Integrating willow-based bioenergy and organic dairy production – the role of tree fodder for feed supplementation

Silvopastoral systems that combine livestock and trees offer two main advantages for the animals. First, trees modify microclimatic conditions which can have beneficial effects on pasture growth and animal welfare. Second, trees also provide alternative feed resources during periods of low forage availability. This paper reports on research carried out within the Sustainable Organic and Low Input Dairying (SOLID) project to investigate the multifunctional potential of a novel integrated willow-based bio-energy/organic dairy production system in the UK, especially the role of tree fodder for feed supplementation in organic dairy systems. The nutritional value of two ages (1st and 2nd year re-growth) of short rotation coppiced willow was assessed in two seasons (late spring and late summer) in 2011

NOVEL FEEDS IN ORGANIC DAIRY CHAINS

The objective of the current work was to collect information on various feeds and thus increase the awareness of various novel feeding solutions suitable for organic and low input dairying

The Anti-Inflammatory Effects of Lipoxygenase and Cyclo-Oxygenase Inhibitors in Inflammation-Induced Human Fetal Glia Cells and the Aβ Degradation Capacity of Human Fetal Astrocytes in an Ex vivo Assay

Chronic inflammation is a common phenomenon present in the background of multiple neurodegenerative diseases, including Alzheimer's disease (AD). The arachidonic acid pathway overproduces proinflammatory eicosanoids during these states and glial cells in the brain gradually lose their vital functions of protecting and supporting neurons. In this study, the role of different key enzymes of the eicosanoid pathway mediating inflammatory responses was examined in vitro and ex vivo using human fetal glial cells. Astrocytes and microglia were exposed to proinflammatory agents i.e., cytokines interleukin 1-beta (IL-1 beta) and tumor necrosis factor (TNF-alpha). ELISA assays were used to examine the effects of inhibitors of key enzymes in the eicosanoid pathway. Inhibitors for 5-lipoxygenase (5-LOX) and cyclo-oxygenase 2 (COX-2) in both cell types and 5-, 12-, and 15-LOX-inhibitor in astrocytes reduced significantly IL-6 secretion, compared to exposed glial cells without inhibitors. The cytokine antibody array showed that especially treatments with 5, -12, and -15 LOX inhibitor in astrocytes, 5-LOX inhibitor in microglia and COX-2 inhibitor in both glial cell types significantly reduced the expression of multiple proinflammatory cytokines. Furthermore, human fetal astrocytes and microglia were cultured on top of AD-affected and control human brain sections for 30h. According to the immunochemical evaluation of the level of total A beta, astrocytes were very efficient at degrading A beta from AD-affected brain sections ex vivo; simultaneously added enzyme inhibitors did not increase their A beta degradation capabilities. Microglia were not able to reduce the level of total A beta during the 30h incubation time

Insuliiniresistenssi, aivot ja muistisairausriski

Tyypin 2 diabetes ja siihen liittyvä insuliiniresistenssi ovat muistisairauden riskitekijöitä. Insuliiniresistenssi ennustaa tiedonkäsittelytoimintojen heikentymistä jo henkilöillä, joille ei vielä ole kehittynyt diabetesta. Insuliinilla on useita tärkeitä säätelytehtäviä keskushermostossa. Se vaikuttaa esimerkiksi synapsien toimintaan ja niiden pitkäkestoiseen vahvistumiseen. Insuliiniresistenssiin liittyvään hyperinsulinemiaan on puolestaan yhdistetty paradoksaalisesti keskushermoston pienentynyt insuliinipitoisuus. Alzheimerin tautia sairastavilla insuliinin vaste keskushermostossa on heikentynyt. Insuliinilla ja Alzheimerin taudille tyypillisellä beeta-amyloidilla on aivoissa yhteinen hajottajaentsyymi. Muutokset tämän entsyymin toiminnassa ja määrässä voivat vaikuttaa beeta-amyloidin kertymään aivoissa. Insuliiniresistenssi voi altistaa kognition heikentymiselle myös aivojen pienten suonten muutosten kautta. Insuliiniresistenssi voi siis vaikuttaa tiedonkäsittelytoimintoihin ja Alzheimerin taudin neuropatologiaan useita eri reittejä.</p

Association of Early Beta-amyloid Accumulation and Neuroinflammation Measured with [11C]PBR28 in Elderly Individuals Without Dementia

OBJECTIVE: To examine whether early β-amyloid (Aβ) accumulation and metabolic risk factors are associated with neuroinflammation in elderly individuals without dementia. METHODS: We examined 54 volunteers (mean age 70.0, 56% women, 51% APOE ε4 carriers) with a TSPO-tracer [11C]PBR28 to assess neuroinflammation and with [11C]Pittsburgh compound B (PiB) to assess cerebral Aβ accumulation. [11C]PBR28 and [11C]PiB standardized uptake value ratios (SUVRs) were quantified in six regions of interests by using the cerebellar cortex as a pseudo-reference/reference region, respectively. Fasting venous glucose, insulin, and high sensitivity C-reactive protein (hs-CRP) values were determined. Homeostatic model assessment of insulin resistance (HOMA-IR) was calculated. A subset of individuals (n=11) underwent CSF sampling, and Aβ40, Aβ42, total-tau, phospho-tau, soluble TREM2 and YKL-40 levels were measured. RESULTS: Among the whole study group, no significant association was found between [11C]PiB and [11C]PBR28 SUVR composite scores (slope 0.02, p=0.30). However, higher [11C]PiB binding was associated with higher [11C]PBR28 binding among amyloid negative ([11C]PiB composite score ≤1.5) (TSPO-genotype, age and sex adjusted slope 0.26, p=0.008) but not among amyloid positive participants (slope: -0.004, p=0.88). Higher CSF sTREM2 (rs 0.72, p=0.01) and YKL-40 (rs=0.63, p=0.04) concentrations were associated with a higher [11C]PBR28 composite score. Higher body mass index, HOMA-IR, and hs-CRP were associated with higher [11C]PBR28 binding in brain regions where Aβ accumulation is first detected in Alzheimer's disease (AD). CONCLUSIONS: While there was no association between amyloid and neuroinflammation in the overall study group, neuroinflammation was associated with amyloid among the subgroup at early stages of amyloid pathology

Limited Effects of Set Shifting Training in Healthy Older Adults

Our ability to flexibly shift between tasks or task sets declines in older age. As this decline may have adverse effects on everyday life of elderly people, it is of interest to study whether set shifting ability can be trained, and if training effects generalize to other cognitive tasks. Here, we report a randomized controlled trial where healthy older adults trained set shifting with three different set shifting tasks. The training group (n = 17) performed adaptive set shifting training for 5 weeks with three training sessions a week (45 min/session), while the active control group (n = 16) played three different computer games for the same period. Both groups underwent extensive pre-and post-testing and a 1-year follow-up. Compared to the controls, the training group showed significant improvements on the trained tasks. Evidence for near transfer in the training group was very limited, as it was seen only on overall accuracy on an untrained computerized set shifting task. No far transfer to other cognitive functions was observed. One year later, the training group was still better on the trained tasks but the single near transfer effect had vanished. The results suggest that computerized set shifting training in the elderly shows long-lasting effects on the trained tasks but very little benefit in terms of generalization

Monoacylglycerol lipase inhibitor JZL184 reduces neuroinflammatory response in APdE9 mice and in adult mouse glial cells

Conclusions: JZL184 decreased the proinflammatory reactions of microglia and reduced the total A beta burden and its precursors in the APdE9 mouse model. It also reduced the proinflammatory responses of microglia and astrocytes isolated from adult mice.</p

Midlife insulin resistance, APOE genotype, and late-life brain amyloid accumulation

ObjectiveTo examine whether midlife insulin resistance is an independent risk factor for brain amyloid accumulation in vivo after 15 years, and whether this risk is modulated by APOE epsilon 4 genotype.MethodsThis observational study examined 60 elderly volunteers without dementia (mean age at baseline 55.4 and at follow-up 70.9 years, 55.5% women) from the Finnish population-based, nationwide Health2000 study with [C-11]Pittsburgh compound B-PET imaging in 2014-2016. The participants were recruited according to their homeostatic model assessment of insulin resistance (HOMA-IR) values in the year 2000, and their APOE epsilon 4 genotype. The exposure group (IR+, n = 30) consisted of individuals with HOMA-IR > 2.17 at baseline (highest tertile of the Health2000 study population), and the control group (IR-, n = 30) consisted of individuals with HOMA-IR < 1.25 at baseline (lowest tertile). The groups were enriched for APOE epsilon 4 carriers, resulting in 50% (n = 15) APOE epsilon 4 carriers in both groups. Analyses were performed with multivariate logistic and linear regression.ResultsAn amyloid-positive PET scan was found in 33.3% of the IR-group and 60.0% of the IR+ group (odds ratio 3.0, 95% confidence interval 1.1-8.9, p = 0.04). The increased risk was seen in carriers and noncarriers of APOE epsilon 4 genotype. Higher midlife, but not late-life continuous HOMA-IR was associated with a greater brain amyloid burden at follow-up after multivariate adjustments for other cognitive and metabolic risk factors (ss = 0.11, 95% confidence interval 0.002-0.22, p = 0.04).ConclusionsThese results indicate that midlife insulin resistance is an independent risk factor for brain amyloid accumulation in elderly individuals without dementia

Insulin Resistance Predicts Cognitive Decline: An 11-Year Follow-up of a Nationally Representative Adult Population Sample

OBJECTIVEThe aim of this study was to examine whether insulin resistance, assessed by HOMA of insulin resistance (HOMA-IR), is an independent predictor of cognitive decline.RESEARCH DESIGN AND METHODSThe roles of HOMA-IR, fasting insulin and glucose, HbA(1c), and hs-CRP as predictors of cognitive performance and its change were evaluated in the Finnish nationwide, population-based Health 2000 Health Examination Survey and its 11-year follow-up, the Health 2011 study (n = 3,695, mean age at baseline 49.3 years, 55.5% women). Categorical verbal fluency, word-list learning, and word-list delayed recall were used as measures of cognitive function. Multivariate linear regression analysis was performed and adjusted for previously reported risk factors for cognitive decline.RESULTSHigher baseline HOMA-IR and fasting insulin levels were independent predictors of poorer verbal fluency performance (P = 0.0002 for both) and of a greater decline in verbal fluency during the follow-up time (P = 0.004 for both). Baseline HOMA-IR and insulin did not predict word-list learning or word-list delayed recall scores. There were no interactions between HOMA-IR and apolipoprotein E epsilon 4 (APOE epsilon 4) genotype, hs-CRP, or type 2 diabetes on the cognitive tests. Fasting glucose and hs-CRP levels at baseline were not associated with cognitive functioning.CONCLUSIONSOur results show that higher serum fasting insulin and insulin resistance predict poorer verbal fluency and a steeper decline in verbal fluency during 11 years in a representative sample of an adult population. Prevention and treatment of insulin resistance might help reduce cognitive decline later in life