SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "LAR1:gu ;pers:(Gustafson Deborah 1966);lar1:(gu)"

Sökning: LAR1:gu > Gustafson Deborah 1966 > Göteborgs universitet

  • Resultat 41-50 av 102
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
41.
  • Gustafson, Deborah, 1966, et al. (författare)
  • CSF Biomarkers for Alzheimer’s Disease
  • 2006
  • Ingår i: Research advances in Alzheimer’s disease and related disorders. Vol 11. Eds. Iqbal K, Winblad B. Alzheimer’s Association. ; , s. 1-6
  • Konferensbidrag (refereegranskat)
  •  
42.
  • Gustafson, Deborah, 1966, et al. (författare)
  • Dietary fatty acids and risk of Alzheimer's disease and related dementias: Observations from the Washington Heights-Hamilton Heights-Inwood Columbia Aging Project (WHICAP)
  • 2020
  • Ingår i: Alzheimer's and Dementia. - : Wiley. - 1552-5260 .- 1552-5279. ; 16:12, s. 1638-1649
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: High dietary intake of long chain, polyunsaturated fatty acids is associated with lower Alzheimer's disease (AD) risk. Methods: Washington Heights-Hamilton Heights-Inwood Columbia Aging Project is a multiethnic, prospective observational study of aging and dementia among elderly (≥ 65 years). Dietary intake was measured using a food frequency questionnaire. Dietary short-, medium-, and long-chain fatty acid intakes were categorized by number of carbons and double bonds. Consensus AD diagnoses were made. Associations between AD risk and dietary fatty acid and cholesterol intakes were estimated using multivariable Cox proportional hazards regression models. Results: Of 2612 multiethnic women (67%) and men (baseline age 76.3 [6.4] years), 380 developed AD over an average 4.5 years follow-up. Lower risk of AD was associated with increasing intakes of docosahexaenoic acid (DHA; hazard ratio [HR] = 0.73, 95% confidence interval [CI]: 0.57 to 0.95, P = 0.018) and eicosapentaenoic acid (EPA; HR = 0.74, 95% CI: 0.57 to 0.95, P = 0.021), and longer AD-free survival (P < 0.05). Discussion: Higher intake of DHA and EPA are protective for AD. © 2020 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association
  •  
43.
  • Gustafson, Deborah, 1966, et al. (författare)
  • High adiposity: Risk factor for dementia and Alzheimer's disease?
  • 2013
  • Ingår i: Alzheimer's Research and Therapy. - : Springer Science and Business Media LLC. - 1758-9193. ; 5:6
  • 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.
  •  
44.
  • Gustafson, Deborah, 1966, et al. (författare)
  • Leptin and dementia over 32 years-The Prospective Population Study of Women
  • 2012
  • Ingår i: Alzheimers & Dementia. - : Wiley. - 1552-5260 .- 1552-5279. ; 8:4, s. 272-277
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: We have shown that high mid-life central adiposity may increase the risk for dementia after 32 years. Leptin, an adipose tissue hormone, is correlated with adiposity measures and may contribute to a better etiological understanding of the relationship between high adiposity and dementia. We explored the relationship between serum leptin in mid-life and dementia, which is a late-life outcome. Methods: A longitudinal cohort study, the Prospective Population Study of Women, in Gothenburg, Sweden, includes a representative sample of 1462 women followed from mid-life ages of 38 to 60 years to late-life ages of 70 to 92 years. Women were examined in 1968, 1974, 1980, 1992, and 2000 using neuropsychiatric, anthropometric, clinical, and other measurements. Serum leptin was measured on samples collected at the 1968 baseline examination, after storage at -20 degrees C for 29 years. Cox proportional hazards regression models estimated incident dementia risk by baseline leptin. Logistic regression models related leptin levels to dementia among surviving participants 32 years later. All models were adjusted for multiple potential confounders. Results: Mid-life leptin was not related to dementia risk using Cox or logistic regression models. This was observed despite positive baseline correlations between leptin and adiposity measures, and given our previous report of high mid-life waist-to-hip ratio being related to a twofold higher dementia risk. Conclusions: Leptin is not a mid-life marker of late-life dementia risk in this population sample of Swedish women born between 1908 and 1930. (C) 2012 The Alzheimer's Association. All rights reserved.
  •  
45.
  • Gustafson, Deborah, 1966, et al. (författare)
  • Mid-life adiposity factors relate to blood-brain barrier integrity in late life.
  • 2007
  • Ingår i: Journal of internal medicine. - : Wiley. - 1365-2796 .- 0954-6820. ; 262:6, s. 643-50
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: We explored the relationship between adiposity factors measured during mid-life and blood-brain barrier (BBB) integrity measured via the cerebrospinal fluid/serum (CSF/S) albumin ratio in late life. Adiposity factors included body mass index and blood levels of sex hormone binding globulin (SHBG) and leptin. Design. Retrospective analyses over 24 years within a longitudinal study. SETTING: Population-based sample. Subjects. Eighty-one women. MAIN OUTCOME MEASURES: CSF/S albumin ratio. RESULTS: The CSF/S albumin ratio measured at age 70-84 years was higher amongst women who were overweight or obese (6.50 +/- 2.79 vs. 5.23 +/- 1.61, age-adjusted P = 0.012), and was inversely correlated with SHBG (age-adjusted r = -0.321, P < 0.005) at age 46-60 years. In stepwise regression models, SHBG predicted the CSF/S albumin ratio (beta = -0.017, R2 = 0.107, P = 0.007). The best model (R2 = 0.187) predicting CSF/S albumin ratio included SHBG, age group (age 46 years versus >46), overweight or obesity, and an age group by SHBG interaction. CONCLUSIONS: Lower levels of SHBG in mid-life were related to worse BBB integrity in women after 24 years in late life, even considering other adiposity factors. SHBG may be important for understanding sex hormone-mediated mechanisms in brain health or as an independent marker of adipose tissue, the largest endocrine organ.
  •  
46.
  • Gustafson, Deborah, 1966, et al. (författare)
  • New Perspectives on Alzheimer's Disease and Nutrition
  • 2015
  • Ingår i: Journal of Alzheimers Disease. - : IOS Press. - 1387-2877 .- 1875-8908. ; 46:4, s. 1111-1127
  • Tidskriftsartikel (refereegranskat)abstract
    • Accumulating evidence shows nutritional factors influence the risk of developing Alzheimer's disease (AD) and its rate of clinical progression. Dietary and lifestyle guidelines to help adults reduce their risk have been developed. However, the clinical dementia picture remains complex, and further evidence is required to demonstrate that modifying nutritional status can protect the brain and prevent, delay, or reduce pathophysiological consequences of AD. Moreover, there is a pressing need for further research because of the global epidemic of overweight and obesity combined with longer life expectancy of the general population and generally observed decreases in body weight with aging and AD. A new research approach is needed, incorporating more sophisticated models to account for complex scenarios influencing the relationship between nutritional status and AD. Systematic research should identify and address evidence gaps. Integrating longitudinal epidemiological data with biomarkers of disease, including brain imaging technology, and randomized controlled interventions may provide greater insights into progressive and subtle neurological changes associated with dietary factors in individuals at risk for or living with AD. In addition, greater understanding of mechanisms involved in nutritional influences on AD risk and progression, such as oxidative stress and loss of neuronal membrane integrity, will better inform possible interventional strategies. There is consensus among the authors that nutritional deficits, and even states of excess, are associated with AD, but more work is needed to determine cause and effect. Appropriately designed diets or nutritional interventions may play a role, but additional research is needed on their clinical-cognitive effectiveness.
  •  
47.
  • Gustafson, Deborah, 1966 (författare)
  • Obesity and intelligence
  • 2006
  • Ingår i: AGRO FOOD INDUSTRY HI-TECH. - 1722-6996. ; 17:5, s. XXXI-XXXIV
  • Tidskriftsartikel (refereegranskat)
  •  
48.
  • Gustafson, Deborah, 1966, et al. (författare)
  • The ACE Insertion Deletion polymorphism relates to dementia by metabolic phenotype, APOEepsilon4, and age of dementia onset.
  • 2010
  • Ingår i: Neurobiology of aging. - : Elsevier BV. - 1558-1497 .- 0197-4580. ; 31:6, s. 910-6
  • Tidskriftsartikel (refereegranskat)abstract
    • The renin-angiotensin system (RAS) may play a role in dementia pathogenesis because of its effects on vascular and metabolic homeostasis, amyloid metabolism, and learning and memory. The angiotensin-converting enzyme (ACE), a pivotal RAS protein, is encoded for by a gene containing a functional ID variant, which has been related to dementia risk. We examined the relationship between the ACE Insertion Deletion (ACE ID) variant and dementia with consideration for metabolic phenotypes, age and APOEepsilon4 using a population-based, cross-sectional sample of 891 Swedish women and men aged 70-92 years, of whom 61 people were demented. The odds of dementia was two-fold higher among those with ACE II genotype, and ranged from 2.18 to 4.35 among those with dementia onset
  •  
49.
  • Haast, Roy A.M., et al. (författare)
  • Sex differences in stroke
  • 2012
  • Ingår i: Journal of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 0271-678X .- 1559-7016. ; 32:12, s. 2100-2107
  • Tidskriftsartikel (refereegranskat)abstract
    • Sex differences in stroke are observed across epidemiologic studies, pathophysiology, treatments, and outcomes. These sex differences have profound implications for effective prevention and treatment and are the focus of this review. Epidemiologic studies reveal a clear age-by-sex interaction in stroke prevalence, incidence, and mortality. While premenopausal women experience fewer strokes than men of comparable age, stroke rates increase among postmenopausal women compared with age-matched men. This postmenopausal phenomenon, in combination with living longer, are reasons for women being older at stroke onset and suffering more severe strokes. Thus, a primary focus of stroke prevention has been based on sex steroid hormone-dependent mechanisms. Sex hormones affect different (patho)physiologic functions of the cerebral circulation. Clarifying the impact of sex hormones on cerebral vasculature using suitable animal models is essential to elucidate male–female differences in stroke pathophysiology and development of sex-specific treatments. Much remains to be learned about sex differences in stroke as anatomic and genetic factors may also contribute, revealing its multifactorial nature. In addition, the aftermath of stroke appears to be more adverse in women than in men, again based on older age at stroke onset, longer prehospital delays, and potentially, differences in treatment.
  •  
50.
  • Hansson, Oskar, et al. (författare)
  • Evaluation of Plasma A beta as Predictor of Alzheimer's Disease in Older Individuals Without Dementia: A Population-Based Study
  • 2012
  • Ingår i: Journal of Alzheimer's Disease. - 1387-2877 .- 1875-8908. ; 28:1, s. 231-238
  • Tidskriftsartikel (refereegranskat)abstract
    • Amyloid-beta (A beta) pathology is a major component in the mechanisms behind Alzheimer's disease (AD). Measurement of A beta(42) in cerebrospinal fluid predicts cognitive decline in patients with mild cognitive impairment and identifies AD in patients with dementia. However, studies on A beta in plasma are contradictory. In this prospective population-based study, plasma A beta(42) and A beta(40) were measured at baseline in 730 adults aged 70 years or older and without dementia. After five years, plasma levels were analyzed again and participants were assessed for development of dementia. During follow-up, 53 individuals (7%) developed dementia of which 37 (5%) were classified as AD. No difference in baseline plasma A beta(42), A beta(40), or A beta(42)/A beta(40) ratio levels were observed between converters to dementia or AD compared to the cognitively stable individuals. However, individuals with plasma A beta(40) levels above the median level for the group at baseline had an increased risk of developing dementia and AD during the follow-up, even after adjustment for age, gender, APOE genotype, and educational level (odds ratio = 2.2, 95% confidence interval = 1.0-4.7, p < 0.05). Neither plasma A beta(42) nor the A beta(42)/A beta(40) ratio influenced the risk of developing dementia or AD. Moreover, A beta(42) and A beta(40) levels increased over the 5 years, whereas the A beta(42)/A beta(40) ratio decreased (p < 0.001). In conclusion, this study suggests that measurement of plasma A beta should not be used clinically to predict dementia or AD. However, plasma A beta(40) may possibly be regarded as a moderate risk marker comparable to other risk markers for AD such as first-degree family history of dementia.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 41-50 av 102
Typ av publikation
tidskriftsartikel (93)
forskningsöversikt (4)
bokkapitel (3)
konferensbidrag (2)
Typ av innehåll
refereegranskat (98)
övrigt vetenskapligt/konstnärligt (4)
Författare/redaktör
Skoog, Ingmar, 1954 (56)
Waern, Margda, 1955 (28)
Östling, Svante, 195 ... (28)
Blennow, Kaj, 1958 (18)
Zetterberg, Henrik, ... (10)
visa fler...
Lissner, Lauren, 195 ... (9)
Bengtsson, Calle, 19 ... (8)
Björkelund, Cecilia, ... (7)
Börjesson-Hanson, An ... (6)
Rosengren, Lars, 195 ... (6)
Sigström, Robert, 19 ... (5)
Sjögren, Magnus (5)
Karlsson, Björn (4)
Arnoldussen, I. A. C ... (4)
Minthon, Lennart (3)
Janson, Per-Olof, 19 ... (3)
Sevlever, G. (3)
Eriksson, Elias, 195 ... (3)
Albani, D (3)
Ongaro, F (3)
Antuono, P (3)
Caberlotto, L (3)
Zanardo, A (3)
Siculi, M (3)
Gallucci, M (3)
Stener-Victorin, Eli ... (3)
Thorvaldsson, Valgei ... (3)
Joas, Erik, 1983 (3)
Zandi, Peter P (3)
Johansson, Boo (3)
Wallin, Anders, 1950 (2)
Landén, Mikael, 1966 (2)
Landgren, Sara, 1980 (2)
Zetterberg, Madelein ... (2)
Palmer, Mona Seibt (2)
Kivipelto, Miia (2)
Mehlig, Kirsten, 196 ... (2)
Fratiglioni, Laura (2)
Kern, Silke (2)
Johansson, Lena, 197 ... (2)
Mazzuco, S (2)
Thelle, Dag, 1942 (2)
Steen, Bertil, 1938 (2)
Anastos, K (2)
Sundh, Valter, 1950 (2)
Hällström, Tore, 193 ... (2)
Holm, Göran, 1942 (2)
Yaffe, K (2)
Cohen, M. (2)
visa färre...
Lärosäte
Karolinska Institutet (8)
Lunds universitet (3)
Stockholms universitet (2)
Högskolan i Skövde (2)
Umeå universitet (1)
visa fler...
Chalmers tekniska högskola (1)
visa färre...
Språk
Engelska (102)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (94)
Samhällsvetenskap (4)
Naturvetenskap (1)
Teknik (1)
Lantbruksvetenskap (1)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy