22 research outputs found
Anthocyanin-rich extract from purple potatoes decreases postprandial glycemic response and affects inflammation markers in healthy men
Our recent clinical study suggested that polyphenol-rich purple potatoes lowered postprandial glycemia and insulinemia compared to yellow potatoes. Here, 17 healthy male volunteers consumed yellow potatoes with or without purple potato extract (PPE, extracted with water/ethanol/acetic acid) rich in acylated anthocyanins (152 mg) and other phenolics (140 mg) in a randomized cross-over trial. Ethanol-free PPE decreased the incremental area under the curve for glucose (p = 0.019) and insulin (p = 0.015) until 120 min after the meal, glucose at 20 min (p = 0.015) and 40 min (p = 0.004), and insulin at 20 min (p = 0.003), 40 min (p = 0.004) and 60 min (p = 0.005) after the meal. PPE affected some of the studied 90 inflammation markers after meal; for example insulin-like hormone FGF-19 levels were elevated at 240 min (p = 0.001). These results indicate that PPE alleviates postprandial glycemia and insulinemia, and affects postprandial inflammation.</p
Physical environments and community reintegration post-stroke : qualitative insights from stroke clubs
NF-E2-related factor 2 activation boosts antioxidant defenses and ameliorates inflammatory and amyloid properties in human Presenilin-1 mutated Alzheimer's disease astrocytes
Alzheimer's disease (AD) is a common dementia affecting a vast number of individuals and significantly impairing quality of life. Despite extensive research in animal models and numerous promising treatment trials, there is still no curative treatment for AD. Astrocytes, the most common cell type of the central nervous system, have been shown to play a role in the major AD pathologies, including accumulation of amyloid plaques, neuroinflammation, and oxidative stress. Here, we show that inflammatory stimulation leads to metabolic activation of human astrocytes and reduces amyloid secretion. On the other hand, the activation of oxidative metabolism leads to increased reactive oxygen species production especially in AD astrocytes. While healthy astrocytes increase glutathione (GSH) release to protect the cells, Presenilin‐1‐mutated AD patient astrocytes do not. Thus, chronic inflammation is likely to induce oxidative damage in AD astrocytes. Activation of NRF2, the major regulator of cellular antioxidant defenses, encoded by the NFE2L2 gene, poses several beneficial effects on AD astrocytes. We report here that the activation of NRF2 pathway reduces amyloid secretion, normalizes cytokine release, and increases GSH secretion in AD astrocytes. NRF2 induction also activates the metabolism of astrocytes and increases the utilization of glycolysis. Taken together, targeting NRF2 in astrocytes could be a potent therapeutic strategy in AD.</p
Co-morbidity and drug treatment in Alzheimer's disease. A cross sectional study of participants in the Dementia Study in Northern Norway
Inappropriate medical treatment of co-morbidities in Alzheimer’s disease (AD) is an increasing
concern in geriatric medicine. The objective of this study was to compare current drug use related to co-morbidity between individuals with a recent diagnosis of AD and a cognitively healthy control group in a population based
clinical trial in Northern Norway.
Setting: Nine rural municipalities with 70 000 inhabitants in Northern Norway. Participants: Participants with and without AD recruited in general practice and by population based screening. 187 participants with a recent diagnosis of AD were recruited among community dwellers. Of 791 respondents without cognitive symptoms, 500 were randomly selected and invited to further clinical and cognitive testing. The
final control group consisted of 200 cognitively healthy individuals from the same municipalities. Demographic characteristics, data on medical history and current medication were included, and a physical and cognitive examination was performed. The statistical analyses were carried out by independent sample t-test, chi-square,
ANCOVA and logistic regression.
A co-morbidity score was significantly higher in AD participants compared to controls. The mean number of drugs was higher for AD participants compared to controls (5.1 ± 3.6 and 2.9 ± 2.4 respectively, p < 0.001 age and gender adjusted), also when adjusted for co-morbidity. AD participants used significantly more anticholinergic, sedative and antidepressant drugs. For nursing home residents with AD the mean number of drugs was significantly higher compared to AD participants living at home (6.9 ± 3.9 and 4.5 ± 3.3, respectively, p < 0.001).
AD participants were treated with a significantly higher number of drugs as compared to cognitively
healthy controls, even after adjustment for co-morbidity. An inappropriate use of anticholinergic and sedative drugs was identified, especially among nursing home residents with AD. The drug burden and the increased risk of adverse reactions among individuals suffering from AD need more attention from prescribing doctors
Recruitment methods in Alzheimer's disease research: general practice versus population based screening by mail
<p>Abstract</p> <p>Background</p> <p>In Alzheimer's disease (AD) research patients are usually recruited from clinical practice, memory clinics or nursing homes. Lack of standardised inclusion and diagnostic criteria is a major concern in current AD studies. The aim of the study was to explore whether patient characteristics differ between study samples recruited from general practice and from a population based screening by mail within the same geographic areas in rural Northern Norway.</p> <p>Methods</p> <p>An interventional study in nine municipalities with 70000 inhabitants was designed. Patients were recruited from general practice or by population based screening of cognitive function by mail. We sent a questionnaire to 11807 individuals ≥ 65 years of age of whom 3767 responded. Among these, 438 individuals whose answers raised a suspicion of cognitive impairment were invited to an extended cognitive and clinical examination. Descriptive statistics, chi-square, independent sample t-test and analyses of covariance adjusted for possible confounders were used.</p> <p>Results</p> <p>The final study samples included 100 patients recruited by screening and 87 from general practice. Screening through mail recruited younger and more self-reliant male patients with a higher MMSE sum score, whereas older women with more severe cognitive impairment were recruited from general practice. Adjustment for age did not alter the statistically significant differences of cognitive function, self-reliance and gender distribution between patients recruited by screening and from general practice.</p> <p>Conclusions</p> <p>Different recruitment procedures of individuals with cognitive impairment provided study samples with different demographic characteristics. Initial cognitive screening by mail, preceding extended cognitive testing and clinical examination may be a suitable recruitment strategy in studies of early stage AD.</p> <p>Clinical Registration</p> <p>ClinicalTrial.gov Identifier: NCT00443014</p
A molecular-based identification resource for the arthropods of Finland
Publisher Copyright: © 2021 The Authors. Molecular Ecology Resources published by John Wiley & Sons Ltd.To associate specimens identified by molecular characters to other biological knowledge, we need reference sequences annotated by Linnaean taxonomy. In this study, we (1) report the creation of a comprehensive reference library of DNA barcodes for the arthropods of an entire country (Finland), (2) publish this library, and (3) deliver a new identification tool for insects and spiders, as based on this resource. The reference library contains mtDNA COI barcodes for 11,275 (43%) of 26,437 arthropod species known from Finland, including 10,811 (45%) of 23,956 insect species. To quantify the improvement in identification accuracy enabled by the current reference library, we ran 1000 Finnish insect and spider species through the Barcode of Life Data system (BOLD) identification engine. Of these, 91% were correctly assigned to a unique species when compared to the new reference library alone, 85% were correctly identified when compared to BOLD with the new material included, and 75% with the new material excluded. To capitalize on this resource, we used the new reference material to train a probabilistic taxonomic assignment tool, FinPROTAX, scoring high success. For the full-length barcode region, the accuracy of taxonomic assignments at the level of classes, orders, families, subfamilies, tribes, genera, and species reached 99.9%, 99.9%, 99.8%, 99.7%, 99.4%, 96.8%, and 88.5%, respectively. The FinBOL arthropod reference library and FinPROTAX are available through the Finnish Biodiversity Information Facility (www.laji.fi) at https://laji.fi/en/theme/protax. Overall, the FinBOL investment represents a massive capacity-transfer from the taxonomic community of Finland to all sectors of society.Peer reviewe
Association of Midlife Inflammatory Markers With Cognitive Performance at 10-Year Follow-up
NF-E2-related factor 2 activation boosts antioxidant defenses and ameliorates inflammatory and amyloid properties in human Presenilin-1 mutated Alzheimer's disease astrocytes
Alzheimer's disease (AD) is a common dementia affecting a vast number of individuals and significantly impairing quality of life. Despite extensive research in animal models and numerous promising treatment trials, there is still no curative treatment for AD. Astrocytes, the most common cell type of the central nervous system, have been shown to play a role in the major AD pathologies, including accumulation of amyloid plaques, neuroinflammation, and oxidative stress. Here, we show that inflammatory stimulation leads to metabolic activation of human astrocytes and reduces amyloid secretion. On the other hand, the activation of oxidative metabolism leads to increased reactive oxygen species production especially in AD astrocytes. While healthy astrocytes increase glutathione (GSH) release to protect the cells, Presenilin-1-mutated AD patient astrocytes do not. Thus, chronic inflammation is likely to induce oxidative damage in AD astrocytes. Activation of NRF2, the major regulator of cellular antioxidant defenses, encoded by the NFE2L2 gene, poses several beneficial effects on AD astrocytes. We report here that the activation of NRF2 pathway reduces amyloid secretion, normalizes cytokine release, and increases GSH secretion in AD astrocytes. NRF2 induction also activates the metabolism of astrocytes and increases the utilization of glycolysis. Taken together, targeting NRF2 in astrocytes could be a potent therapeutic strategy in AD.Peer reviewe
Postprandial response on fatty meal is affected by sea buckthorn (Hippophae rhamnoides) supplementation: NMR metabolomics study
Nuclear magnetic resonance fingerprinting (H-1 NMR) combined with different statistical tools was used to assess the effect of phenolics-rich sea buckthorn berries on postprandial plasma and urine after consumption of a fatty meal and to obtain information about the absorption and excretion of ethyl-O-beta-D-glucopyranoside and various inositols in sea buckthorn berries. Analyses of plasma samples indicated the delayed postprandial increase of lipid levels and the restrained increase of 3-hydroxy butanoic acid and N-acetyl glycoproteins when sea buckthorn meal was compared to control. The rise of acetic acid concentration and the occurrence of methyl-O-beta-D-glucopyranoside and ethyl-O-beta-D-glucopyranoside, but no inositols, were noticed after sea buckthorn meal in plasma. The methylglucoside was detected for the first time in plasma in relation to sea buckthorn containing diet, and the compound has subsequently been identified for the first time in sea buckthorn. Analyses of postprandial urine samples revealed a lower creatinine and dimethylamine concentrations and a higher hippuric acid concentration in urine after the berry meal when compared to the control. Excretion of the ethylglucoside in urine was detected after the sea buckthorn meal which indicates that this alkyl sugar is not efficiently metabolized by human body. (C) 2013 Elsevier Ltd. All rights reserved