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  • 1. Ahmed, Niaz
    et al.
    Davalos, Antoni
    Eriksson, Niclas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniskt forskningscentrum (UCR).
    Ford, Gary A.
    Glahn, Joerg
    Hennerici, Michael
    Mikulik, Robert
    Kaste, Markku
    Lees, Kennedy R.
    Lindsberg, Perttu J.
    Toni, Danilo
    Association of Admission Blood Glucose and Outcome in Patients Treated With Intravenous Thrombolysis2010Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 67, nr 9, s. 1123-1130Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: To determine the association between admission blood glucose and outcome in ischemic stroke patients treated with thrombolysis. Design: A prospective, open, multinational, observational study. Setting: An ongoing Internet-based, academic-driven, interactive thrombolysis register. Patients: Between 2002 and 2007, 16 049 patients were recorded in the SITS-ISTR. Main Outcome Measure: Blood glucose was recorded at admission. Blood glucose was divided into the following categories: less than 80,80-120 (reference range), 121-140, 141-160, 161-180, 181-200, and greater than 200 mg/dL. Outcomes were mortality and independence (modified Rankin Scale score of 0-2) at 3 months and symptomatic intracerebral hemorrhage (SICH) (National Institutes of Health Stroke Scale deterioration >= points within 24 hours and type 2 parenchymal hemorrhage). Results: In multivariable analysis, blood glucose as a continuous variable was independently associated with a higher mortality (P < .001), lower independence (P < .001), and an increased risk of SICH (P = .005). Blood glucose greater than 120 mg/dL as a categorical variable was associated with a significantly higher odds for mortality (odds ratio [OR], 1.24; 95% confidence interval [Cl], 1.07-1.44; P = .004) and a lower odds for independence (OR, 0.58; 95% CI, 0.48-0.70; P < .001), and blood glucose from 181 to 200 mg/dL was associated with an increased risk of SICH (OR, 2.86; 95% CI, 1.69-4.83; P < .001) compared with the reference level. The trends of associations between blood glucose and outcomes were similar in patients with diabetes (17%) or without such history, except for mortality (P = .23) and SICH (P = .06) in which the association was not statistically significant in patients with diabetes. Conclusions: Admission hyperglycemia was an independent predictor for poor outcome after stroke/thrombolysis, though SICH rates did not increase significantly until reaching 180 mg/dL. These results suggest that tight control of blood glucose may be indicated in the hyperacute phase following thrombolysis. Randomized trial data are needed.

  • 2.
    Basun, Hans
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Bogdanovic, Nenad
    Ingelsson, Martin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Almkvist, Ove
    Näslund, Jan
    Axelman, Karin
    Bird, Thomas D
    Nochlin, David
    Schellenberg, Gerard D
    Wahlund, Lars-Olof
    Lannfelt, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Clinical and Neuropathological Features of the Arctic APP Gene Mutation Causing Early-Onset Alzheimer Disease2008Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 65, nr 4, s. 499-505Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: A majority of mutations within the beta-amyloid region of the amyloid precursor protein (APP) gene cause inherited forms of intracerebral hemorrhage. Most of these mutations may also cause cognitive impairment, but the Arctic APP mutation is the only known intra-beta-amyloid mutation to date causing the more typical clinical picture of Alzheimer disease. Objective: To describe features of 1 Swedish and 1 American family with the previously reported Arctic APP mutation. Design, Setting, and Participants: Affected and non-affected carriers of the Arctic APP mutation from the Swedish and American families were investigated clinically. In addition, 1 brain from each family was investigated neuropathologically. Results: The clinical picture, with age at disease onset in the sixth to seventh decade of life and dysfunction in multiple cognitive areas, is indicative of Alzheimer disease and similar to the phenotype for other Alzheimer disease APP mutations. Several affected mutation carriers displayed general brain atrophy and reduced blood flow of the parietal lobe as demonstrated by magnetic resonance imaging and single-photon emission computed tomography. One Swedish case and 1 American case with the Arctic APP mutation came to autopsy, and both showed no signs of hemorrhage but revealed severe congophilic angiopathy, region-specific neurofibrillary tangle pathological findings, and abundant amyloid plaques. Intriguingly, most plaques from both of these cases had a characteristic ringlike character. Conclusions: Overall, our findings corroborate that the Arctic APP mutation causes a clinical and neuropathological picture compatible with Alzheimer disease.

  • 3.
    Fang, Fang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland.
    Bellocco, Rino
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Department of Statistics, University of Milano-Bicocca, Milan, Italy.
    Ronnevi, Lars-Olof
    Department of Neurology, Karolinska Hospital Stockholm.
    Sparén, Pär
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Fall, Katja
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Amyotrophic lateral sclerosis in Sweden, 1991-20052009Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 66, nr 4, s. 515-9Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objectives: To investigate the temporal trend of amyotrophic lateral sclerosis (ALS) incidence in Sweden between January 1, 1991, and December 31, 2005, and to explore incidence variations according to major demographic factors.

    Design: Population-based study.

    Setting: Academic research.

    Participants: All incident cases of ALS identified through the Swedish Inpatient Register between January 1, 1991, and December 31, 2005.

    Main outcome measure: Age-standardized incidence rates were calculated by applying the observed age-specific incidence rates to the age distribution of the Swedish population in 1991. A linear regression model was used to assess the potential trend of the incidence during calendar years. We also followed up the entire population registered in the 1990 Population and Housing Census for incidence of ALS. Relative risk and 95% confidence interval of ALS associated with demographic variables were estimated using Poisson regression models.

    Results: The age-standardized incidence rates increased from 2.32 per 100,000 person-years in 1991-1993 to 2.98 per 100,000 person-years in 2003-2005, representing an annual increase of approximately 2% during the 15 years (P value for trend, .002). The age-specific incidence rates increased in all age groups except those younger than 50 years. The observed increase remained significant when restricting the analysis to individuals born in Sweden (P value for trend, <.001). Compared with individuals born from April through June, those born from October through December were at 11% increased risk of ALS (95% confidence interval, 1.01-1.23).

    Conclusions: The incidence of ALS has been increasing during the last 15 years in Sweden. Further studies are warranted to explore the underlying reasons for this observed trend.

  • 4. Freund-Levi, Yvonne
    et al.
    Eriksdotter-Jonhagen, Maria
    Cederholm, Tommy
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Basun, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Faxén-Irving, Gerd
    Garlind, Anita
    Vedin, Inger
    Vessby, Bengt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Wahlund, Lars-Olof
    Palmblad, Jan
    Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease: OmegAD study - A randomized double-blind trial2006Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 63, nr 10, s. 1402-1408Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Epidemiologic and animal studies have suggested that dietary fish or fish oil rich in omega-3 fatty acids, for example, docosahexaenoic acid and eicosapentaenoic acid, may prevent Alzheimer disease (AD).

    Objective: To determine effects of dietary omega-3 fatty acid supplementation on cognitive functions in patients with mild to moderate AD.

    Design: Randomized, double-blind, placebo-controlled clinical trial.

    Participants: Two hundred four patients with AD (age range [mean +/- SD], 74 +/- 9 years) whose conditions were stable while receiving acetylcholine esterase inhibitor treatment and who had a Mini-Mental State Examination (MMSE) score of 15 points or more were randomized to daily intake of 1.7 g of docosahexaenoic acid and 0.6 g of eicosapentaenoic acid (omega-3 fatty acid-treated group) or placebo for 6 months, after which all received omega-3 fatty acid supplementation for 6 months more.

    Main Outcome Measures: The primary outcome was cognition measured with the MMSE and the cognitive portion of the Alzheimer Disease Assessment Scale. The secondary outcome was global function as assessed with the Clinical Dementia Rating Scale; safety and tolerability of omega-3 fatty acid supplementation; and blood pressure determinations.

    Results: One hundred seventy-four patients fulfilled the trial. At baseline, mean values for the Clinical Dementia Rating Scale, MMSE, and cognitive portion of the Alzheimer Disease Assessment Scale in the 2 randomized groups were similar. At 6 months, the decline in cognitive functions as assessed by the latter 2 scales did not differ between the groups. However, in a subgroup (n=32) with very mild cognitive dysfunction (MMSE > 27 points), a significant (P <.05) reduction in MMSE decline rate was observed in the omega-3 fatty acid-treated group compared with the placebo group. A similar arrest in decline rate was observed between 6 and 12 months in this placebo subgroup when receiving omega-3 fatty acid supplementation. The omega-3 fatty acid treatment was safe and well tolerated.

    Conclusions: Administration of omega-3 fatty acid in patients with mild to moderate AD did not delay the rate of cognitive decline according to the MMSE or the cognitive portion of the Alzheimer Disease Assessment Scale. However, positive effects were observed in a small group of patients with very mild AD (MMSE > 27 points).

  • 5.
    Freund-Levi, Yvonne
    et al.
    Department of Neurobiology, Caring Sciences and Society, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Eriksdotter-Jönhagen, Maria
    Department of Neurobiology, Caring Sciences and Society, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Cederholm, Tommy
    Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism, Uppsala University Hospital, Uppsala, Sweden.
    Basun, Hans
    Division of Geriatrics, Uppsala University Hospital, Uppsala, Sweden.
    Faxén-Irving, Gerd
    Department of Neurobiology, Caring Sciences and Society, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Garlind, Anita
    Department of Neurobiology, Caring Sciences and Society, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Vedin, Inger
    Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Vessby, Bengt
    Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism, Uppsala University Hospital, Uppsala, Sweden.
    Wahlund, Lars-Olof
    Department of Neurobiology, Caring Sciences and Society, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Palmblad, Jan
    Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden; Department of Medicine, M54, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease: OmegAD study - A randomized double-blind trial2006Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 63, nr 10, s. 1402-1408Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Epidemiologic and animal studies have suggested that dietary fish or fish oil rich in omega-3 fatty acids, for example, docosahexaenoic acid and eicosapentaenoic acid, may prevent Alzheimer disease (AD).

    OBJECTIVE: To determine effects of dietary omega-3 fatty acid supplementation on cognitive functions in patients with mild to moderate AD.

    DESIGN: Randomized, double-blind, placebo-controlled clinical trial.

    PARTICIPANTS: Two hundred four patients with AD (age range [mean +/- SD], 74 +/- 9 years) whose conditions were stable while receiving acetylcholine esterase inhibitor treatment and who had a Mini-Mental State Examination (MMSE) score of 15 points or more were randomized to daily intake of 1.7 g of docosahexaenoic acid and 0.6 g of eicosapentaenoic acid (omega-3 fatty acid-treated group) or placebo for 6 months, after which all received omega-3 fatty acid supplementation for 6 months more.

    MAIN OUTCOME MEASURES: The primary outcome was cognition measured with the MMSE and the cognitive portion of the Alzheimer Disease Assessment Scale. The secondary outcome was global function as assessed with the Clinical Dementia Rating Scale; safety and tolerability of omega-3 fatty acid supplementation; and blood pressure determinations.

    RESULTS: One hundred seventy-four patients fulfilled the trial. At baseline, mean values for the Clinical Dementia Rating Scale, MMSE, and cognitive portion of the Alzheimer Disease Assessment Scale in the 2 randomized groups were similar. At 6 months, the decline in cognitive functions as assessed by the latter 2 scales did not differ between the groups. However, in a subgroup (n = 32) with very mild cognitive dysfunction (MMSE >27 points), a significant (P<.05) reduction in MMSE decline rate was observed in the omega-3 fatty acid-treated group compared with the placebo group. A similar arrest in decline rate was observed between 6 and 12 months in this placebo subgroup when receiving omega-3 fatty acid supplementation. The omega-3 fatty acid treatment was safe and well tolerated.

    CONCLUSIONS: Administration of omega-3 fatty acid in patients with mild to moderate AD did not delay the rate of cognitive decline according to the MMSE or the cognitive portion of the Alzheimer Disease Assessment Scale. However, positive effects were observed in a small group of patients with very mild AD (MMSE >27 points).

  • 6.
    Huang, Wenyong
    et al.
    Aging Research Center, Division of Geriatric Epidemiology and Medicine, Department of Neurotec, Karolinska Institutet and Stockholm Gerontology Research Center, Stockholm.
    Qiu, Chengxuan
    Aging Research Center, Division of Geriatric Epidemiology and Medicine, Department of Neurotec, Karolinska Institutet and Stockholm Gerontology Research Center, Stockholm.
    von Strauss, Eva
    Aging Research Center, Division of Geriatric Epidemiology and Medicine, Department of Neurotec, Karolinska Institutet and Stockholm Gerontology Research Center, Stockholm.
    Winblad, Bengt
    Aging Research Center, Division of Geriatric Epidemiology and Medicine, Department of Neurotec, Karolinska Institutet and Stockholm Gerontology Research Center, Stockholm.
    Fratiglioni, Laura
    Aging Research Center, Division of Geriatric Epidemiology and Medicine, Department of Neurotec, Karolinska Institutet and Stockholm Gerontology Research Center, Stockholm.
    APOE Genotype, Family History of Dementia, and Alzheimer Disease Risk: A 6-Year Follow-up Study2004Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 61, nr 12, s. 1930-1934Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background Both family aggregation and apolipoprotein E (APOE) ε4 allele are well-known risk factors for dementia, but the relation between these two factors remains unclear.

    Objective To explore whether the risk of dementia and Alzheimer disease (AD) due to a positive family history is explained by APOE genotypes.

    Design Community-based cohort study.

    Setting The Kungsholmen district of Stockholm, Sweden.

    Participants A total of 907 nondemented people 75 years or older, followed up for 6 years to detect incident dementia and AD cases according to the diagnostic criteria of the Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition.

    Main Outcome Measures Risk of dementia and AD by Cox proportional hazards models after controlling for several potential confounders.

    Results Subjects who had at least 2 siblings with dementia were at an increased risk of AD. Individuals with both APOE ε4 allele and at least 2 affected first-degree relatives had a higher risk of dementia and AD compared with those without these 2 factors. Similar results were obtained for history of dementia separately in parents or siblings. Among the ε4 allele carriers, subjects with 2 or more first-degree demented relatives had increased risk of dementia and AD, whereas no increased risk was detected among non–ε4 carriers.

    Conclusions Family history of dementia was associated with an increased risk of dementia and AD in this very old population, but only among APOE ε4 carriers. This suggests the existence of other genetic or environmental risk factors that may be active in the presence of the APOE ε4 allele.

    The role of both family history of dementia and the apolipoprotein E (APOE) gene in the development of Alzheimer disease (AD) has been extensively investigated. There is strong evidence to suggest that APOE ε4 allele carriers, as well as subjects with a family history of dementia, have an increased risk of AD.Familial aggregation and genetic risk factors appear to be most influential in AD at relatively early ages.However, there are reports supporting an effect of both familial aggregation and APOE ε4 even in late-onset AD,although a lower effect in comparison with early-onset cases has been detected.

    It is hypothesized that APOE ε4 allele might explain the association between family history of dementia and AD. Previous studies have tried to evaluate this hypothesis, but to what extent familial aggregation is due to the association between the ε4 allele and AD remains equivocal. Some studies indicated that ε4-positive patients with AD tended to have a higher rate of family history of dementia than ε4-negative patients. Conversely, patients with family history of AD are also more likely to carry the ε4 allele than patients without family history.Other studies, however, showed that the APOE ε4 allele was not related to familial aggregation of AD.

    Most previous analyses have been hospital-based case-control studies. Because of ascertainment bias and severe truncation of data, these studies might overestimate the effects of family history and APOE ε4 allele, especially in very old people. Only a small-scale prospective study has examined both family history of dementia and APOE ε4 allele in relation to AD risk among people 75 years or older.

    In a previous study within the Kungsholmen Project, a strong familial aggregation was detected among prevalent cases of late-onset AD, but the contribution of the APOE ε4 allele was not considered. In the present study, we examined the 6-year follow-up data from the same project to explore whether the risk of dementia and AD due to a positive family history is explained by APOE genotypes.

  • 7. Leinonen, Ville
    et al.
    Alafuzoff, Irina
    Department of Neuroscience and Neurology, University of Kuopio Finland .
    Aalto, Sargo
    Suotunen, Timo
    Savolainen, Sakari
    Någren, Kjell
    Tapiola, Tero
    Pirttilä, Tuula
    Rinne, Jaakko
    Jääskeläinen, Juha E
    Soininen, Hilkka
    Rinne, Juha O
    Assessment of beta-amyloid in a frontal cortical brain biopsy specimen and by positron emission tomography with carbon 11-labeled Pittsburgh Compound B.2008Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 65, nr 10, s. 1304-9Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: To compare carbon 11-labeled Pittsburgh Compound B ([11C]PiB) positron emission tomography (PET) findings in patients with and without Alzheimer disease lesions in frontal cortical biopsy specimens.

    DESIGN: Cross-sectional study of [11C]PiB PET findings in patients with or without beta-amyloid (Abeta) aggregates in frontal cortical biopsy specimens.

    SETTING: Two university hospitals in Finland. Patients Ten patients who had undergone intraventricular pressure monitoring with a frontal cortical biopsy (evaluated for Abeta aggregates and hyperphosphorylated tau) for suspected normal-pressure hydrocephalus.

    INTERVENTIONS: [11C]PiB PET and evaluation for cognitive impairment using a battery of neuropsychological tests.

    MAIN OUTCOME MEASURES: Immunohistochemical evaluation for Abeta aggregates and hyperphosphorylated tau in the frontal cortical biopsy specimen and [11C]PiB PET.

    RESULTS: In patients with Abeta aggregates in the frontal cortical biopsy specimen, PET imaging revealed higher [11C]PiB uptake (P < .05) in the frontal, parietal, and lateral temporal cortices and in the striatum as compared with the patients without frontal Abeta deposits.

    CONCLUSIONS: Our study supports the use of noninvasive [11C]PiB PET in the assessment of Abeta deposition in the brain. Large prospective studies are required to verify whether [11C]PiB PET will be a diagnostic aid, particularly in early Alzheimer disease.

  • 8. Malm, J.
    et al.
    Kristensen, B.
    Karlsson, Thomas
    Linköpings universitet, Filosofiska fakulteten. Linköpings universitet, Institutionen för beteendevetenskap, Avdelningen för kognition, utveckling och handikapp, CDD.
    Fagerlund, M.
    Elfverrson, J.
    Ekstedt, J.
    The predictive value of cerebrospinal fluid dynamic tests in patients with the idiopathic adult hydrocephalus syndrome1995Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 52, s. 783-789Artikkel i tidsskrift (Fagfellevurdert)
  • 9. Qiu, Chengxuan
    et al.
    von Strauss, Eva
    Fastbom, Johan
    Winblad, Bengt
    Fratiglioni, Laura
    Low blood pressure and risk of dementia in the Kungsholmen project: a 6-year follow-up study2003Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 60, nr 2, s. 223-228Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Previous studies have reported a higher prevalence of dementia in persons with low blood pressure.

    Objective: To examine whether low blood pressure is prospectively associated with the occurrence of Alzheimer disease and dementia in elderly people.

    Subjects and Methods: A community-based, dementia-free cohort (n = 1270) aged 75 to 101 years was longitudinally examined twice within 6 years to detect incident dementia using the Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria. Cox proportional hazards models were used to analyze blood pressure in association with dementia after adjustment for several potential confounders.

    Results: During the 6-year period, 339 subjects were diagnosed with dementia, including 256 persons with Alzheimer disease. Subjects with very high systolic pressure (&gt;180 vs 141-180 mm Hg) had an adjusted relative risk of 1.5 (95% confidence interval [CI], 1.0-2.3; P =.07) for Alzheimer disease, and 1.6 (95% CI, 1.1-2.2) for dementia. Low systolic pressure (&lt;/=140 mm Hg) was not related to incident dementia. In contrast, high diastolic pressure (&gt;90 mm Hg) was not associated with dementia incidence, whereas extremely low diastolic pressure (&lt;/=65 vs 66-90 mm Hg) produced an adjusted relative risk of 1.7 (95% CI, 1.1-2.4) for Alzheimer disease and 1.5 (95% CI, 1.0-2.1; P =.03) for dementia. The latter association was pronounced particularly in persons who used antihypertensive drugs.

    Conclusions: Both low diastolic and high systolic pressure are associated with an increased risk of Alzheimer disease and dementia in this elderly population. The atherosclerotic process may explain the observed associations. In addition, low diastolic pressure may increase dementia risk by affecting cerebral perfusion.

  • 10. Stanton, Biba R
    et al.
    Shinhmar, Daisy
    Turner, Martin R
    Williams, Victoria C
    Williams, Steven C R
    Blain, Camilla R V
    Giampietro, Vincent P
    Catani, Marco
    Leigh, P Nigel
    Andersen, Peter M
    Umeå universitet, Medicinska fakulteten, Institutionen för farmakologi och klinisk neurovetenskap, Neurologi.
    Simmons, Andrew
    Diffusion tensor imaging in sporadic and familial (D90A SOD1) forms of amyotrophic lateral sclerosis2009Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 66, nr 1, s. 109-115Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: The basis of heterogeneity in the clinical presentation and rate of progression of amyotrophic lateral sclerosis (ALS) is poorly understood. OBJECTIVES: To use diffusion tensor imaging as a measure of axonal pathologic features in vivo in ALS and to compare a homogeneous form of familial ALS (homozygous D90A SOD1 [superoxide dismutase 1]) with sporadic ALS. DESIGN: Cross-sectional diffusion tensor imaging study. SETTING: Tertiary referral neurology clinic. PATIENTS: Twenty patients with sporadic ALS, 6 patients with homozygous D90A SOD1 ALS, and 21 healthy control subjects. MAIN OUTCOME MEASURE: Fractional anisotropy in cerebral white matter. RESULTS: Patients with homozygous D90A SOD1 ALS showed less extensive pathologic white matter in motor and extramotor pathways compared with patients with sporadic ALS, despite similar disease severity assessed clinically using a standard functional rating scale. Fractional anisotropy correlated with clinical measures of severity and upper motor neuron involvement. CONCLUSION: In vivo diffusion tensor imaging measures demonstrate differences in white matter degeneration between sporadic ALS and a unique familial form of the disease, indicating that genotype influences the distribution of cerebral pathologic features in ALS.

  • 11. Sundelöf, J
    et al.
    Giedraitis, V
    Irizarry, M
    Sundström, J
    Ingelsson, E
    Rönnemaa, E
    Ärnlöv, Johan
    Högskolan Dalarna, Akademin Utbildning, hälsa och samhälle, Medicinsk vetenskap.
    Degerman Gunnarsson, M
    Hyman, B
    Basun, H
    Ingelsson, M
    Kilander, L
    Lannfelt, L
    Plasma Aß and the risk of Alzheimer's disease and dementia in elderly men: a prospective population-based cohort study2008Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 65, nr 2, s. 256-63Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Beta amyloid (Abeta) protein accumulates in the brains of individuals with Alzheimer disease (AD) and is detectable in cerebrospinal fluid and plasma. OBJECTIVE: To examine plasma levels of Abeta peptides Abeta(40) and Abeta(42) as predictors of incident AD and other types of dementia. DESIGN: Prospective, population-based cohort study. SETTING: The Uppsala Longitudinal Study of Adult Men. PARTICIPANTS: Plasma Abeta(40) and Abeta(42) levels were analyzed as predictors of incident AD in 1045 men at age 70 years and 680 men at age 77 years using Cox proportional hazards analyses. Alzheimer disease and other types of dementia were diagnosed by standardized screening, clinical evaluation, and medical record review. MAIN OUTCOME MEASURES: Hazard ratios of AD (primary outcome) and vascular dementia or other dementia (secondary outcomes) according to baseline levels of plasma Abeta(40) and Abeta(42). RESULTS: From the age of 77 years at baseline, 46 individuals developed AD at follow-up (median, 5.3 years). A low plasma Abeta(40) level at age 77 years was associated with higher incidence of AD. The multivariate-adjusted hazard ratio was 4.87 (95% confidence interval, 1.63-14.6) for the lowest Abeta(40) tertile compared with the highest tertile. On follow-up from age 70 years at baseline (median, 11.2 years), 82 individuals developed AD. Plasma Abeta(40) and Abeta(42) levels measured at age 70 years were not significantly associated with incident AD. CONCLUSIONS: Low plasma Abeta(40) levels predicted incident AD in elderly men independently of potential confounders. Plasma Abeta(42) levels were not significantly associated with AD incidence. The clinical value of Abeta measurement in plasma remains to be established in future studies.

  • 12.
    Sundelöf, Johan
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Giedraitis, Vilmantas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Irizarry, Michael C
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Rönnemaa, Elina
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Arnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Gunnarsson, Malin Degerman
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Hyman, Bradley T
    Basun, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Ingelsson, Martin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Lannfelt, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Kilander, Lena
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Plasma β Amyloid and the Risk of Alzheimer Disease and Dementia in Elderly Men: A Prospective, Population-Based Cohort Study2008Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 65, nr 2, s. 256-63Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Beta amyloid (Abeta) protein accumulates in the brains of individuals with Alzheimer disease (AD) and is detectable in cerebrospinal fluid and plasma. OBJECTIVE: To examine plasma levels of Abeta peptides Abeta(40) and Abeta(42) as predictors of incident AD and other types of dementia. DESIGN: Prospective, population-based cohort study. SETTING: The Uppsala Longitudinal Study of Adult Men. PARTICIPANTS: Plasma Abeta(40) and Abeta(42) levels were analyzed as predictors of incident AD in 1045 men at age 70 years and 680 men at age 77 years using Cox proportional hazards analyses. Alzheimer disease and other types of dementia were diagnosed by standardized screening, clinical evaluation, and medical record review. MAIN OUTCOME MEASURES: Hazard ratios of AD (primary outcome) and vascular dementia or other dementia (secondary outcomes) according to baseline levels of plasma Abeta(40) and Abeta(42). RESULTS: From the age of 77 years at baseline, 46 individuals developed AD at follow-up (median, 5.3 years). A low plasma Abeta(40) level at age 77 years was associated with higher incidence of AD. The multivariate-adjusted hazard ratio was 4.87 (95% confidence interval, 1.63-14.6) for the lowest Abeta(40) tertile compared with the highest tertile. On follow-up from age 70 years at baseline (median, 11.2 years), 82 individuals developed AD. Plasma Abeta(40) and Abeta(42) levels measured at age 70 years were not significantly associated with incident AD. CONCLUSIONS: Low plasma Abeta(40) levels predicted incident AD in elderly men independently of potential confounders. Plasma Abeta(42) levels were not significantly associated with AD incidence. The clinical value of Abeta measurement in plasma remains to be established in future studies.

  • 13.
    Tajsharghi, Homa
    et al.
    Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden.
    Kimber, Eva
    Departments of Pediatrics, Institute for Clinical Sciences, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden / Department of Neuropediatrics, Uppsala University Children's Hospital, Uppsala, Sweden.
    Kroksmark, Anna-Karin
    Departments of Pediatrics, Institute for Clinical Sciences, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden / Queen Silvia's Children's Hospital, Göteborg, Sweden.
    Jerre, Ragnar
    Department of Orthopedics, Sahlgrenska University Hospital, Göteborg, Sweden.
    Tulinius, Mar
    Departments of Pediatrics, Institute for Clinical Sciences, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden / Queen Silvia's Children's Hospital, Göteborg, Sweden.
    Oldfors, Anders
    Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden.
    Embryonic myosin heavy-chain mutations cause distal arthrogryposis and developmental myosin myopathy that persists postnatally2008Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 65, nr 8, s. 1083-1090Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Myosin is a molecular motor and the essential part of the thick filament of striated muscle. The expression of myosin heavy-chain (MyHC) isoforms is developmentally regulated. The embryonic isoform encoded from MYH3 (OMIM *160720) is expressed during fetal life. Recently, mutations in MYH3 were demonstrated to be associated with congenital joint contractures, that is, Freeman-Sheldon and Sheldon-Hall syndromes, which are both distal arthrogryposis syndromes. Mutations in other MyHC isoforms cause myopathy. It is unknown whether MYH3 mutations cause myopathy because muscle tissue has not been studied.

    OBJECTIVES: To determine whether novel MYH3 mutations are associated with distal arthrogryposis and to demonstrate myopathic changes in muscle biopsy specimens from 4 patients with distal arthrogryposis and MYH3 mutations.

    DESIGN: In a cohort of patients with distal arthrogryposis, we analyzed the entire coding sequence of MYH3. Muscle biopsy specimens were obtained, and in addition to morphologic analysis, the expression of MyHC isoforms was investigated at the protein and transcript levels.

    RESULTS: We identified patients from 3 families with novel MYH3 mutations. These mutations affect developmentally conserved residues that are located in different regions of the adenosine triphosphate-binding pocket of the MyHC head. The embryonic (MYH3) isoform was not detected in any of the muscle biopsy samples, indicating a normal developmental downregulation of MYH3 in these patients. However, morphologic analysis of muscle biopsy specimens from the 4 patients revealed mild and variable myopathic features and a pathologic upregulation of the fetal MyHC isoform (MYH8) in 1 patient.

    CONCLUSIONS: Distal arthrogryposis associated with MYH3 mutations is secondary to myosin myopathy, and postnatal muscle manifestations are variable.

  • 14. Tajsharghi, Homa
    et al.
    Kimber, Eva
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa.
    Kroksmark, Anna-Karin
    Jerre, Ragnar
    Tulinius, Mar
    Oldfors, Anders
    Embryonic myosin heavy-chain mutations cause distal arthrogryposis and developmental myosin myopathy that persists postnatally2008Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 65, nr 8, s. 1083-1090Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Myosin is a molecular motor and the essential part of the thick filament of striated muscle. The expression of myosin heavy-chain (MyHC) isoforms is developmentally regulated. The embryonic isoform encoded from MYH3 (OMIM *160720) is expressed during fetal life. Recently, mutations in MYH3 were demonstrated to be associated with congenital joint contractures, that is, Freeman-Sheldon and Sheldon-Hall syndromes, which are both distal arthrogryposis syndromes. Mutations in other MyHC isoforms cause myopathy. It is unknown whether MYH3 mutations cause myopathy because muscle tissue has not been studied. Objectives: To determine whether novel MYH3 mutations are associated with distal arthrogryposis and to demonstrate myopathic changes in muscle biopsy specimens from 4 patients with distal arthrogryposis and MYH3 mutations. Design: In a cohort of patients with distal arthrogryposis, we analyzed the entire coding sequence of MYH3. Muscle biopsy specimens were obtained, and in addition to morphologic analysis, the expression of MyHC isoforms was investigated at the protein and transcript levels. Results: We identified patients from 3 families with novel MYH3 mutations. These mutations affect developmentally conserved residues that are located in different regions of the adenosine triphosphate-binding pocket of the MyHC head. The embryonic (MYH3) isoform was not detected in any of the muscle biopsy samples, indicating a normal developmental downregulation of MYH3 in these patients. However, morphologic analysis of muscle biopsy specimens from the 4 patients revealed mild and variable myopathic features and a pathologic upregulation of the fetal MyHC isoform (MYH8) in 1 patient. Conclusions: Distal arthrogryposis associated with MYH3 mutations is secondary to myosin myopathy, and postnatal muscle manifestations are variable.

  • 15.
    Tajsharghi, Homa
    et al.
    Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden.
    Ohlsson, Monica
    Department of Internal Medicine, Sahlgrenska University Hospital, Göteborg, Sweden.
    Lindberg, Christopher
    Department of Neurology, Sahlgrenska University Hospital, Göteborg, Sweden.
    Oldfors, Anders
    Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden.
    Congenital myopathy with nemaline rods and cap structures caused by a mutation in the beta-tropomyosin gene (TPM2)2007Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 64, nr 9, s. 1334-1338Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: To describe the clinical, morphologic, and genetic findings in a family in which one woman had nemaline myopathy, whereas her daughter showed features of cap disease.

    PATIENTS: A 66-year-old woman and her 35-year-old daughter had congenital, slowly progressive muscle weakness. They had weakness in both proximal and distal muscles and facial diplegia with bilateral ptosis, a long narrow face, a high arched palate, and micrognathia.

    RESULTS: Muscle biopsy specimens in the mother at age 57 years had shown nemaline myopathy, whereas a biopsy specimen at age 32 years had demonstrated no rods. Muscle biopsy specimens in the daughter at age 26 years had shown features of cap disease and no apparent nemaline rods. A missense mutation, Glu41Lys, in the beta-tropomyosin gene TPM2 was identified in both patients but was absent in their healthy relatives.

    CONCLUSIONS: The results indicate that mutations in TPM2 may cause nemaline myopathy as well as cap disease with a dominant mode of inheritance. These disorders may thus be phenotypic variants of the same genetic defect.

  • 16. Tapiola, Tero
    et al.
    Alafuzoff, Irina
    Department of Neuroscience and Neurology, University of Kuopio Finland .
    Herukka, Sanna-Kaisa
    Parkkinen, Laura
    Hartikainen, Päivi
    Soininen, Hilkka
    Pirttilä, Tuula
    Cerebrospinal fluid {beta}-amyloid 42 and tau proteins as biomarkers of Alzheimer-type pathologic changes in the brain2009Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 66, nr 3, s. 382-389Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: There is a clear need to develop an objective diagnostic test for Alzheimer disease (AD). Changes in the levels of cerebrospinal fluid (CSF) tau protein and beta-amyloid 42 (Abeta42) peptide in patients with AD have been well documented, but the relationship between these biomarkers and neuropathologic changes in the brain is not established. OBJECTIVE: To study the relationship between antemortem CSF biomarker levels and Alzheimer-type neuropathologic changes in the brain. DESIGN: Cross-sectional study to correlate levels of CSF Abeta42, total tau, and phosphorylated tau protein with neuropathologic changes in the brain. SETTING: Academic research. Patients The study included 123 patients (79 with clinically diagnosed AD, 29 with other dementia, and 15 with other neurologic disease). All underwent clinical evaluation and provided antemortem lumbar CSF samples, and neuropathologic data were collected from September 11, 1990, to March 13, 2003, in the Department of Neuroscience and Neurology, University of Kuopio, Kuopio, Finland. MAIN OUTCOME MEASURES: Levels of CSF Abeta42, total tau, and phosphorylated tau protein were measured using standard commercial immunoassays. Neuropathologic evaluations included the classic silver impregnation method and immunohistochemistry for Abeta, hyperphosphorylated tau, and alpha-synuclein. RESULTS: Cerebrospinal fluid Abeta42 and tau protein levels were related to amyloid load and the presence of neurofibrillary pathologic abnormalities in the brain. Cerebrospinal fluid Abeta42 level correlated inversely with total Abeta load in the brain, and CSF tau level correlated with results of immunohistochemistry for hyperphosphorylated tau and with the presence of neocortical neurofibrillary tangles. In multivariate logistic regression analysis, the number of neuritic plaques in the brain remained a significant predictor of decreased CSF Abeta42 level and of increased CSF tau level. Based on the ratio of phosphorylated tau level to Abeta42 level, sensitivity was 91.6%, and specificity was 85.7%, with an overall accuracy of 90.2% for the presence of pathologic neuritic plaque in the brain. CONCLUSIONS: Cerebrospinal fluid Abeta42 and tau proteins are biomarkers of AD-associated pathologic changes in the brain. The combination of abnormally low CSF Abeta42 level and abnormally high CSF tau level predicted the presence of AD pathologic features with high accuracy. This combination assay may be helpful in diagnosing the presence of AD pathologic changes in the brain.

  • 17. Tomson, T
    et al.
    Nilsson, B Y
    Richard, Levi
    Impaired visual contrast sensitivity in epileptic patients treated with carbamazepine.1988Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 45, nr 8, s. 897-900Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Critical flicker fusion frequencies and visual contrast sensitivity were determined in 27 adult epileptic patients receiving carbamazepine monotherapy and in 24 healthy, drug-free control subjects. Flicker fusion thresholds were the same in patients and control subjects, whereas the contrast sensitivity was significantly reduced in the patient group at all spatial frequencies. There was a significant negative correlation between the plasma concentration of carbamazepine and the contrast sensitivity at 11.4 and 22.8 cycles per degree, indicating that the reduced contrast sensitivity was due to the drug therapy.

  • 18.
    Tomson, Torbjörn
    et al.
    Karolinska Inst, Stockholm, Sweden.
    Nilsson, Bengt Y
    Karolinska Inst, Stockholm, Sweden.
    Levi, Richard
    Karolinska Inst, Stockholm, Sweden.
    Impaired visual contrast sensitivity in epileptic patients treated with carbamazepine.1988Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 45, nr 8, s. 897-900Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Critical flicker fusion frequencies and visual contrast sensitivity were determined in 27 adult epileptic patients receiving carbamazepine monotherapy and in 24 healthy, drug-free control subjects. Flicker fusion thresholds were the same in patients and control subjects, whereas the contrast sensitivity was significantly reduced in the patient group at all spatial frequencies. There was a significant negative correlation between the plasma concentration of carbamazepine and the contrast sensitivity at 11.4 and 22.8 cycles per degree, indicating that the reduced contrast sensitivity was due to the drug therapy.

  • 19.
    von Strauss, Eva
    et al.
    Stockholm Gerontology Research Center, Division of Geriatric Medicine, Neurotec, Karolinska Institute, Stockholm.
    Viitanen, Matti
    Stockholm Gerontology Research Center, Division of Geriatric Medicine, Neurotec, Karolinska Institute, Stockholm.
    De Ronchi, Diana
    Stockholm Gerontology Research Center, Division of Geriatric Medicine, Neurotec, Karolinska Institute, Stockholm.
    Winblad, Bengt
    Stockholm Gerontology Research Center, Division of Geriatric Medicine, Neurotec, Karolinska Institute, Stockholm.
    Fratiglioni, Laura
    Stockholm Gerontology Research Center, Division of Geriatric Medicine, Neurotec, Karolinska Institute, Stockholm.
    Aging and the occurrence of dementia: Findings From a Population-Based Cohort With a Large Sample of Nonagenarians1999Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 56, nr 5, s. 587-592Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Context In spite of numerous studies on the occurrence of dementia, many questions remain, such as the relation between age, aging, and dementing disorders. This question is relevant both for understanding the pathogenetic mechanism of the dementias and for the public health prospective because of the increasing number of 85-year-old or older persons in our population.

    Objective To estimate the occurrence of dementia in the very old, including nonagenarians, in relation to age, gender, and different dementia types.

    Design An epidemiological survey where all participants were clinically examined by physicians, assessed by psychologists, and interviewed by nurses. The Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition (DSM-III-R) criteria for dementia were followed. A category of "questionable dementia" was added when all criteria were not fulfilled. A double diagnostic procedure was used for all subjects.

    Setting Community-based population, including all inhabitants of 2 areas in central Stockholm, Sweden (N=1848).

    Participants Of the 1848 subjects in the study population, 168 (9.1%) had died and 56 (3%) moved before examination. Of the remaining subjects, 1424 (87.7%) were examined, and the refusal rate was 12.3%.

    Main Outcome Measures Age- and gender-specific prevalence figures, and gender- and education-adjusted odds ratios were used.

    Results At the end of the diagnostic procedure, 358 clinically definite cases of dementia and 101 questionable cases of dementia were identified. Alzheimer disease (AD) contributed to 76.5%, and vascular dementia (VaD) to 17.9%. The prevalence of dementia increases from 13% in the 77- to 84-year-old subjects to 48% among persons 95 years and older (from 18% to 61% when questionable cases were included). The odds ratio for subjects 90 to 94 years and 95 years and older in comparison with 77- to 84-year-old subjects was 3.7 (95% confidence interval [CI], 2.7-5.1) and 6.5 (95% CI, 3.9-10.8) for dementia, 4.8 (95% CI, 3.3-7.0) and 8.0 (95% CI, 4.6-14.0) for persons with AD, 2.3 (95% CI, 1.3-4.2) and 4.6 (95% CI, 1.9-11.2) for VaD, respectively.

    Conclusions Dementia prevalence continues to increase even in the most advanced ages. This increase is especially evident among women and is more clear for AD. We believe that our prevalence data reflect the differential distribution of dementia risk.

  • 20. Winnberg Almqvist, Elisabeth
    et al.
    Huntington Study Group PHAROS Investigators, The
    At risk for Huntington disease: The PHAROS (Prospective Huntington At Risk Observational Study) cohort enrolled.2006Inngår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 63, nr 7, s. 991-6Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: To identify the emerging clinical precursors that indicate the early onset of Huntington disease (HD) in a reliable and gene-specific manner. This information is critical for the development of therapeutic trials aimed at postponing clinical onset in HD gene carriers. METHODS: Between July 1999 and January 2004, 1001 adults at 50-50 risk for HD agreed to provide longitudinal clinical data and a blood DNA sample under consent provisions that require their individual clinical and genetic information to never be revealed. RESULTS: The Prospective Huntington At Risk Observational Study (PHAROS) cohort is characterized by a 2:1 predominance of women to men, high educational attainment, and gainful employment. Despite the gender disparity, the demographic, hereditary, and clinical characteristics of the female and male participants were similar. Investigators, who are unaware of individual gene status, characterized the baseline cohort to be highly functional with minimal motor or cognitive impairment; 92.3% of participants were judged to have no or nonspecific motor abnormalities; 6.7%, to have possible or probable motor signs; and only 1.0%, to have unequivocal HD. CONCLUSION: The baseline characteristics of the PHAROS cohort make it well suited to generate objective and prospective data about gene-specific clinical precursors that can be used as outcomes in controlled trials aimed at postponing the onset of HD.

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