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Sökning: WFRF:(Börjesson Hanson Anne)

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1.
  • Abdullah, Laila, et al. (författare)
  • The Influence of Baseline Alzheimer's Disease Severity on Cognitive Decline and CSF Biomarkers in the NILVAD Trial.
  • 2020
  • Ingår i: Frontiers in neurology. - : Frontiers Media SA. - 1664-2295. ; 11
  • Tidskriftsartikel (refereegranskat)abstract
    • We examined the effects of a dihydropyridine calcium channel blocker nilvadipine with anti-inflammatory properties on cognition and cerebrospinal fluid (CSF) biomarkers by baseline Alzheimer's disease (AD) severity. Exploratory analyses were performed on the dataset (n = 497) of a phase III randomized placebo-controlled trial to examine the response to nilvadipine in AD subjects stratified by baseline AD severity into very mild (MMSE ≥ 25), mild (MMSE 20-24) and moderate AD (MMSE < 20). The outcome measures included total and subscale scores of the Alzheimer's Disease Assessment Scale Cognitive 12 (ADAS-Cog 12), the Clinical Dementia Rating Scale sum of boxes (CDR-sb) and the AD composite score (ADCOMS). Cerebrospinal fluid biomarkers Aβ38, Aβ40, Aβ42, neurofilament light chain (NFL), neurogranin, YKL-40, total tau and P181 tau (ptau) were measured in a subset of samples (n = 55). Regression analyses were adjusted for confounders to specifically examine the influence of nilvadipine and baseline AD severity on cognitive outcomes over 78-weeks. Compared to their respective placebo-controls, nilvadipine-treated, very mild AD subjects showed less decline, whereas moderate AD subjects showed a greater cognitive decline on the ADAS-Cog 12 test and the ADCOMS. A lower decline was observed after nilvadipine treatment for a composite memory trait in very mild AD subjects and a composite language trait in mild AD subjects. Cerebrospinal fluid Aβ42/Aβ40 ratios were increased in mild AD and decreased in moderate AD patients treated with nilvadipine, compared to their respective controls. Among moderate AD subjects, levels of ptau, total tau, neurogranin and YKL-40 increased in subjects treated with nilvadipine compared to placebo. These studies suggest that baseline AD severity influenced the treatment outcome in the NILVAD trial and that future clinical trials of nilvadipine should be restricted to mild and very mild AD patients. Trial Registration: NCT02017340 Registered 20 December 2013, https://clinicaltrials.gov/ct2/show/NCT02017340 EUDRACT Reference Number 2012-002764-27 Registered 04 February 2013, https://www.clinicaltrialsregister.eu/ctr-search/search?query=2012-002764-27.
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2.
  • Bjerke, Maria, 1977, et al. (författare)
  • Cerebrospinal Fluid Fatty Acid-Binding Protein 3 is Related to Dementia Development in a Population-Based Sample of Older Adult Women Followed for 8 Years.
  • 2016
  • Ingår i: Journal of Alzheimer's disease : JAD. - 1875-8908. ; 49:3, s. 733-741
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Increased fatty acid-binding protein 3 (FABP-3) levels have been reported in neurodegenerative diseases, including Alzheimer's disease (AD). Cerebrospinal fluid (CSF) FABP-3 has therefore been proposed as a putative marker for dementia. Population-based studies examining whether CSF FABP-3 predicts later development of dementia are lacking. OBJECTIVE: The aim of this study was to examine CSF levels of FABP-3 in relation to later development of dementia in elderly women and in relation to Aβ42, T-tau, P-tau181, and CSF: serum albumin ratio. METHODS: 86 non-demented women aged 70-84 years who participated in the Prospective Population Study of Women in Gothenburg, Sweden took part in a lumbar puncture in 1992-93. CSF-FABP-3, Aβ42, T-tau, P-tau181, and the CSF: serum albumin ratio were measured at baseline. Participants were examined with a neuropsychiatric exam at baseline and at follow-up in 2000. Dementia was diagnosed in accordance with DSM-III-R criteria. RESULTS: Between 1992 and 2000, 8 women developed dementia (4 AD, 3 vascular dementia, 1 mixed vascular dementia and AD). Higher levels of CSF-FABP-3 at baseline were related to development of dementia (OR 1.36 CI [1.05-1.76] p = 0.022) and the subtype AD (OR 1.38 CI [1.06-1.82), p = 0.019) during follow-up. FABP-3 correlated with CSF T-tau (r = 0.88, p <  0.001), P-tau181 (r = 0.619, p <  0.001), and CSF:serum albumin ratio (r = 0.233, p = 0.031), but not with Aβ42 (r = -0.08, p = 0.444)Conclusion: CSF FABP-3 may be an early marker for later development of dementia, probably related to neuronal degeneration, but independent of Aβ metabolism.
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3.
  • Börjesson-Hanson, Anne, 1959 (författare)
  • Dementia and other mental disorders among 95-year olds
  • 2008
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • The aims of this study were to estimate the prevalence of mental disorders and age related differences in the very elderly. In addition, five-year mortality after age 95 in relation to dementia and cognitive function in non-demented, was examined. A population sample of 338 95-year olds (response rate 65%) living in Gothenburg, Sweden, was compared with 85- (N=494) and 75-year olds (N=303) from the same birth cohort. All participants were examined by psychiatrists. The assessments included the Comprehensive Psychopathological Rating Scale, cognitive tests, the Mini Mental State Examination (MMSE), medical history, physical examination and a telephone interview with a key informant. Dementia, depression, anxiety and psychosis were classified according to DSM-III-R criteria, Alzheimer?s disease according to NINCDS-ADRDA criteria and vascular dementia (VaD) according to NINDS-AIREN criteria. Two-thirds (66%) of the 95-year olds fulfilled criteria for a mental disorder. Dementia was more common (52% vs. 30%; p<0.001) and more severe in 95-year olds than in 85-year olds. Among 95-year olds, dementia was more common in women than in men (56% vs. 37%; p=0.006). The proportion of VaD was lower among 95-year olds than among 85-year olds (30% vs. 40%; p<0.001). Almost one-third (29%) of the non-demented 95-year olds had a psychiatric disorder (depression 17%, anxiety disorders 9%, psychotic disorder 7%). Psychotic symptoms among non-demented 95-year olds were not associated with other psychiatric symptoms, sensory impairments or cognitive function. The prevalence of psychiatric disorders among non-demented was higher for 85- and 95-year olds than for 75-year olds. Five-year survival after age 95 was similar in men and women, but when controlling for dementia, male sex predicted mortality. Dementia was the leading predictor for death after age 95 and attributed to 40% of deaths. For each point increase in the MMSE score among the non-demented 95-year olds, mortality decreased by 13% (RR 0.87; p<0.0002). The high prevalence of psychiatric disorders emphasizes the importance of detecting and treating psychiatric problems among the oldest old, and also the need for further research on mental health in this age group. There is a concern that psychiatric symptoms among the very old are considered ?normal for age? and therefore neglected by the patients themselves, their relatives and health care professionals.
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4.
  • Börjesson-Hanson, Anne, 1959, et al. (författare)
  • Five-year mortality in relation to dementia and cognitive function in 95-year-olds.
  • 2007
  • Ingår i: Neurology. - : Ovid Technologies (Wolters Kluwer Health). - 0028-3878 .- 1526-632X. ; 69:22, s. 2069-75
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Dementia is a known predictor of mortality, but most studies include small numbers of participants above age 90. The influence of dementia or cognition on mortality in this age group is therefore uncertain. OBJECTIVE: To examine 5-year mortality in relation to dementia and cognitive performance at age 95. METHODS: A population sample of 338 individuals examined at age 95 was followed to age 100. Dementia was diagnosed according to DSM-III-R criteria. Cognitive function was measured using the Mini-Mental State Examination (MMSE). Information on severe physical disorders was obtained from the Swedish Hospital Discharge Register, and date of death from the Swedish Population Register. RESULTS: Five-year mortality was higher in 95-year-olds with dementia than in 95-year-olds without dementia (96% vs 73%; p < 0.0001), even when adjusting for severe physical disorders. A Cox regression analysis with calculation of population attributable risk (PAR), calculated from adjusted relative risks, showed that mortality was predicted by dementia (PAR 42%), cardiac disease (PAR 17%), cancer (PAR 6%), and male sex (PAR 7%), but not by stroke. Among the subjects without dementia, cognitive performance measured using the MMSE (n = 133 with complete tests; 81% of the subjects without dementia) predicted mortality. For each point increase in the MMSE, mortality decreased by 13%. CONCLUSIONS: In 95-year-olds, dementia, as well as cognitive performance in the subjects without dementia, influences mortality. When controlling for other severe medical conditions we found dementia to be the leading cause of deaths among the oldest old. The reason why dementia and cognitive function predict life expectancy requires further elucidation.
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5.
  • Börjesson-Hanson, Anne, 1959, et al. (författare)
  • One-Month Prevalence of Mental Disorders in a Population Sample of 95-Year Olds.
  • 2011
  • Ingår i: The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry. - 1545-7214. ; 19:3, s. 284-91
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE:: To determine the 1-month prevalence of mental disorders among 95-year olds. DESIGN:: Cross-sectional population sample of 95-year olds. SETTING:: All 95-year olds born in the period 1901-1903 living in Gothenburg, Sweden, were invited. Elderly living in both community settings and nursing homes were included. PARTICIPANTS:: In total, 338 95-year olds (response rate: 65%) were examined (263 women, 75 men). MEASUREMENTS:: All participants were examined by psychiatrists using the Comprehensive Psychopathological Rating Scale and cognitive tests. Mental disorders were classified according to Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised criteria. RESULTS:: Two-third of all 95-year olds had a mental disorder. In the total sample of 95-year olds, the 1-month prevalence was 52% for dementia, 8% for depression, 4% for anxiety, and 3% for psychotic disorders. Almost one-third (29%) of the nondemented 95-year olds fulfilled criteria for a psychiatric disorder: 17% had depression, 9% anxiety, and 7% psychotic disorder. CONCLUSIONS:: The combined prevalence of mental disorders was high among 95-year olds, even after excluding dementia. These findings emphasize the importance of research, care, and detection of psychiatric problems in this age group.
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7.
  • Craggs, L. J. L., et al. (författare)
  • Clusterin/Apolipoprotein J immunoreactivity is associated with white matter damage in cerebral small vessel diseases
  • 2016
  • Ingår i: Neuropathology and Applied Neurobiology. - : Wiley. - 0305-1846 .- 1365-2990. ; 42:2, s. 194-209
  • Tidskriftsartikel (refereegranskat)abstract
    • AimBrain clusterin is known to be associated with the amyloid- deposits in Alzheimer's disease (AD). We assessed the distribution of clusterin immunoreactivity in cerebrovascular disorders, particularly focusing on white matter changes in small vessel diseases. MethodsPost-mortem brain tissues from the frontal or temporal lobes of a total of 70 subjects with various disorders including cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), cerebral amyloid angiopathy (CAA) and AD were examined using immunohistochemistry and immunofluorescence. We further used immunogold electron microscopy to study clusterin immunoreactivity in extracellular deposits in CADASIL. ResultsImmunostaining with clusterin antibodies revealed strong localization in arterioles and capillaries, besides cortical neurones. We found that clusterin immunostaining was significantly increased in the frontal white matter of CADASIL and pontine autosomal dominant microangiopathy and leukoencephalopathy subjects. In addition, clusterin immunostaining correlated with white matter pathology severity scores. Immunostaining in axons ranged from fine punctate deposits in single axons to larger confluent areas with numerous swollen axon bulbs, similar to that observed with known axon damage markers such as non-phosphorylated neurofilament H and the amyloid precursor protein. Immunofluorescence and immunogold electron microscopy experiments showed that whereas clusterin immunoreactivity was closely associated with vascular amyloid- in CAA, it was lacking within the granular osmiophilic material immunolabelled by NOTCH3 extracelluar domain aggregates found in CADASIL. ConclusionsOur results suggest a wider role for clusterin associated with white matter damage in addition to its ability to chaperone proteins for clearance via the perivascular drainage pathways in several disease states.
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8.
  • Craggs, Lucinda, et al. (författare)
  • Quantitative vascular pathology and phenotyping familial and sporadic cerebral small vessel diseases
  • 2013
  • Ingår i: Brain Pathology. - : Wiley. - 1015-6305 .- 1750-3639. ; 23:5, s. 547-557
  • Tidskriftsartikel (refereegranskat)abstract
    • We quantified vascular changes in the frontal lobe and basal ganglia of four inherited small vessel diseases (SVDs) including cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), pontine autosomal dominant microangiopathy and leukoencephalopathy (PADMAL), hereditary multi-infarct dementia of Swedish type (Swedish hMID), and hereditary endotheliopathy with retinopathy, nephropathy, and stroke (HERNS). Vascular pathology was most severe in CADASIL, and varied with marginally greater severity in the basal ganglia compared to the frontal lobe. The overall sclerotic index values in frontal lobe were in the order CADASIL ≥ HERNS > PADMAL > Swedish hMID > sporadic SVD, and in basal ganglia CADASIL > HERNS > Swedish hMID > PADMAL> sporadic SVD. The subcortical white matter was almost always more affected than any gray matter. We observed glucose transporter-1 (GLUT-1) protein immunoreactivities were most affected in the white matter indicating capillary degeneration whereas collagen IV (COL4) immunostaining was increased in PADMAL cases in all regions and tissue types. Overall, GLUT-1 : COL4 ratios were higher in the basal ganglia indicating modifications in capillary density compared to the frontal lobe. Our study shows that the extent of microvascular degeneration varies in these genetic disorders exhibiting common end-stage pathologies but is the most aggressive in CADASIL.
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9.
  • de Heus, R. A. A., et al. (författare)
  • Blood Pressure Lowering With Nilvadipine in Patients With Mild-to-Moderate Alzheimer Disease Does Not Increase the Prevalence of Orthostatic Hypotension
  • 2019
  • Ingår i: Journal of the American Heart Association. - : Ovid Technologies (Wolters Kluwer Health). - 2047-9980. ; 8:10
  • Tidskriftsartikel (refereegranskat)abstract
    • Background-Hypertension is common among patients with Alzheimer disease. Because this group has been excluded from hypertension trials, evidence regarding safety of treatment is lacking. This secondary analysis of a randomized controlled trial assessed whether antihypertensive treatment increases the prevalence of orthostatic hypotension (OH) in patients with Alzheimer disease. Methods and Results-Four hundred seventy-seven patients with mild-to-moderate Alzheimer disease were randomized to the calcium-channel blocker nilvadipine 8 mg/day or placebo for 78 weeks. Presence of OH (blood pressure drop >= 20/>= 10 mm Hg after 1 minute of standing) and OH-related adverse events (dizziness, syncope, falls, and fractures) was determined at 7 follow-up visits. Mean age of the study population was 72.2 +/- 8.2 years and mean Mini-Mental State Examination score was 20.4 +/- 3.8. Baseline blood pressure was 137.8 +/- 14.0/77.0 +/- 8.6 mm Hg. Grade I hypertension was present in 53.4% (n=255). After 13 weeks, blood pressure had fallen by -7.8/-3.9 mm Hg for nilvadipine and by -0.4/-0.8 mm Hg for placebo (P<0.001). Across the 78-week intervention period, there was no difference between groups in the proportion of patients with OH at a study visit (odds ratio [95% CI] 1.1 [0.8-1.5], P 0.62), nor in the proportion of visits where a patient met criteria for OH, corrected for number of visits (7.7 +/- 13.8% versus 7.3 +/- 11.6%). OH-related adverse events were not more often reported in the intervention group compared with placebo. Results were similar for those with baseline hypertension. Conclusions-This study suggests that initiation of a low dose of antihypertensive treatment does not significantly increase the risk of OH in patients with mild-to-moderate Alzheimer disease.
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10.
  • Dyer, A. H., et al. (författare)
  • Cognitive Outcomes of Long-term Benzodiazepine and Related Drug (BDZR) Use in People Living With Mild to Moderate Alzheimer's Disease: Results From NILVAD
  • 2020
  • Ingår i: Journal of the American Medical Directors Association. - : Elsevier BV. - 1525-8610. ; 21:2, s. 194-200
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Benzodiazepines and related drugs (BDZRs) have been associated with an increased risk of Alzheimer's disease (AD) in later life. Despite this, it remains unclear whether ongoing BDZR use may further accelerate cognitive decline in those diagnosed with mild to moderate AD. Design: This study was embedded within NILVAD, a randomized controlled trial of nilvadipine in mild to moderate AD. Cognition was measured at baseline and 18 months using the Alzheimer Disease Assessment Scale, Cognitive Subsection (ADAS-Cog). We assessed predictors of long-term BDZR use and analyzed the effect of ongoing BDZR use on ADAS-Cog scores at 18 months. Additionally, the impact of BDZR use on adverse events, incident delirium, and falls over 18-month follow-up was assessed adjusting for relevant covariates. Setting and Participants: 448 participants with mild to moderate AD recruited from 23 academic centers in 9 European countries. Results: Overall, 14% (62/448) were prescribed an ongoing BDZR for the study duration. Increasing total number of (non-BDZR) medications was associated with a greater likelihood of BDZR prescription (odds ratio 1.16, 95% confidence interval 1.05-1.29). At 18 months, BDZR use was not associated with greater cognitive decline on the ADAS-Cog controlling for baseline ADAS-Cog scores, age, gender, study arm, and other clinical covariates (beta = 1.62, -1.34 to 4.56). However, ongoing BDZR use was associated with a greater likelihood of adverse events [incidence rate ratio (IRR) 1.19, 1.05-1.34], incident delirium (IRR 2.31, 1.45-3.68), and falls (IRR 1.66, 1.02-2.65) over 18 months that persisted after robust adjustment for covariates. Conclusions and Implications: This study found no effect of ongoing BDZR use on ADAS-Cog scores in those with mild to moderate AD over 18 months. However, ongoing use of these medications was associated with an increased risk of adverse events, delirium, and falls. Thus, BDZR use should be avoided where possible and deprescribing interventions should be encouraged in older adults with AD. (C) 2019 AMDA - The Society for Post-Acute and Long-Term Care Medicine.
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