Metabolic syndrome impact on cognitive composites domain scores and on white matter hyperintensities in subjective cognitive decline: The FACEHBI Cohort

Abstract Background To explore whether the combination of white matter hyperintensities (WMHs) and amyloid-beta (Aβ) deposition is associated with worse cognitive performance on cognitive composites (CCs) domain scores in individuals with subjective cognitive decline (SCD). Methods Two hundred participants from the FACEHBI cohort underwent structural magnetic resonance imaging (MRI), 18F-florbetaben positron emission tomography (FBB-PET), and neuropsychological assessment. WMHs were addressed through the Fazekas scale, the Age-Related White Matter Changes (ARWMC) scale, and the FreeSurfer pipeline. Eight CCs domain scores were created using the principal component analysis (PCA). Age, sex, education, and apolipoprotein E (APOE) were used as adjusting variables. Results Adjusted multiple linear regression models showed that FreeSurfer (B − .245; 95% CI − .1.676, − .393, p = .016) and β burden (SUVR) (B − .180; 95% CI − 2.140, − .292; p = .070) were associated with face–name associative memory CCs domain score, although the latest one was not statistically significant after correction for multiple testing (p = .070). There was non-significant interaction of these two factors on this same CCs domain score (p = .54). However, its cumulative effects on face–name associative performance indicated that those individuals with either higher WMH load or higher Aβ burden showed the worst performance on the face–name associative memory CCs domain score. Conclusions Our results suggest that increased WMH load and increased Aβ are independently associated with poorer episodic memory performance in SCD individuals, indicating a cumulative effect of the combination of these two pathological conditions in promoting lower cognitive performance, an aspect that could help in terms of treatment and prevention.

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Evidence of a Relation Between Hippocampal Volume, White Matter Hyperintensities, and Cognition in Subjective Cognitive Decline and Mild Cognitive Impairment

The Journals of Gerontology Series B ◽

10.1093/geronb/gbz120 ◽

2019 ◽

Vol 75 (7) ◽

pp. 1382-1392 ◽

Cited By ~ 4

Author(s):

Marie Caillaud ◽

Carol Hudon ◽

Benjamin Boller ◽

Simona Brambati ◽

Simon Duchesne ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cognitive Impairment ◽

Mild Cognitive Impairment ◽

White Matter ◽

Episodic Memory ◽

Cognitive Decline ◽

White Matter Hyperintensities ◽

Hippocampal Volume ◽

Subjective Cognitive Decline

Abstract Objective The concepts of mild cognitive impairment (MCI) and subjective cognitive decline (SCD) have been proposed to identify individuals in the early stages of Alzheimer’s disease (AD), or other neurodegenerative diseases. One approach to validate these concepts is to investigate the relationship between pathological brain markers and cognition in those individuals. Method We included 126 participants from the Consortium for the Early Identification of Alzheimer’s disease-Quebec (CIMA-Q) cohort (67 SCD, 29 MCI, and 30 cognitively healthy controls [CH]). All participants underwent a complete cognitive assessment and structural magnetic resonance imaging. Group comparisons were done using cognitive data, and then correlated with hippocampal volumes and white matter hyperintensities (WMHs). Results Significant differences were found between participants with MCI and CH on episodic and executive tasks, but no differences were found when comparing SCD and CH. Scores on episodic memory tests correlated with hippocampal volumes in both MCI and SCD, whereas performance on executive tests correlated with WMH in all of our groups. Discussion As expected, the SCD group was shown to be cognitively healthy on tasks where MCI participants showed impairment. However, SCD’s hippocampal volume related to episodic memory performances, and WMH to executive functions. Thus, SCD represents a valid research concept and should be used, alongside MCI, to better understand the preclinical/prodromal phase of AD.

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White matter hyperintensities may be an early marker for age-related cognitive decline in the ADNI cohort

10.1101/2021.09.23.461560 ◽

2021 ◽

Author(s):

Cassandra Morrison ◽

Mahsa Dadar ◽

Sylvia Villeneuve ◽

D. Louis Collins

Keyword(s):

White Matter ◽

Cognitive Decline ◽

White Matter Hyperintensities ◽

White Matter Hyperintensity ◽

Subjective Cognitive Decline ◽

Age Related ◽

Lower Baseline ◽

Age Related Cognitive Decline ◽

Linear Regressions

Background: Previous research suggests that white matter hyperintensities, amyloid, and tau contribute to age-related cognitive decline. It remains unknown as to how these factors relate to one another and how they jointly contribute to cognitive decline in normal aging. This project examines the association between these pathologies and their relationship to cognitive decline. Methods: Cognitively normal older adult data from the Alzheimers Disease Neuroimaging Initiative were examined. Participants were included if they had no subjective cognitive decline, had baseline white matter hyperintensity, CSF AB42/40, CSF pTau181, and cognitive scores. Of the 102 participants included, only 79 had follow-up cognitive scores. Linear regressions examined the influence of white matter hyperintensities, amyloid, and tau on baseline and follow-up cognitive scores. Linear regressions also examined the association of amyloid and tau on white matter hyperintensities and between tau and amyloid. Results: Increased white matter hyperintensity load was associated with lower baseline memory (B= -0.20, p =.046), follow-up executive functioning (B= -0.32, p<.001), and follow-up ADAS-13 (B=2.69, p<.001) scores. White matter hyperintensities were not related to pTau or AB42/40. Lower AB42/40 was associated with increased pTau (p=.025). pTau was not associated with decline in any cognitive score. Lower AB42/40 was associated with lower baseline (p=.015) but not follow-up executive function. Discussion: White matter hyperintensities may be one of the earliest pathologies observed in healthy older adults that contribute to cognitive decline. The inclusion of white matter hyperintensities as an additional marker for early cognitive decline may improve our current understanding of age-related changes.

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White Matter Hyperintensities Relate to Clinical Progression in Subjective Cognitive Decline

Stroke ◽

10.1161/strokeaha.115.009475 ◽

2015 ◽

Vol 46 (9) ◽

pp. 2661-2664 ◽

Cited By ~ 39

Author(s):

Marije R. Benedictus ◽

Argonde C. van Harten ◽

Annebet E. Leeuwis ◽

Teddy Koene ◽

Philip Scheltens ◽

...

Keyword(s):

White Matter ◽

Cognitive Decline ◽

White Matter Hyperintensities ◽

Subjective Cognitive Decline ◽

Clinical Progression

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P2-340: Diffusion Tensor Imaging Study in the Detection of White Matter Degeneration in Subjective Cognitive Decline

Alzheimer s & Dementia ◽

10.1016/j.jalz.2016.06.1470 ◽

2016 ◽

Vol 12 ◽

pp. P773-P773

Author(s):

Xuanyu Li ◽

Zhenyu Liu ◽

Zhenchao Tang ◽

Ying Han

Keyword(s):

Diffusion Tensor Imaging ◽

White Matter ◽

Cognitive Decline ◽

Diffusion Tensor ◽

Imaging Study ◽

Subjective Cognitive Decline ◽

White Matter Degeneration ◽

Diffusion Tensor Imaging Study

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Predictors for cognitive decline in patients with confluent white matter hyperintensities

Alzheimer s & Dementia ◽

10.1016/j.jalz.2011.10.004 ◽

2012 ◽

Vol 8 ◽

pp. S96-S103 ◽

Cited By ~ 13

Author(s):

Vincent Mok ◽

Yunyun Xiong ◽

Kelvin K. Wong ◽

Adrian Wong ◽

Reinhold Schmidt ◽

...

Keyword(s):

White Matter ◽

Cognitive Decline ◽

White Matter Hyperintensities

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Role of white matter hyperintensities, hemoglobin and vitamin B‐12 on cognitive decline: Two‐year follow‐up data from the Tata Longitudinal Study of Ageing (TLSA)

Alzheimer s & Dementia ◽

10.1002/alz.045683 ◽

2020 ◽

Vol 16 (S6) ◽

Author(s):

Aditi Balakrishnan ◽

Vivek Tiwari ◽

M.L. Abhishek ◽

Naren P. Rao ◽

Vijayalakshmi Ravindranath ◽

...

Keyword(s):

Longitudinal Study ◽

White Matter ◽

Cognitive Decline ◽

White Matter Hyperintensities ◽

Vitamin B ◽

Vitamin B 12

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Prestroke Statins, Progression of White Matter Hyperintensities, and Cognitive Decline in Stroke Patients with Confluent White Matter Hyperintensities

Neurotherapeutics ◽

10.1007/s13311-014-0270-5 ◽

2014 ◽

Vol 11 (3) ◽

pp. 606-611 ◽

Cited By ~ 24

Author(s):

Yunyun Xiong ◽

Adrian Wong ◽

Margherita Cavalieri ◽

Reinhold Schmidt ◽

Winnie W. C. Chu ◽

...

Keyword(s):

White Matter ◽

Cognitive Decline ◽

White Matter Hyperintensities ◽

Stroke Patients

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Abstract TP181: Serum Eiocosapentaenoic Acids Is Protective Against White Matter Lesions

Stroke ◽

10.1161/str.44.suppl_1.atp181 ◽

2013 ◽

Vol 44 (suppl_1) ◽

Author(s):

Daiki Takano ◽

Takashi Yamazaki ◽

Tetsuya Maeda ◽

Yuichi Satoh ◽

Yasuko Ikeda ◽

...

Keyword(s):

White Matter ◽

Cognitive Decline ◽

White Matter Hyperintensities ◽

Small Vessel Disease ◽

White Matter Lesions ◽

White Matter Hyperintensity ◽

Partial Regression Coefficient ◽

The Relationship ◽

Total Pufa ◽

Periventricular Hyperintensity

[Introduction] White matter hyperintensities (WMH) are considered manifestation of arteriosclerotic small vessel disease and WMH burden increases risk of ischemic stroke and cognitive decline. There are only a few evidences concerning the relationship between polyunsaturated fatty acids (PUFA) and WMH. The present study was designed to elucidate the association between WMH and PUFA profile including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and arachidonic acid (AA) in patients with Alzheimer’s disease (AD). [Methods] The present study was based on 119 patients who were diagnosed as having a probable AD according to the NINCDS-ADRDA criteria. Their mean age was 78.3 years old. All subjects underwent neuropsychological evaluation including mini mental state exam (MMSE) and 1.5-Tesla MRI. Fasting blood samples were also collected for the PUFA measurements. We measured the ratio of serum EPA, DHA and AA concentration to the total PUFA concentration. The WMH were evaluated on T2-weight images and classified into periventricular hyperintensity (PVH) and deep white matter hyperintensity (DWMH). The severity of WMH was graded 5 categories. We investigated the relationship between WMH and PUFA profiles. [Results] The EPA ratio correlated negatively with both PVH (rs=-0.2036, p=0.0264) and DWMH grade (rs=-0.3155, p=0.0005). It remained still significant after adjustment for age, sex, statins use, antithrombotics use, mean blood pressure and presence of hypertension (standardized partial regression coefficient(β)=-0.2516, p=0.0122 for PVH, β=-0.3598, p=0.0001 for DWMH). Neither DHA nor AA ratio correlated with DWMH or PVH grade. The EPA ratio but not DHA or AA ratio correlated positively with total MMSE score (rs=0.2310, p=0.0115). [Conclusions] Our data revealed that the serum EPA was protective against WMH as well as cognitive decline in AD patients. Pathophysiology underlying WMH is complex and the possible mechanisms involved in the pathogenesis of WMH encompass incomplete brain ischemia, increased permeability of blood-brain barrier, and inflammation responses. The relationship between serum EPA and WMH can be partly explained by those anti-ischemic and anti-arteriosclerotic effects of EPA.

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