B‐vitamins reduce the long‐term risk of depression after stroke: The VITATOPS‐DEP trial

Almeida, Osvaldo P.; Marsh, Kylie; Alfonso, Helman; Flicker, Leon; Davis, Timothy; Hankey, Graeme J.

doi:10.1002/ana.22189

Cited by 92 publications

(83 citation statements)

References 47 publications

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“…It is a major challenge to develop consistently effective therapy for ischemic stroke. [2][3][4][5][6][7] A core of necrotic cell death is surrounded by a zone of tissue, termed the penumbra, in which the energy metabolism is preserved by constrained blood supply. 8 The penumbra is an important target area for both basic investigators of cerebral ischemia and clinicians who treat stroke patients, whereas the necrotic lesion is irreversible.…”

Section: Introductionmentioning

confidence: 99%

Induction of autophagy contributes to the neuroprotection of nicotinamide phosphoribosyltransferase in cerebral ischemia

Wang

Guan²,

Du³

et al. 2012

Autophagy

291

241

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Recent reports indicate that autophagy serves as a stress response and may participate in the pathophysiology of cerebral ischemia. Nicotinamide phosphoribosyltransferase (Nampt, also known as visfatin), the rate-limiting enzyme in mammalian NAD + biosynthesis, protects against ischemic stroke through inhibiting neuronal apoptosis and necrosis. This study sought to determine the involvement of autophagy in neuroprotection of Nampt in cerebral ischemia. Middle cerebral artery occlusion (MCAO) in rats and oxygen-glucose deprivation (OGD) in cultured cortical neurons were performed. Nampt was overexpressed or knocked down using lentivirus-mediated gene transfer in vivo and in vitro. Immunochemistry (LC3-II), electron microscope and immunoblotting assays (LC3-II, Beclin 1, mammalian target of rapamycin [mTOR], S6K1 and tuberous sclerosis complex-2 [TSC2]) were performed to assess autophagy. We found that overexpression of Nampt increased autophagy (LC3 puncta immunochemistry staining, LC3-II/Beclin 1 expression and autophagosomes number) both in vivo and in vitro at 2 h after MCAO. At the early stage of OGD, autophagy-inducer rapamycin protected against neuronal injury induced by Nampt knockdown, whereas autophagy-inhibitor 3-methyladenine partly abolished the neuroprotective effect of Nampt. Overexpression or knockdown of Nampt regulated the phosphorylation of mTOR and S6K1 signaling pathway upon OGD stress through enhancing phosphorylation of TSC2 at Ser1387 but not Thr1462 site. Furthermore, in cultured SIRT1-knockout neurons, the regulation of Nampt on autophagic proteins LC3-II and Beclin 1 was abolished. Our results demonstrate that Nampt promotes neuronal survival through inducing autophagy via regulating the TSC2-mTOR-S6K1 signaling pathway in a SIRT1-dependent manner during cerebral ischemia.

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Section: Introductionmentioning

confidence: 99%

Induction of autophagy contributes to the neuroprotection of nicotinamide phosphoribosyltransferase in cerebral ischemia

Wang

Guan²,

Du³

et al. 2012

Autophagy

291

241

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“…France (Astorg, et al, 2008), Greece (Dimopoulos, et al, 2007), Japan (Murakami, et al, 2008;Nanri, Mizoue, et al, 2010) Norway (Bjelland, et al, 2003), Singapore (Ng, Niti, Zaw, & Kua, 2009), Spain (Sanchez-Villegas, Doreste, et al, 2009Sanchez-Villegas, et al, 2006), and Australia before 2009 (Almeida, et al, 2010;Sachdev et al, 2005). Fortification of flour with folic acid may have attenuated the effect of folate, which corroborates the aforementioned hypothesis that lower vitamin status may be more strongly associated with depression compared to higher vitamin status due to mandatory fortification.…”

Section: Discussionmentioning

confidence: 99%

“…There was no improvement in depression scores in the treatment group compared to the placebo group 3 months after the start of the treatment (Hvas, Juul, Lauritzen, Nexo, & Ellegaard, 2004). In Australia, five double-blinded, placebo-controlled randomized trials involving older adults tested the potential effect of B-vitamin supplementation on depression risk in post-stroke patients (Almeida et al, 2010), on cognition and mood in women (Bryan, Calvaresi, & Hughes, 2002), on the potentiation of antidepressant medication or on the 2-year depression risk in communitydwelling seniors with elevated psychological distress (H. Christensen et al, 2011;Walker et al, 2010), and on the 2-year depression risk in elderly men with a history of or being treated for hypertension (Ford et al, 2008). Only the trial with stroke survivors (n=137, 63.0 ± 11.4y) found a protective effect of daily supplementation with 2 mg folic acid, 25 mg vitamin B6, and 0.5 mg vitamin B12…”

Section: B Vitamins and Depressionmentioning

confidence: 99%

Nutritional predictors of depression in a cohort of community-dwelling elderly Canadians: NuAge cohort

GougeonLaura¹

2014

Appl. Physiol. Nutr. Metab.

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Depression is associated with decreased quality of life and high mortality risk at all ages and, despite having lower prevalence in community-dwelling seniors compared to other stages of the life span or institutionalized elderly, it negatively affects seniors' health outcomes. Most evidence linking late-life depression, defined as first onset after 65 years of age, with dietary factors comes from cross-sectional studies, which cannot provide information on whether declines in diet were a consequence of depression-the reverse causality hypothesis. The Quebec Longitudinal Study on Nutrition and Aging (NuAge) provides an ideal setting to explore such a relationship among a healthy, community-dwelling elderly population. Diet is hypothesized to be a factor associated with depression. Some longitudinal evidence from studies with middle-aged adults suggests that dietary patterns such as the Mediterranean or patterns deemed "healthy" are protective against depression, while "western" and "unhealthy" patterns are risk factors for the disease. B-vitamins are important cofactors in neurotransmitter synthesis and in the enzymes of the one-carbon metabolism, which has been hypothesized to have an aetiological role in depression through its neurotoxic derivates, such as homocysteine. Nonetheless, it is still largely unknown how depression affects nutrient intake in the elderly population, raising the question of the directionality of the association. Therefore, ii the three objectives of this thesis were to explore the longitudinal associations of i) dietary patterns and macronutrient intake and of ii) B6, B12 and folate intakes with the incidence of depression in late life; and iii) to investigate whether depression significantly affects short-term nutrient intakes (reverse causality effect) in comparison to intakes among non-depressed seniors.Data for this study have been obtained from the NuAge cohort, a 4-y longitudinal study of 1,793 community-dwelling men and women aged 68 to 82 years at baseline. The main outcome is incidence of depression as defined by scores in the 30-item Geriatric Depression Scale ≥11 and or antidepressant medication use over the three years of follow-up. Participants were free of depression at the study's baseline through the exclusion of those with GDS scores ≥11 or antidepressant use at the time of the recruitment. Individuals with invalid or missing dietary information were also excluded. Dietary patterns were created through principal component analysis on amount (grams) of food items consumed in each of the 32 predefined food categories. Sex-specific tertiles of intake were created from the mean of three non-consecutive 24h-recalls. Multiple logistic regression models were adjusted for several demographic, health, and social confounders. For the study of the reverse causality hypothesis, we conducted a case-control nested within the NuAge cohort. Participants free of iii depression at baseline who developed depression at some point of follow-up were matched by age group and sex with...

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“…Homocysteine can mediate the formation of cardiovascular disease by several different mechanisms including increased proliferation of vascular smooth muscle cells, endothelial dysfunction, oxidative damage, and collagen synthesis. Treatment with B vitamins may reduce homocysteine by ~30% in stroke survivors [32] and reduce the risk of overall stroke in participants with known cardiovascular disease [33,34]. However, numerous factors may modulate the impact of B vitamins on cardiovascular risk in stroke survivors.…”

Section: B Vitamin Supplementation and Cardiovascular Riskmentioning

confidence: 99%

Dietary Intake and Intervention in Chronic Stroke: Review of the Evidence

Serra¹

2017

J Neurol Neurophysiol

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Despite evidence for a role of nutrition in the development of metabolic dysfunction, physical deconditioning, and psychological dysfunction common post-stroke, very little is known about the dietary habits and nutritional needs of chronic (>6 months) stroke survivors. This review summarizes the available evidence regarding dietary intake adequacy in chronic stroke survivors. It appears that a combination of screening methods, including food record, laboratory and malnutrition screening tools assessments may be beneficial to assess the dietary intake adequacy of stroke survivors. We also review the evidence suggesting the need for dietary modification by summarizing the strongest evidence (i.e., randomized controlled trial data) supporting and refuting the impact of nutritional interventions on clinical outcomes post-stroke. Data suggest that the B vitamins, omega 3s and vitamin D have promising effects on recovery post-stroke; however, to date, study limitations make drawing definitive conclusions regarding the impact of nutritional supplementation difficult. Further research is needed to provide insight on the ideal supplement dose and duration and about how different rehabilitation therapies (i.e., nutritional supplements, medications, exercise and caloric restriction) may interact to affect recovery. A better understanding of the role of nutrition during chronic stroke is needed as this information may one day help to individualize rehabilitation approaches to optimize patient outcomes.

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B‐vitamins reduce the long‐term risk of depression after stroke: The VITATOPS‐DEP trial

Cited by 92 publications

References 47 publications

Induction of autophagy contributes to the neuroprotection of nicotinamide phosphoribosyltransferase in cerebral ischemia

Induction of autophagy contributes to the neuroprotection of nicotinamide phosphoribosyltransferase in cerebral ischemia

Nutritional predictors of depression in a cohort of community-dwelling elderly Canadians: NuAge cohort

Dietary Intake and Intervention in Chronic Stroke: Review of the Evidence

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