cognitive decline.

    “The co-presence of APOE ε4 and APOC1 risk alleles has been reported to be more strongly associated with AD than APOE ε4 alone, indicating that the interaction between these two genes may contribute to the development of AD and cognitive decline [96].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [96] Chuang W-L, et al. Association of apolipoproteins e4 and c1 with onset age and memory: a study of sporadic Alzheimer disease in Taiwan. Journal of geriatric psychiatry and neurology. 2010;23(1):42–8. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given

    Cortical thickness and hippocampal volume were the only measures utilized to assess brain atrophy.

    “Third, CTh and HV were the only measures utilized to assess brain atrophy.”
    Quote in the paperNot a substantial claim

  • It may state two separate claims as one.

    Premisecitation

    APOC1 is involved in amyloid-β accumulation and contributes to cognitive decline and memory impairment, similar to the effects observed with APOE ε4.

    “Multiple studies have confirmed that APOC1 is involved in amyloid-β (Aβ) accumulation and contributes to cognitive decline and memory impairment, similar to the effects observed with APOE ε4 [13, 14].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [13] Cudaback E, et al. Apolipoprotein CI is an APOE genotype-dependent suppressor of glial activation. Journal of neuroinflammation. 2012;9:1–13. source
    • cites [14] Petit-Turcotte C, et al. Apolipoprotein CI expression in the brain in Alzheimer’s disease. Neurobiology of disease. 2001;8(6):953–63. source

  • It may state two separate claims as one.

    Interpretationcitation

    Our findings reinforce the connection between synaptic dysfunction and AD pathogenesis, suggesting that disruptions in synaptic integrity contribute to cortical thinning and cognitive decline.

    “Our findings, consistent with previous studies [72, 74–76], reinforce the connection between synaptic dysfunction and AD pathogenesis, suggesting that disruptions in synaptic integrity contribute to cortical thinning and cognitive decline.”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [72] Cai S, et al. Cortical thickness differences are associated with chemical synaptic transmission upregulated genes in degeneration of mild cognitive impairment. Frontiers in aging neuroscience. 2021;13: 745381. source
    • cites [74] Ferrari RR, et al. A map of transcriptomic signatures of different brain areas in Alzheimer’s disease. International Journal of Molecular Sciences. 2024;25(20):11117. source
    • cites [75] Scheff SW, DeKosky ST, Price DA. Quantitative assessment of cortical synaptic density in Alzheimer’s disease. Neurobiology of aging. 1990;11(1):29–37. source
    • cites [76] Nguyen DPQ, et al. Multiple transcriptomic analyses explore potential synaptic biomarker rabphilin-3A for Alzheimer’s disease. Scientific reports. 2024;14(1):18717. source

  • It may state two separate claims as one.

    Premisecitation

    Previous transcriptomic studies and investigations into cortical synaptic density in AD have underscored the link between synaptic transmission and AD pathogenesis, demonstrating that disruptions in synaptic integrity contribute to cortical thinning in AD.

    “Other previous transcriptomic studies and investigations into cortical synaptic density in AD have underscored the link between synaptic transmission and AD pathogenesis, demonstrating that disruptions in synaptic integrity contribute to cortical thinning in AD [74, 75].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [74] Ferrari RR, et al. A map of transcriptomic signatures of different brain areas in Alzheimer’s disease. International Journal of Molecular Sciences. 2024;25(20):11117. source
    • cites [75] Scheff SW, DeKosky ST, Price DA. Quantitative assessment of cortical synaptic density in Alzheimer’s disease. Neurobiology of aging. 1990;11(1):29–37. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    Reduced hippocampal volume is closely associated with cognitive decline and progression to dementia.

    “and reduced HV is closely associated with cognitive decline and progression to dementia [91–93].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [91] Den Heijer T, et al. A 10-year follow-up of hippocampal volume on magnetic resonance imaging in early dementia and cognitive decline. Brain. 2010;133(4):1163–72. source
    • cites [92] Barnes J, et al. A meta-analysis of hippocampal atrophy rates in Alzheimer’s disease. Neurobiology of aging. 2009;30(11):1711–23. source
    • cites [93] Henneman W, et al. Hippocampal atrophy rates in Alzheimer disease: added value over whole brain volume measures. Neurology. 2009;72(11):999–1007. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Premisecitation

    A study found that the association of APOC1 H2 with AD remained significant even after adjusting for APOE ε4 status, suggesting that the APOC1 allele may act as an independent risk factor.

    “For example, a study found that the association of APOC1 H2 with AD remained significant even after adjusting for APOE ε4 status, suggesting that the APOC1 allele may act as an independent risk factor [15].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [15] Ki C-S, et al. Genetic association of an apolipoprotein CI (APOC1) gene polymorphism with late-onset Alzheimer’s disease. Neuroscience letters. 2002;319(2):75–8. source

  • Probably not a substantial claim. It may be too vague to check against evidence. It may state two separate claims as one.

    Interpretationreasoning

    These findings contribute to a deeper understanding of the impact of APOC1 expression on AD progression and its mechanistic role in AD pathology, providing a foundation for developing new therapeutic targets.

    “These findings contribute to a deeper understanding of the impact of APOC1 expression on AD progression and its mechanistic role in AD pathology, providing a foundation for developing new therapeutic targets.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Interpretationreasoning

    These findings suggest that the co-expression or co-regulation of APOC1 with APOE may heighten cortical vulnerability, especially in memory-related brain regions, through synergistic influences within the brain's lipid and inflammatory environments.

    “These findings suggest that the co-expression or co-regulation of APOC1 with APOE may heighten cortical vulnerability, especially in memory-related brain regions, through synergistic influences within the brain’s lipid and inflammatory environments.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim. It may be too vague to check against evidence. It may state two separate claims as one.

    Interpretationreasoning

    These findings suggested that APOC1 is a potential biomarker and therapeutic target.

    “These findings suggested that APOC1 is a potential biomarker and therapeutic target”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognition.
    • Rests on an assumption: The mediation analyses assume no unmeasured confounding between APOC1 expression, cortical atrophy, and cognitive outcomes.

  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Premisecitation

    While several studies support a synergistic effect between APOC1 and APOE ε4 in influencing AD risk, others point to APOC1's independent role in AD pathology.

    “While several studies support a synergistic effect between APOC1 and APOE ε4 in influencing AD risk, others point to APOC1’s independent role in AD pathology.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim.

    Study design and conductcitation

    Site effects were adjusted using ComBat harmonization.

    “site effects were adjusted using ComBat harmonization [40].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [40] Fortin J-P, et al. Harmonization of cortical thickness measurements across scanners and sites. Neuroimage. 2018;167:104–20. source

  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Interpretationcitation

    These results align with previous research highlighting the differential impacts of these genes on cortical atrophy and memory decline, particularly in the elderly with memory impairments.

    “These results align with previous research highlighting the differential impacts of these genes on cortical atrophy and memory decline, particularly in the elderly with memory impairments [25].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [25] Serra-Grabulosa J, et al. Apolipoproteins E and C1 and brain morphology in memory impaired elders. Neurogenetics. 2003;4:141–6. source
58 of 58

  • The paper relies on this without support.

    The relationship between APOC1 expression and brain atrophy lacks evidence and requires further investigation.

    “However, the relationship between APOC1 expression and brain atrophy lacks evidence and requires further investigation.”

  • The paper relies on this without support.

    APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognitive decline.

    “We performed mediation analyses to assess whether elevated APOC1 expression levels in the peripheral blood of patients with ADNI mediate accelerated cognitive decline via CTh.”

  • The paper relies on this without support.

    The AHBA post-mortem gene expression data from six donors without psychiatric or neuropathological disorders are representative of cortical APOC1 expression in the study population.

    “The AHBA data were used to extract transcriptional profiles across brain regions, providing a database of microarray-based log expression levels for 15,632 genes from the post-mortem brains of six donors without psychiatric or neuropathological disorders.”

  • The paper relies on this without support.

    The mediation model’s assumed causal ordering (baseline APOC1 expression → cortical thickness change → cognitive decline) is correct.

    “Mediation analysis was conducted to test whether adjusted APOC1 levels in peripheral blood measured at baseline influenced cognitive impairment through their effects on CTh.”

  • The paper relies on this without support.

    APOC1 mRNA expression measured in peripheral blood reflects APOC1 expression or activity in the brain relevant to cortical atrophy and cognition.

    “We examined the differential effects of APOE and APOC1 on CTh changes and memory performance through spatial associations with post-mortem gene expression in the human brain, as well as through mediation analyses using mRNA expression levels in peripheral blood.”

  • The paper relies on this without support.

    The mediation analyses assume no unmeasured confounding between APOC1 expression, cortical atrophy, and cognitive outcomes.

    “Finally, the impact of APOC1 expression on cognitive decline was mediated by cortical atrophy.”

  • The paper relies on this without support.

    Spatial correlation between post-mortem AHBA gene expression and in vivo cortical thickness change maps reflects regionally specific gene expression effects relevant to AD progression.

    “We discovered that the spatial correlation between the CTh change map and APOE mRNA expression from AHBA was significant, but weaker than that of APOC1 (APOE: r = −0.20, pspin = 0.046, APOC1: r = −0.31, pspin = 0.004; Fig. S8).”

  • The paper relies on this without support.

    The GAMLSS normative model derived from healthy aging individuals is appropriate for identifying deviations in cortical atrophy in those at risk of conversion to AD.

    “Normative CTh trajectories established using the GAMLSS model in healthy aging individuals have helped identify deviations in cortical atrophy in those at risk of conversion to AD.”

  • The paper relies on this without support.

    The APOC1 SNPs identified are functional or affect APOC1 expression.

    “Specific SNPs within the APOC1 region further differentiated conversion risk according to the presence of the variant.”

  • The paper relies on this without support.

    The sample of 636 cognitively normal participants is representative of normal aging for normative modeling.

    “We assessed hippocampal atrophy in the normal-aging group using the GAMLSS model in 636 participants with CN status.”

  • The paper relies on this without support.

    AD is a genetically heterogeneous disorder necessitating investigation of additional genetic contributors beyond APOE ε4.

    “Although APOE ε4 has been identified as a key genetic risk factor for AD, it is evident that AD is a genetically heterogeneous disorder, necessitating the investigation of additional genetic contributors beyond APOE ε4.”
11 of 11

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Increased MMSE score is described as no cognitive improvement

    Minor

    The stated inclusion criterion equates no cognitive improvement with an increased MMSE score at follow-up. An increased score indicates improvement, the opposite of the stated criterion.

1 of 1

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Metadata

Authors
Oh, S., Kim, S., Kim, J. P., Seo, S. W., Park, B.-Y., & Park, H.
Affiliations
  • Institute for Basic Science (KR)
  • Korea University (KR)
  • Samsung Medical Center (KR)
Corresponding author
  • Park, Bo-yong
  • Park, Hyunjin
ORCID
Venue
GeroScience
Publisher
Springer Science and Business Media LLC
Published
2025-05-15
Volume
47
Issue
6
Pages
6665-6682
ISSN
  • 2152-4041 (ISSN-L)
  • 2509-2723
DOI
10.1007/s11357-025-01695-6
PMC
PMC12638608
OpenAlex
W4410351674
Cited by
4
References
97
Citations by year
2026: 3 · 2025: 1
FWCI
2.13
Type
journal article
Language
en
Open access
Licence
Locations
  • GeroScience (publishedVersion, public-domain)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • National Research Foundation grant funded by the Korea government (NRF-2020M3E5D2A01084892, RS-2024-00408040)
  • AI Graduate School Support Program (RS-2019-II190421)
  • ICT Creative Consilience program (RS-2020-II201821)
  • Institute for Information and Communications Technology Planning and Evaluation (IITP) funded by the Korea Government (No.2022-0-00448/RS-2022-II220448, Deep Total Recall: Continual Learning for Human-Like Recall of Artificial Neural Networks, RS-2021-II212068, Artificial Intelligence Innovation Hub)
  • Sungkyunkwan University
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
Keywords
APOC1, Alzheimer's disease, mild cognitive impairment, cortical thickness, cortical atrophy, conversion to Alzheimer's disease, apolipoprotein E, gene expression, memory, entorhinal cortex, parahippocampal gyrus, paralimbic regions, longitudinal brain changes, genetic risk
MeSH terms
Brain Cortical Thickness, Aged, Aged, 80 and over, Alzheimer Disease, Atrophy, Cerebral Cortex, Female, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Disease Progression, Apolipoprotein C-I, Cognitive Dysfunction

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