“…We predicted more pronounced white matter glia reductions in APOE ε4 compared to ε2 and/or ε3 carriers, as cholesterol transport for myelin repair in the brain has been proposed to be less efficient in ε4 carriers 50–53 . In addition, we assessed lifestyle-related risk factors associated with the metabolic syndrome, notably central obesity, hypertension, alcohol consumption and sedentary lifestyle 54,55 (Table 1). We were particularly interested in the effects of central adiposity, as obesity is globally on the rise, and is associated with chronic inflammation, insulin resistance and vascular problems 54,55 as well as with accelerated aging in brain regions that include limbic white matter 56,57 .…”
Section: Introductionmentioning
confidence: 99%
“…In addition, we assessed lifestyle-related risk factors associated with the metabolic syndrome, notably central obesity, hypertension, alcohol consumption and sedentary lifestyle 54,55 (Table 1). We were particularly interested in the effects of central adiposity, as obesity is globally on the rise, and is associated with chronic inflammation, insulin resistance and vascular problems 54,55 as well as with accelerated aging in brain regions that include limbic white matter 56,57 . Finally, episodic memory performance was assessed with standard neuropsychological tests of verbal and non-verbal recall 58,59 (Table 1).…”
Aging leads to gray and white matter decline but their causation remains unclear. We explored two classes of models of age and dementia risk related brain changes. The first class of models emphasises the importance of gray matter: age and risk-related processes cause neurodegeneration and this causes damage in associated white matter tracts. The second class of models reverses the direction of causation: aging and risk factors cause white matter damage and this leads to gray matter damage. We compared these models with linear mediation analysis and quantitative MRI indices (from diffusion, quantitative magnetization transfer and relaxometry imaging) of tissue properties in two limbic structures implicated in age-related memory decline: the hippocampus and the fornix in 166 asymptomatic individuals (aged 38–71 years). Aging was associated with apparent glia but not neurite density damage in the fornix and the hippocampus. Mediation analysis supported white matter damage causing gray matter decline; controlling for fornix glia damage, the correlations between age and hippocampal damage disappear, but not vice versa. Fornix and hippocampal differences were both associated with reductions in episodic memory performance. These results suggest that fornix white matter glia damage may cause hippocampal gray matter damage during age-dependent limbic decline.
“…We predicted more pronounced white matter glia reductions in APOE ε4 compared to ε2 and/or ε3 carriers, as cholesterol transport for myelin repair in the brain has been proposed to be less efficient in ε4 carriers 50–53 . In addition, we assessed lifestyle-related risk factors associated with the metabolic syndrome, notably central obesity, hypertension, alcohol consumption and sedentary lifestyle 54,55 (Table 1). We were particularly interested in the effects of central adiposity, as obesity is globally on the rise, and is associated with chronic inflammation, insulin resistance and vascular problems 54,55 as well as with accelerated aging in brain regions that include limbic white matter 56,57 .…”
Section: Introductionmentioning
confidence: 99%
“…In addition, we assessed lifestyle-related risk factors associated with the metabolic syndrome, notably central obesity, hypertension, alcohol consumption and sedentary lifestyle 54,55 (Table 1). We were particularly interested in the effects of central adiposity, as obesity is globally on the rise, and is associated with chronic inflammation, insulin resistance and vascular problems 54,55 as well as with accelerated aging in brain regions that include limbic white matter 56,57 . Finally, episodic memory performance was assessed with standard neuropsychological tests of verbal and non-verbal recall 58,59 (Table 1).…”
Aging leads to gray and white matter decline but their causation remains unclear. We explored two classes of models of age and dementia risk related brain changes. The first class of models emphasises the importance of gray matter: age and risk-related processes cause neurodegeneration and this causes damage in associated white matter tracts. The second class of models reverses the direction of causation: aging and risk factors cause white matter damage and this leads to gray matter damage. We compared these models with linear mediation analysis and quantitative MRI indices (from diffusion, quantitative magnetization transfer and relaxometry imaging) of tissue properties in two limbic structures implicated in age-related memory decline: the hippocampus and the fornix in 166 asymptomatic individuals (aged 38–71 years). Aging was associated with apparent glia but not neurite density damage in the fornix and the hippocampus. Mediation analysis supported white matter damage causing gray matter decline; controlling for fornix glia damage, the correlations between age and hippocampal damage disappear, but not vice versa. Fornix and hippocampal differences were both associated with reductions in episodic memory performance. These results suggest that fornix white matter glia damage may cause hippocampal gray matter damage during age-dependent limbic decline.
“…Obesity and MetS are identified as risk factors for adult-onset AD and vascular dementia [13,38]. Moreover, the combination of obesity, metabolic imbalances, and arterial hypertension occurring in MetS [39] have been associated with cognitive decline and their treatment is accompanied by a significantly decreased risk of dementia [40].…”
Metabolic syndrome (MetS) is an association between obesity, dyslipidemia, hyperglycemia, hypertension, and insulin resistance. A relationship between MetS and vascular dementia was hypothesized. The purpose of this work is to investigate brain microanatomy alterations in obese Zucker rats (OZRs), as a model of MetS, compared to their counterparts lean Zucker rats (LZRs). 12-, 16-, and 20-weeks-old male OZRs and LZRs were studied. General physiological parameters and blood values were measured. Immunochemical and immunohistochemical techniques were applied to analyze the brain alterations. The morphology of nerve cells and axons, astrocytes and microglia were investigated. The blood–brain barrier (BBB) changes occurring in OZRs were assessed as well using aquaporin-4 (AQP4) and glucose transporter protein-1 (GLUT1) as markers. Body weight gain, hypertension, hyperglycemia, and hyperlipidemia were found in OZRs compared to LZRs. In the frontal cortex and hippocampus, a decrease of neurons was noticeable in the older obese rats in comparison to their age-matched lean counterparts. In OZRs, a reduction of neurofilament immunoreaction and gliosis was observed. The BBB of older OZRs revealed an increased expression of AQP4 likely related to the development of edema. A down-regulation of GLUT1 was found in OZRs of 12 weeks of age, whereas it increased in older OZRs. The behavioral analysis revealed cognitive alterations in 20-week-old OZRs. Based on these results, the OZRs may be useful for understanding the mechanisms through which obesity and related metabolic alterations induce neurodegeneration.
“…Modern epidemiological studies show that whole grain foods can prevent chronic diseases such as type 2 diabetes, coronary heart disease, and bowel cancer [39][40][41][42][43][44]. Although the mechanisms underlying these effects are not fully understood, they are likely to be closely related to the antioxidant activity of whole grains [45,46].…”
Phenolic compounds are important products of secondary metabolism in plants. They cannot be synthesized in the human body and are mainly taken from food. Cereals, especially whole grains, are important sources of dietary polyphenols. Compared with vegetables and fruits, the content and biological activities of polyphenols in cereals have long been underestimated. Polyphenols in whole grains are non-nutritive compounds, which are distributed in all structural areas of cereal substances, mainly phenolic acids, flavonoids, and lignans. In recent years, the health effects of whole grains are closely related to their phenolic compounds and their antioxidant activities. Now, different physicochemical processing treatments and their effects have been summarized in order to provide the basis for promoting the development and utilization of food. The various functions of whole grains are closely related to the antioxidant effect of polyphenols. As the basic research on evaluating the antioxidant effect of active substances, in vitro antioxidant tests are faster and more convenient.
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