A blood‐based nutritional risk index explains cognitive enhancement and decline in the multidomain Alzheimer prevention trial

Bowman, Gene L.; Dodge, Hiroko H.; Guyonnet, Sophie; Zhou, Nina; Donohue, Juliana; Bichsel, Aline; Schmitt, J.A.J.; Hooper, Claudie; Bartfai, Tamás; Andrieu, Sandrine; Vellas, Bruno; Carrié, Isabelle; Brigitte, Lauréane; Faisant, C.; Lala, Françoise; Delrieu, Julien; Villars, H.; Combrouze, Emeline; Badufle, Carole; Zueras, Audrey; Cantet, Christelle; Morin, Christophe; Kan, Gabor Abellán van; Dupuy, Charlotte; Rolland, Yves; Caillaud, Céline; Ousset, Pierre‐Jean

doi:10.1016/j.trci.2019.11.004

Cited by 22 publications

(24 citation statements)

References 71 publications

(100 reference statements)

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“…Considering that the accumulation of deficits can be related with the ability of an individual to respond to stressors (15), it is possible that combined deficiencies in homocysteine, vitamin D, and omega-3 PUFAs would work synergistically to determine physical performance over time. This concept had been supported by the findings of a previous study, which have indicated that an increasing number of nutritional deficits were associated with faster cognitive decline (16). In another study, the nutritional index, which was constructed with 41 nutrition-related parameters from anthropometric, plasma, and nutrient intake measurements, had shown a stronger prediction of frailty and mortality risk compared with single nutritional parameters separately (15).…”

Section: Introductionmentioning

confidence: 63%

“…Details of nutritional marker assessment are described in Supplementary Materials . Nutritional deficits were determined at baseline according to the clinical cutoffs below: (1) vitamin D deficiency, if 25(OH)D <20 ng/ml ( 26 ); (2) HHcy, if homocysteine >14 μmol/L ( 27 ); (3) low omega-3 PUFA index, defined as omega-3 index ( 28 ) [% docosahexaenoic acid (DHA) + % eicosapentaenoic acid (EPA)] below the lower quartile of study population (≤4.87%) ( 16 ). The participants were then classified into three groups based on the counting of nutritional deficits: no deficit, 1 deficit, and ≥2 deficits.…”

Section: Methodsmentioning

confidence: 99%

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Associations Between Nutritional Deficits and Physical Performance in Community-Dwelling Older Adults

Giudici

Rolland

et al. 2021

Front. Nutr.

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Background: Whether multiple nutritional deficiencies have a synergic effect on mobility loss remains unknown. This study aims to evaluate associations between multi-nutritional deficits and physical performance evolution among community-dwelling older adults.Methods: We included 386 participants from the Multidomain Alzheimer Preventive Trial (MAPT) (75.6 ± 4.5 years) not receiving omega-3 polyunsaturated fatty acid (PUFA) supplementation and who had available data on nutritional deficits. Baseline nutritional deficits were defined as plasma 25 hydroxyvitamin D <20 ng/ml, plasma homocysteine >14 μmol/L, or erythrocyte omega-3 PUFA index ≤ 4.87% (lower quartile). The Short Physical Performance Battery (SPPB), gait speed, and chair rise time were used to assess physical performance at baseline and after 6, 12, 24, 36, 48, and 60 months. We explored if nutrition-physical performance associations varied according to the presence of low-grade inflammation (LGI) and brain imaging indicators.Results: Within-group comparisons showed that physical function (decreased SPPB and gait speed, increased chair rise time) worsened over time, particularly in participants with ≥2 nutritional deficits; however, no between-group differences were observed when individuals without deficit and those with either 1 or ≥2 deficits were compared. Our exploratory analysis on nutritional deficit-LGI interactions showed that, among people with ≥2 deficits, chair rise time was increased over time in participants with LGI (adjusted mean difference: 3.47; 95% CI: 1.03, 5.91; p = 0.017), compared with individuals with no LGI.Conclusions: Accumulated deficits on vitamin D, homocysteine, and omega-3 PUFA were not associated with physical performance evolution in older adults, but they determined declined chair rise performance in subjects with low-grade inflammation.Clinical Trial Registration: [https://clinicaltrials.gov/ct2/show/NCT00672685], identifier [NCT00672685].

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Section: Introductionmentioning

confidence: 63%

Section: Methodsmentioning

confidence: 99%

Associations Between Nutritional Deficits and Physical Performance in Community-Dwelling Older Adults

Giudici

Rolland

et al. 2021

Front. Nutr.

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“…However, underlying mechanisms are still not fully understood. Nutritional compounds such as linoleic acid, vitamins or polyunsaturated fatty acids have been discussed as being preventive for decades, accordingly (for example: [ 3 ]). Many of these nutritional substances are correlated to immune modulatory probabilities and AD patients also have been demonstrated to show altered immune stimulation [ 4 , 5 ] as well as mutations in microglial genes such as triggering receptor expressed on myeloid cells 2 (TREM2; [ 6 ]).…”

Section: Introductionmentioning

confidence: 99%

Dietary Wheat Amylase Trypsin Inhibitors Impact Alzheimer’s Disease Pathology in 5xFAD Model Mice

Guilherme

Zevallos

Pesi

et al. 2020

IJMS

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Wheat amylase trypsin inhibitors (ATIs) represent a common dietary protein component of gluten-containing cereals (wheat, rye, and barley). They act as toll-like receptor 4 ligands, and are largely resistant to intestinal proteases, eliciting a mild inflammatory response within the intestine after oral ingestion. Importantly, nutritional ATIs exacerbated inflammatory bowel disease and features of fatty liver disease and the metabolic syndrome in mice. For Alzheimer’s disease (AD), both inflammation and altered insulin resistance are major contributing factors, impacting onset as well as progression of this devastating brain disorder in patients. In this study, we evaluated the impact of dietary ATIs on a well-known rodent model of AD (5xFAD). We assessed metabolic, behavioral, inflammatory, and microbial changes in mice consuming different dietary regimes with and without ATIs, consumed ad libitum for eight weeks. We demonstrate that ATIs, with or without a gluten matrix, had an impact on the metabolism and gut microbiota of 5xFAD mice, aggravating pathological hallmarks of AD. If these findings can be translated to patients, an ATI-depleted diet might offer an alternative therapeutic option for AD and warrants clinical intervention studies.

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“…Changes in nutritional status including weight loss and lower nutrient levels are often prevalent before the onset of Alzheimer's disease (AD)‐type dementia 1–4 . Impaired nutritional status has been associated with faster cognitive decline in community‐based populations 5–7 . Nutritional biomarker levels in blood or cerebrospinal fluid (CSF) can be used to identify nutritional factors that may contribute to faster cognitive decline in AD.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, large population‐based studies have reported higher levels of homocysteine and cholesterol to be a risk factor for AD‐type dementia 8,9 . A recent study proposed a nutritional risk index including levels of omega‐3 fatty acids, vitamin D, and homocysteine that might help to identify non‐demented elderly at risk for cognitive decline 6 . These findings suggest that nutritional biomarkers have potential to aid in the identification of targets for dietary interventions.…”

Section: Introductionmentioning

confidence: 99%

LDL cholesterol and uridine levels in blood are potential nutritional biomarkers for clinical progression in Alzheimer's disease: The NUDAD project

Leeuw

Tijms

Doorduijn

et al. 2020

Alzheimer's & Dementia: Diagnosis, Assessment &

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INTRODUCTION We examined associations between nutritional biomarkers and clinical progression in individuals with subjective cognitive decline (SCD), mild cognitive impairment (MCI), and Alzheimer's disease (AD)‐type dementia. METHODS We included 528 individuals (64 ± 8 years, 46% F, follow‐up 2.1 ± 0.87 years) with SCD (n = 204), MCI (n = 130), and AD (n = 194). Baseline levels of cholesterol, triglycerides, glucose, homocysteine, folate, vitamin A, B12, E and uridine were measured in blood and S‐adenosylmethionine and S‐adenosylhomocysteine in cerebrospinal fluid. We determined associations between nutritional biomarkers and clinical progression using Cox proportional hazard models. RESULTS Twenty‐two (11%) patients with SCD, 45 (35%) patients with MCI, and 100 (52%) patients with AD showed clinical progression. In SCD, higher levels of low‐density lipoprotein (LDL) cholesterol were associated with progression (hazard ratio [HR] [95% confidence interval (CI)] 1.88 [1.04 to 3.41]). In AD, lower uridine levels were associated with progression (0.79 [0.63 to 0.99]). DISCUSSION Our findings suggest that LDL cholesterol and uridine play a—stage‐dependent—role in the clinical progression of AD.

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A blood‐based nutritional risk index explains cognitive enhancement and decline in the multidomain Alzheimer prevention trial

Cited by 22 publications

References 71 publications

Associations Between Nutritional Deficits and Physical Performance in Community-Dwelling Older Adults

Associations Between Nutritional Deficits and Physical Performance in Community-Dwelling Older Adults

Dietary Wheat Amylase Trypsin Inhibitors Impact Alzheimer’s Disease Pathology in 5xFAD Model Mice

LDL cholesterol and uridine levels in blood are potential nutritional biomarkers for clinical progression in Alzheimer's disease: The NUDAD project

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