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Träfflista för sökning "hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Psykiatri) srt2:(2000-2009);srt2:(2005)"

Sökning: hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Psykiatri) > (2000-2009) > (2005)

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2.
  • Passant, Ulla, et al. (författare)
  • Psychiatric Symptoms and Their Psychosocial Consequences in Frontotemporal Dementia.
  • 2005
  • Ingår i: Alzheimer Disease and Associated Disorders. - 0893-0341. ; 19 Suppl 1, s. 15-18
  • Tidskriftsartikel (refereegranskat)abstract
    • Based on a retrospective study of 19 neuropathologically verified cases with frontotemporal dementia (FTD), neuropsychiatric symptoms related to behavioral disturbances and their psychosocial consequences were studied. The results indicate that frontotemporal dementia is often misdiagnosed early in the clinical course. Behavioural features with impaired social interactions, impaired personal regulation, and loss of insight were seen in all patients. The psychosocial consequences reported in this paper challenge future research in frontotemporal dementia.
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3.
  • Höglund, Kina, 1976, et al. (författare)
  • The effect of simvastatin treatment on the amyloid precursor protein and brain cholesterol metabolism in patients with Alzheimer's disease
  • 2005
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 19:5-6, s. 256-265
  • Tidskriftsartikel (refereegranskat)abstract
    • During the last years, several clinical studies have been published trying to elucidate the effect of statin treatment on amyloid precursor protein (APP) processing and metabolism of brain cholesterol in Alzheimer’s disease (AD) in humans. We present an open biochemical study where 19 patients with AD have been treated with simvastatin (20 mg/day) for 12 months. The aim was to further investigate the effect of simvastatin treatment on cerebrospinal fluid (CSF) biomarkers of APP processing, AD biomarkers as total tau and tau phosphorylated at threonine 181, brain cholesterol metabolism as well as on cognitive decline in patients with AD. Despite biochemical data suggesting that treatment with 20 mg/day of simvastatin for 12 months does affect the brain cholesterol metabolism, we did not find any change in CSF or plasma levels of β-amyloid (Aβ)<sub>1–42</sub>. However, by analysis of APP isoforms, we found that statin treatment may favor the nonamyloidogenic pathway of APP processing. The relevance and mechanism between statin treatment and AD has to be further elucidated by using statins of different lipophility in different dosages over a longer period of time.
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4.
  • Johansson, Annica, 1969, et al. (författare)
  • Genetic association of CDC2 with cerebrospinal fluid tau in Alzheimer's disease
  • 2005
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 20:6, s. 367-374
  • Tidskriftsartikel (refereegranskat)abstract
    • We have recently reported that a polymorphism in the cell division cycle <i>(CDC2) </i>gene, designated Ex6 + 7I/D, is associated with Alzheimer’s disease (AD). The <i>CDC2</i> gene is located on chromosome 10q21.1 close to the marker D10S1225 linked to AD. Active cdc2 accumulates in neurons containing neurofibrillary tangles (NFT), a process that can precede the formation of NFT. Therefore, <i>CDC2 </i>is a promising candidate susceptibility gene for AD. We investigated the possible effects of the <i>CDC2</i> polymorphism on cerebrospinal fluid (CSF) biomarkers in AD patients. <i>CDC2</i> genotypes were evaluated in relation to CSF protein levels of total tau, phospho-tau and β-amyloid<sub>(1–42)</sub> in AD patients and control individuals, and in relation to the amount of senile plaques and NFT in the frontal cortex and in the hippocampus in patients with autopsy-proven AD and controls. The <i>CDC2</i> Ex6 + 7I allele was associated with a gene dose-dependent increase of CSF total tau levels (F<sub>2, 626</sub> = 7.0, p = 0.001) and the homozygous <i>CDC2</i> Ex6 + 7II genotype was significantly more frequent among AD patients compared to controls (p = 0.006, OR = 1.57, 95% CI 1.13–2.17). Our results provide further evidence for an involvement of cdc2 in the pathogenesis of AD.
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5.
  • Nilsson, Christer, et al. (författare)
  • Transitorisk global amnesi - godartat tillstånd som även kan drabba unga
  • 2005
  • Ingår i: Läkartidningen. - 0023-7205. ; 102:24, s. 7-1905
  • Tidskriftsartikel (refereegranskat)abstract
    • Transient global amnesia (TGA) occurs mostly in middle-aged and elderly individuals, and is generally believed to be very rare in individuals less than 40 years of age. We present three cases of TGA in young persons (16-22 years). They all had a medical history and presented symptoms fulfilling the criteria for TGA. Physical examinations and investigations were all normal. All three presented their symptoms while playing football. Reviewing the literature the suggested causes are partly different for TGA in old and young people, respectively. The present report confirms that TGA may also occur in younger individuals. We propose that single TGA is a benign condition also in younger persons and that the investigation should be similar to that of TGA in older age groups.
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6.
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7.
  • Nägga, Katarina, 1962-, et al. (författare)
  • Evaluation of factors of importance for clinical dementia diagnosis
  • 2005
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 19:5-6, s. 289-298
  • Tidskriftsartikel (refereegranskat)abstract
    • Diagnosing clinical dementia is based on an assessment of different variables, such as the patient’s medical history, known risk factors, and biochemical features. Partial least squares discriminant analysis was used to evaluate variables of importance for diagnosing dementia in a clinical dementia population. Polymorphism for genotypes of glutathione S-transferase (GST) and sulfotransferase 1A1, hypothetically of importance in dementia disorders, was also included in the analysis. The study population consisted of 73 patients with Alzheimer’s disease (AD), 14 with mixed dementia, 75 patients with vascular dementia, and 28 control cases. We found that several of the variables, such as the presence of ApoE4 allele, high cerebrospinal fluid levels of total tau protein, low levels of β-amyloid<sub>(1–42)</sub>, and a low score on the Mini-Mental State Examination, facilitated a discrimination between the diagnoses compared with the controls. The different diagnoses overlapped. There were indications that genotypes of GSTs contributed to a subgrouping within AD.
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8.
  • Andin, Ulla, et al. (författare)
  • A Clinico-Pathological Study of Heart and Brain Lesions in Vascular Dementia.
  • 2005
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 19:4, s. 222-228
  • Tidskriftsartikel (refereegranskat)abstract
    • All vascular dementia (VaD) cases, neuropathologically verified in a longitudinal prospective dementia project, were classified according to the vascular brain lesion type and related to the dementia type and cardiovascular pathology. From 1976 to 1995, there were 175 VaD cases, 49 of which were pure, without Alzheimer pathology and only one type of cerebrovascular lesion. Furthermore, it was found that 6 cases suffered hypoxic hypoperfusive disease, while 7 were found to have large vessel disease and 36 small vessel disease. In addition to Alzheimer pathology, more than one type of vascular brain pathology was found in the remaining 126 cases. In these cases, diagnosed in accordance with the predominant type of VaD, hypoxic-hypoperfusive lesions were found in 55, large vessel lesions in 50 and small vessel lesions in 110 cases. It should be stressed that 87% of all cases with hypoxic hypoperfusive lesions also had Alzheimer pathology. Cardiovascular and aortic pathologies were more prevalent in small vessel dementia than in the other VaD groups. Clinically diagnosed arterial hypertension was significantly associated with small vessel dementia, but not with hypoxic-hypoperfusive dementia. Cardiovascular symptoms varied considerably in frequency between different dementia groups. VaD is a heterogeneous group regarding lesions caused by different pathophysiological mechanisms and with different combinations of brain pathologies. It is therefore necessary to identify the various types of vascular brain lesions for a correlation with clinical symptoms and for diagnostic purposes in the search for risk factors and therapeutic strategies.
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10.
  • Gräsbeck, Anne, et al. (författare)
  • Dementia in First-Degree Relatives of Patients with Frontotemporal Dementia. A Family History Study.
  • 2005
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 19:2-3, s. 145-153
  • Tidskriftsartikel (refereegranskat)abstract
    • Several studies have found a clustering of dementia in relatives of patients with frontotemporal dementia (FTD). This study analysed the familial aggregation of FTD specifically as well as the occurrence of dementia in general in first-degree relatives of patients with FTD. A family history study was carried out on 478 first-degree relatives of 74 index patients suffering from FTD. Cases of organic dementia and of FTD were diagnosed according to internationally accepted diagnostic criteria. Age- and sex-specific incidences of organic dementia and of FTD were calculated as was the proportion of FTD in relation to organic dementia in general; comparisons with clinical and population studies were made. There was a tenfold increase in the incidence of FTD in the first-degree relatives of FTD patients compared with the incidence of FTD in a population study. The proportion of FTD in relation to all types of organic dementia was much higher in relatives of FTD patients compared to the corresponding proportions in clinical and population-based studies. There was a small, non-significant difference between the present family history study and the population studies as regards the incidence of organic dementia. The findings suggest that hereditary and/or shared environmental factors are strongly involved in the aetiology of FTD. There were no indications of familial clustering of organic dementia in general in relatives of FTD patients.
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