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- Lehtisalo, J., et al.
(författare)
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Association of long-term dietary fat intake, exercise, and weight with later cognitive function in the Finnish Diabetes Prevention Study
- 2016
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Ingår i: The Journal of Nutrition, Health & Aging. - : Springer Science and Business Media LLC. - 1279-7707 .- 1760-4788. ; 20:2, s. 146-154
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Tidskriftsartikel (refereegranskat)abstract
- Objectives: To investigate associations of long-term nutrient intake, physical activity and obesity with later cognitive function among the participants in the Finnish Diabetes Prevention Study, in which a lifestyle intervention was successful in diabetes prevention. Design: An active lifestyle intervention phase during middle age (mean duration 4 years) and extended follow-up (additional 9 years) with annual lifestyle measurements, followed by an ancillary cognition assessment. Setting: 5 research centers in Finland. Participants: Of the 522 middle-aged, overweight participants with impaired glucose tolerance recruited to the study, 364 (70%) participated in the cognition assessment (mean age 68 years). Measurements: A cognitive assessment was executed with the CERAD test battery and the Trail Making Test A on average 13 years after baseline. Lifestyle measurements included annual clinical measurements, food records, and exercise questionnaires during both the intervention and follow-up phase. Results: Lower intake of total fat (p=0.021) and saturated fatty acids (p=0.010), and frequent physical activity (p=0.040) during the whole study period were associated with better cognitive performance. Higher BMI (p= 0.012) and waist circumference (p= 0.012) were also associated with worse performance, but weight reduction prior to the cognition assessment predicted worse performance as well (decrease vs. increase, p= 0.008 for BMI and p= 0.002 for waist). Conclusions: Long-term dietary fat intake, BMI, and waist circumference have an inverse association with cognitive function in later life among people with IGT. However, decreases in BMI and waist prior to cognitive assessment are associated with worse cognitive performance, which could be explained by reverse causality.
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| 4. |
- Andrieu, S, et al.
(författare)
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IAGG Workshop: Health promotion program on prevention of late onset dementia
- 2011
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Ingår i: Journal of nutrition healt & aging. - 1279-7707. ; 15:7, s. 562-575
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Tidskriftsartikel (refereegranskat)abstract
- IAGG, WHO, and SFGG organized a international workshop on Health promotion programs on prevention of late on-set dementia. Thirty world specialists coming from Europe, North America, Asia, South America, Africa and Australia, shared their experience on methods and results of large epidemiological interventions to reduce incidents of dementia or delay its on-set. Chaired by Laura FRATIGLIONI, an expert in Epidemiological studies on dementia issues, the workshop gave opportunity for discussions and controversies about the state-of-the-art. Based on different national and international trials (ADAPT, MAPT, FINGER, GUDIAGE, GEM etc) the questions remained opened for different aspects of methodology, the choice of domain or multi domain intervention, the choice and the definition of the target populations, the best age of candidates, the issues related to the discrepancy between late effects, and interventions' duration. We are please to publish in the Journal, the presentations presented to this workshop. These publications will complete previously task force published in the journal in the last two years on methodological issues for Alzheimer's trials including end point, biomarkers, and the experience of past therapeutic trials.
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| 6. |
- Gustafson, Deborah, 1966, et al.
(författare)
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High adiposity: Risk factor for dementia and Alzheimer's disease?
- 2013
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Ingår i: Alzheimer's Research and Therapy. - : Springer Science and Business Media LLC. - 1758-9193. ; 5:6
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Tidskriftsartikel (refereegranskat)abstract
- Higher levels of total and central adiposity, measured as higher body mass index (BMI) (in kilograms per square meter), waist circumference, or waist-to-hip ratio, have been associated with late-onset Alzheimer's disease (AD). However, some epidemiologic studies do not support this association, and potential underlying biological mechanisms that provide biological plausibility are not clear in terms of providing direct links to adipose tissue. Studies linking adiposity to AD have considered adiposity measures from mid-life and late-life. Given an evolving background trajectory of BMI that exists over the life course and the influence of dementia processes on BMI, results have been conflicting depending on when BMI is measured in relationship to clinical AD onset. This has made interpretation of the BMI-AD literature difficult. This debate will briefly review the epidemiologic evidence for and against an association between higher adiposity and AD, issues of timing of the adiposity measure in relation to AD onset, potential biological mechanisms for observed associations, and explanations for conflicting evidence. © 2013 BioMed Central Ltd.
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| 7. |
- Luchsinger, J. A., et al.
(författare)
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Tracking the potential involvement of metabolic disease in Alzheimer's disease—Biomarkers and beyond
- 2020
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Ingår i: International Review of Neurobiology. Vol. 154. - : Elsevier. - 0074-7742. - 9780128200766 ; , s. 51-77
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Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- There is a vast literature linking systemic metabolic conditions to dementia due to Alzheimer's disease (AD). Advances in in vivo measurements of AD neuropathology using brain imaging, cerebrospinal fluid (CSF), and/or blood biomarkers have led to research in AD that uses in vivo biomarkers as outcomes, focusing primarily on amyloid, tau, and neurodegeneration as constructs. Studies of Type 2 Diabetes Mellitus (T2DM) and AD biomarkers seem to show that T2DM is not related to amyloid deposition, but is related to neurodegeneration and tau deposition. There is a dearth of studies examining adiposity, insulin resistance, and metabolic syndrome in relation to AD biomarkers and the associations in these studies are inconsistent. Metabolomics studies have reported associations of unsaturated fatty acids with AD neuropathology at autopsy, and sphingolipids and glycerophospholipids in relation to neurodegeneration and amyloid and tau. There are other neurodegenerative diseases, such as Lewy body disease that may overlap with AD, and specific biomarkers for these pathologies are being developed and should be integrated into AD biomarker research. More longitudinal studies are needed with concurrent assessment of metabolic factors and AD biomarkers in order to improve the opportunity to assess causality. Ideally, AD biomarkers should be integrated into clinical trials of interventions that affect metabolic factors. Advances in blood-based AD biomarkers, which are less costly and invasive compared with CSF and brain imaging biomarkers, could facilitate widespread implementation of AD biomarkers in studies examining the metabolic contribution to AD. © 2020 Elsevier Inc.
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