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Träfflista för sökning "LAR1:gu ;pers:(Blennow Kaj 1958);pers:(Gustafson Deborah 1966)"

Sökning: LAR1:gu > Blennow Kaj 1958 > Gustafson Deborah 1966

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1.
  • Abramsson, Alexandra, 1973-, et al. (författare)
  • No association of LOXL1 gene polymorphisms with Alzheimer's disease.
  • 2011
  • Ingår i: Neuromolecular medicine. - 1559-1174. ; 13:2, s. 160-6
  • Tidskriftsartikel (refereegranskat)abstract
    • Aggregation of amyloid-beta is one of the major characteristics in brains of patients with Alzheimer's disease (AD). Although several mechanisms behind the formation of such aggregates have been suggested the regulatory factors are still unknown. The present study aimed at investigating the association of lysyl oxidase-like 1 (LOXL1) polymorphisms with AD diagnosis and cerebrospinal fluid biomarkers (CSF) for the disease. Proteins of the lysyl oxidase (LOX) family are involved in cross-linking extracellular matrix proteins to insoluble fibers and have been associated with neurodegenerative diseases including AD. Genetic polymorphisms in LOXL1 (rs1048661, rs3825942, and rs2165241) have been linked to exfoliation syndrome and exfoliation glaucoma, conditions that have shown association with AD. The polymorphisms were genotyped by Taqman allelic discrimination in a study sample including AD patients (n = 318) and controls (n = 575). In a subgroup of the population, the polymorphisms were analyzed in relation to APOE epsilon 4 genotype and to CSF (T-tau, P-tau, and A beta(1-42)). No evidence for associations of these polymorphisms with risk for AD or any of the studied CSF biomarkers measured was found. These results do not support LOXL1 as being a major risk gene for AD.
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3.
  • Bäckman, Kristoffer, 1979-, et al. (författare)
  • 37 years of body mass index and dementia: observations from the prospective population study of women in Gothenburg, Sweden.
  • 2012
  • Ingår i: Journal of Alzheimer's disease : JAD. - 1875-8908. ; 28:1, s. 163-71
  • Tidskriftsartikel (refereegranskat)abstract
    • Level of adiposity is linked to dementia in epidemiological studies. Overweight and obesity in mid- and late-life may increase risk for dementia, whereas decline in body weight or body mass index (BMI) and underweight in years preceding and at the time of a dementia diagnosis may also relate to dementia. Longitudinal studies with sufficient follow-up are necessary to estimate trajectories that allow better understanding of the relationship between adiposity indices and dementia over the life course. We evaluated the natural history of BMI in relationship to clinical dementia over 37 years in the Prospective Population Study of Women (PPSW) in Sweden. PPSW is a systematic sample of 1462 women born 1908, 1914, 1918, 1922, and 1930 and aged 38-60 years at baseline. Examinations occurred in 1968, 1974, 1980, 1992, 2000, and 2005. Statistical analyses were conducted using mixed effects regression models. Trajectories of BMI over 37 years as a function of age differed between women who did versus did not develop dementia. Women developing dementia evidenced a lesser increase in BMI from age 38 to 70 years. After age 70, the BMI slope decreased similarly (no "accelerated decline") irrespective of dementia status. A lower BMI before and during dementia onset was observed. Women with similar BMI at mid-life exhibited a different pattern of BMI change as they approached late-life that was related to dementia onset. BMI may be a potential marker of dementia-related neuropathologies in the brain. Dementia is related to a common risk factor, BMI, from mid-to late-life.
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4.
  • Daborg, Jonny, et al. (författare)
  • Association of the RAGE G82S polymorphism with Alzheimer's disease
  • 2010
  • Ingår i: Journal of Neural Transmission. - 0300-9564. ; 117:7, s. 861-867
  • Tidskriftsartikel (refereegranskat)abstract
    • The receptor for advanced glycation end-products (RAGE) has been implicated in several pathophysiological processes relevant to Alzheimer's disease (AD), including transport and synaptotoxicity of AD-associated amyloid beta (A beta) peptides. A recent Chinese study (Li et al. in J Neural Transm 117:97-104, 2010) suggested an association between the 82S allele of the functional single nucleotide polymorphism (SNP) G82S (rs2070600) in the RAGE-encoding gene AGER and risk of AD. The present study aimed to investigate associations between AGER, AD diagnosis, cognitive scores and cerebrospinal fluid AD biomarkers in a European cohort of 316 neurochemically verified AD cases and 579 controls. Aside from G82S, three additional tag SNPs were analyzed to cover the common genetic variation in AGER. The 82S allele was associated with increased risk of AD (P (c) = 0.04, OR = 2.0, 95% CI 1.2-3.4). There was no genetic interaction between AGER 82S and APOE epsilon 4 in producing increased risk of AD (P = 0.4), and none of the AGER SNPs showed association with A beta(42), T-tau, P-tau(181) or mini-mental state examination scores. The data speak for a weak, but significant effect of AGER on risk of AD.
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5.
  • Gudmundsson, Pia, 1978-, et al. (författare)
  • Is there a CSF biomarker profile related to depression in elderly women?
  • 2010
  • Ingår i: Psychiatry Research. - 0165-1781. ; 176:2-3, s. 174-178
  • Tidskriftsartikel (refereegranskat)abstract
    • In light of our previous observation of higher levels of cerebrospinal fluid (CSF) amyloid beta-42 (Aβ42) and CSF/serum albumin ratio in major depressive disorder (MDD), we analyzed two additional CSF biomarkers reflecting neurodegeneration—neurofilament protein light (NFL) and glial fibrillary acidic protein (GFAp)—in relationship to prevalent geriatric depression. Neuropsychiatric, physical, and lumbar puncture examinations, with DSM-III-R-based depression diagnoses and measurement of CSF levels of NFL and GFAp, were evaluated among a population-based sample of 78 elderly women (mean age, 73.9±3.2 years) without dementia for at least 10 years after CSF collection. Eleven (13.1%) women had MDD, and higher levels of NFL compared with women without depression. A multivariate model including age, NFL, Aβ42 and the CSF/serum albumin ratio showed that each biomarker was independently and positively associated with MDD, and that this biomarker profile explained more variation in the model compared with single or combined biomarkers. A CSF profile with higher levels of NFL, Aβ42, and CSF/serum albumin ratio may indicate neuropathological and vascular events in depression etiology. This contrasts with the well-characterized pattern of low Aβ42, higher CSF/serum albumin ratio, and higher NFL in Alzheimer's disease.
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6.
  • Gudmundsson, Pia, 1978-, et al. (författare)
  • The relationship between cerebrospinal fluid biomarkers and depression in elderly women.
  • 2007
  • Ingår i: The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry. - 1064-7481. ; 15:10, s. 832-8
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Cerebrospinal fluid (CSF) biomarkers including the 42 amino-acid form of beta-amyloid (Abeta42), total tau protein (T-tau), and the CSF/serum albumin ratio are markers of brain pathology and metabolism. Abeta42 and T-tau are sometimes used to discriminate geriatric depression from mild forms of Alzheimer disease (AD) in clinical studies. However, studies focusing on the relationship between these CSF biomarkers and geriatric depression are lacking. METHODS: This was a cross-sectional study with a population-based sample of 84 nondemented elderly women in Sweden. Measurements included neuropsychiatric, physical, and lumbar puncture examinations, with Diagnostic and Statistical Manual of Mental Disorders, Third Revision-based depression diagnoses and measurement of CSF levels of Abeta42, T-tau, albumin, and serum albumin. RESULTS: Fourteen women (mean age: 72.6 years) had any depression (11 with major depressive disorder [MDD]). Compared to women without depression, women with MDD had higher levels of Abeta42 and the CSF/serum albumin ratio. The CSF/serum albumin ratio was also higher in women with any depression. No differences in T-tau were observed; however, T-tau increased with age. CONCLUSION: Higher levels of CSF Abeta42 were observed among elderly depressed women, in contrast to lower levels usually observed in AD, indicating potential neuropathological differences between the two disorders. Higher CSF/serum albumin ratios observed in depressed women point to potential vascular processes.
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8.
  • Gustafson, Deborah, 1966-, et al. (författare)
  • Cerebrospinal fluid beta-amyloid 1-42 concentration may predict cognitive decline in older women.
  • 2007
  • Ingår i: Journal of neurology, neurosurgery, and psychiatry. - 1468-330X. ; 78:5, s. 461-4
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Low levels of cerebrospinal fluid (CSF) beta-amyloid 1-42 (Abeta42) and high total tau (T-tau) are diagnostic for manifest Alzheimer's disease. It is not known, however, whether these biomarkers may be risk indicators for cognitive decline in otherwise healthy older people. METHODS: The longitudinal relationship between CSF markers, Abeta42 and T-tau, measured in 1992, and change in Mini-Mental State Examination (deltaMMSE) score between 1992 and 2002 were investigated in 55 women (aged 70-84 years, mean (SD) MMSE score = 28.3 (1.5)), who were participants in the Prospective Population Study of Women in Gothenburg, Sweden. These women did not have dementia when they experienced lumbar puncture in 1992-3. RESULTS: Over the 8-year follow-up period, deltaMMSE (range = +3 to -21 points) was correlated with Abeta42 (Spearman's r = 0.40, p = 0.002), such that lower levels of Abeta42 were related to greater decline. This was also observed after excluding 4 women who developed dementia between 1992 and 2002 (Spearman's r = 0.34, p = 0.019). A multivariate logistic regression model predicting a decline of > or = 5 points on the MMSE (observed in six women), or a risk of developing dementia over the 8-year follow-up period (observed in four women), including age, education, Abeta42 and T-tau as covariates, showed that Abeta42 was the sole predictor of significant cognitive decline or dementia (OR per 100 pg/ml Abeta42 = 2.24, 95% CI 1.19 to 4.22, p = 0.013). CONCLUSIONS: Low levels of CSF Abeta42 may predict cognitive decline among older women without dementia.
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9.
  • 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)
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10.
  • 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. - 1365-2796. ; 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.
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