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H Basun

Publications and source records attributed to H Basun.

At least 55 records · Page 3Linked to original sources
PubMed1996

Apolipoprotein E polymorphism and stroke in a population sample aged 75 years or more.

BACKGROUND AND PURPOSE: We investigated apolipoprotein E polymorphism stroke risk in a population sample of 1810 persons aged 75 years or more in Stockholm (the Kungsholmen Project). Information on cognition at cohort inception (from 1987 to 1989) and on stroke occurrence (from 1969 to 1994) is available for the cohort. In the cohort, cognitive impairment is associated with the epsilon 4 allele, and longer survival in subjects aged > or = 85 years with good cognition is associated with the epsilon 2 allele and the absence of epsilon 4. METHODS: We compared stroke incidence in the 1077 of 1124 genotyped subjects who carried epsilon 2/3, epsilon 3/3, or epsilon 3/4 and estimated the proportion of cognitive impairment attributable to stroke. RESULTS: Risk of stroke did not vary with apolipoprotein E polymorphism (P = .82): 24% of 87 incident stroke patients during follow-up compared with 25% of 827 subjects with normal cognition and no stroke diagnosis at baseline carried the epsilon 3/4 genotype. An estimated 9% of cognitive impairment was attributable to stroke. Notably, a reduced epsilon 3/4 frequency of 20% was found in subjects who survived a prior stroke and were included in the cohort, and risk of hemorrhagic stroke tended to be associated with the presence of the epsilon 3/4 genotype and the absence of epsilon 2/3. CONCLUSIONS: This population-based study indicates that apolipoprotein E polymorphism is not a risk factor for ischemic stroke in subjects aged > or = 75 years (although it might possibly influence survival after stroke occurrence and be a risk factor for infrequent hemorrhagic stroke) and that approximately 10% of cognitive impairment in this age group is attributable to stroke.

Aged↗
PubMed1995

Amyloid beta-peptide in cerebrospinal fluid in individuals with the Swedish Alzheimer amyloid precursor protein mutation.

The neuropathological hallmarks of Alzheimer's disease (AD) are amyloid-containing plaques and neurofibrillary tangles. The main constituent of senile plaques is amyloid beta-peptide (A beta) and in recent years, pathogenic mutations in the amyloid precursor protein (APP) gene have been discovered in some AD families. The APP670/671 mutation, found in a Swedish AD family, has revealed over-production of A beta as one pathogenic mechanism for the development of AD. In the present study we have used an immunoassay to measure A beta levels in cerebrospinal fluid (CSF) from APP670/671 mutation-carriers and non-carriers. A correlation was seen between decrease in A beta levels and duration of disease although no difference was found in levels of A beta between the groups (14.5 +/- 3.3 ng/ml versus 14.9 +/- 2.3 ng/ml).

Adult↗
PubMed1995

Increased cerebrospinal fluid tau in patients with Alzheimer's disease.

One of the pathological features in Alzheimer's disease (AD) is neurofibrillary tangles in the brain. The main constituent of tangles is the microtubuli-associated protein tau in a hyperphosphorylated state. Tau is also released into cerebrospinal fluid (CSF), and in this study we have used an enzyme linked immunosorbent assay to measure tau in CSF from AD and control cases. Our findings show that tau levels in AD cases are significantly elevated compared to healthy control individuals. We suggest that tau may serve as a biochemical marker of Alzheimer's disease.

Aged↗
PubMed1995

Apolipoprotein epsilon 4 allele and disease progression in patients with late-onset Alzheimer's disease.

A random sample of 60 late-onset Alzheimer's disease (AD) cases from a population-based study were apolipoprotein E (apoE) genotyped and clinically examined with a 3-year interval. The epsilon 4 allele carriers had a significantly lower age of disease onset compared to non-epsilon 4 carriers. However, no significant differences were observed between epsilon 4 allele carries and non-carriers for Mini-Mental State Examination (MMSE) test scores at the first examination, in spite of a longer disease duration in the epsilon 4 allele carriers. After 3 years, MMSE test scores were still not significantly different between epsilon 4 carries and non-carriers but more than twice as many non-carriers had died. All other clinical features were similar between epsilon 4 allele carriers and non-carriers. This study indicates that the epsilon 4 allele is associated with a better prognosis of the disease in late-onset AD but that there are probably factors other than the epsilon 4 allele that are important for the AD phenotype.

Age of Onset↗
PubMed1995

EEG in successful aging; a 5 year follow-up study from the eighth to ninth decade of life.

Fifteen out of 25 successfully aged individuals completed a 5 year EEG follow-up study from the eighth to ninth decade of life with comprehensive neuropsychological investigation. One subject suffered from stroke and one developed symptoms of dementia during the follow-up. Of 13 subjects who completed the follow-up as being healthy, MRI showed subtle enlargement of ventricles or subarachnoid spaces and mild signal hyperintensities in a few regions in 2 subjects. General cognitive decline was not observed (WAIS-R IQ: 113.4 at entry, 114.3 five years later). There were no EEG dominant frequencies below 8 c-sec and no more background slowing than a few theta waves per 10 sec, either at entry or 5 years later. Intermittent slowing was observed in 9 subjects at entry and in 8 subjects 5 years later. The prevalence of intermittent slowing was suggested to increase with advancing age when compared to previous studies with younger elderly. However, intermittent slowing occurred only a few times in an EEG test and lasted for less than 2 sec. Moreover, the presence of intermittent slowing did not correlate with any neuropsychological decline or any MRI change. This type of intermittent slowing was regarded as non-specific and clinically silent.

Aged↗
PubMed1995

Decreased alpha-secretase-cleaved amyloid precursor protein as a diagnostic marker for Alzheimer's disease.

The neuropathologic hallmarks of Alzheimer's disease (AD) are extracellular plaques and intracellular neurofibrillary tangles. A constituent of senile plaques in AD is beta-amyloid, a hydrophobic peptide of 39-43 amino acids and a fragment of the amyloid precursor protein (APP). APP can be metabolized by at least two pathways, one of which involves generation of soluble APP by an unidentified enzyme named alpha-secretase. This cleavage generates alpha-secretase-cleaved, soluble APP (alpha-sAPP), which in this investigation was measured by a new assay in cerebrospinal fluid (CSF) from members of a Swedish AD family with a pathogenic mutation at APP670/671 (ref. 2). Family members who carry the mutation and are diagnosed with AD had low levels of alpha-sAPP (160 +/- 48 ng ml-1), with no overlap compared with non-carriers (257 +/- 48 ng ml-1). Carriers of the presymptomatic mutation showed intermediate alpha-sAPP levels. Today there exists no antemortem marker in AD with sufficient sensitivity and specificity, but measurement of alpha-sAPP represents a new and promising diagnostic marker.

Adult↗
PubMed1995

Microsatellite D21S210 (GT-12) allele frequencies in sporadic Alzheimer's disease.

Four disease-causing mutations have so far been described in the amyloid precursor protein gene on chromosome 21 in familial early-onset Alzheimer's disease. Linkage analysis with a fourteen-allele microsatellite at D21S210 named GT-12 has proven useful in the elucidation of amyloid precursor protein gene involvement in Alzheimer's disease families, as it is closely linked to the gene. Most cases of Alzheimer's disease are thought to be sporadic and not familial. However, evidence from earlier studies suggests an important genetic contribution also in sporadic cases, where gene-environment interaction may contribute to the disease. We have determined frequencies of the GT-12 alleles in 78 Swedish and 49 British sporadic Alzheimer's disease cases and 104 healthy elderly control subjects, to investigate if the disease associates with a particular genotype in GT-12. However, no differences in allele frequencies were observed between any of the groups.

Aged↗
PubMed1994

A large Swedish family with Alzheimer's disease with a codon 670/671 amyloid precursor protein mutation. A clinical and genealogical investigation.

OBJECTIVE: To describe clinical and genealogic features in a Swedish family with Alzheimer's disease with a double mutation of the amyloid precursor protein gene at codon 670/671 and to study the effects of anticipation and imprinting. DESIGN: Interviews with relatives, clinical investigations of the diseased, pedigree analysis, studies of medical records, and comparison with other families affected by Alzheimer's disease with amyloid precursor protein mutations. SETTING: The Alzheimer's Disease Research Centre, Department of Clinical Neuroscience, Section of Geriatric Medicine, Karolinska Institute, Huddinge (Sweden) University Hospital. PATIENTS AND OTHER PARTICIPANTS: Individuals with the amyloid precursor protein codon 670/671 mutation and their relatives (N = 66). RESULTS: The trait was traced through eight generations, and an autosomal dominant inheritance with very high penetrance was observed. Onset occurred between 44 and 61 years of age (mean, 53 years). The mean duration of disease was 8.5 years (range, 3 to 13 years). The earliest clinical manifestations were deficits in memory function and abstract reasoning. Myoclonic jerks and seizures were common symptoms late in the disease. Anticipation and imprinting effects were not found in this family. CONCLUSIONS: The disease in this family has a single origin--a double mutation in the amyloid precursor protein gene at codon 670/671 transmitted as an autosomal dominant trait. The wide range in age at onset and the clinical symptoms in this pedigree give a characteristic phenotype similar to that seen in some of the other pedigrees with amyloid precursor protein mutations.

Adult↗
PubMed1994

Cadmium in blood in Alzheimer's disease and non-demented subjects: results from a population-based study.

Blood cadmium concentrations were studied in Alzheimer's disease (AD) and non-demented subjects. The 29 individuals were randomized from the ongoing population survey on ageing and dementia in Stockholm, the Kungsholmen Project. Smokers had, as expected, higher cadmium levels than non-smokers. Cadmium concentrations in blood were related to diastolic blood pressure in non-smoking, non-demented individuals. In contrast to previous reports no differences in blood cadmium levels were found between AD sufferers and non-demented subjects. Furthermore, there were no correlations between cadmium levels in blood and age or cognitive functions. The importance of quality assurance in sample collection and analysis of cadmium as well as scrutinizing smoking habits is emphasized.

Aged↗
PubMed1994

White matter hyperintensities in dementia: does it matter?

The aim of the study was to investigate whether the regional distribution of white matter hyperintensities (WMH) observed by magnetic resonance imaging differed between vascular dementia and patients with late onset Alzheimer's disease. Another aim was to investigate the relations between the occurrence and degree of WMH and clinical and laboratory data as well as measures of cognitive decline. White matter hyperintensities were assessed with a low field magnetic resonance imager on 23 subjects with probable Alzheimer's disease, 25 with possible Alzheimer's disease and 31 subjects with vascular dementia. The degree and regional distribution of the WMH (expressed as relative volumes) were calculated and compared in the three groups. The relation between cognitive impairment and the degree of the WMH was also studied. The regional distribution of the WMH differed between the groups with significantly more changes in the posterior part of the brain (p < .0001) as well as in the right hemisphere (p < .0005) in the vascular demented as compared to the patients with Alzheimer's disease. No significant correlations between cognitive impairment and the degree of the WMH were found in any of the groups. The total volume of the WMH as well as the regional distribution of these changes differed significantly between vascular dementia and Alzheimer's disease. White matter hyperintensities seem not to be related to the degree of global cognitive decline in dementia and whether it plays a causative role in the development of dementia symptoms needs to be more thoroughly investigated.

Aged↗
PubMed1994

Cobalamin levels are not reduced in Alzheimer's disease: results from a population-based study.

OBJECTIVE: To determine whether there is a relationship between serum cobalamin levels, normal aging, and Alzheimer's Disease (AD). DESIGN: Cross-sectional survey. SETTING: A district (Kungsholmen) in Stockholm, Sweden. PARTICIPANTS: Population-based cohort of 545 subjects aged more than 74 years. The sample was selected on the basis of evidence of cognitive impairment from all inhabitants in an area of Stockholm (2368 individuals), both living at home or in institutions. MEASUREMENTS: Serum cobalamin levels and diagnostic evaluation for a diagnosis of dementia and type of dementia. RESULTS: The serum cobalamin levels in non-demented individuals decreased 5.5 pmol/L with an increase of 1 year of age (regression coefficient = -5.53; P < 0.0001). However, the regression coefficient was 0.21 (P = 0.91) in demented people and 2.57 (P = 0.32) in AD subjects. There was no difference between serum cobalamin levels in demented, AD, and non-demented subjects, except for the oldest ages where demented people and AD sufferers showed higher values. AD patients still living in their own homes had significantly lower cobalamin concentrations compared with institutionalized AD sufferers. The prevalence rate of cobalamin deficiency was 15.5% (95% CI = 11.5-19.5) in normal aging and 18.1% (95% CI = 10.3-25.9) in AD. CONCLUSIONS: These data suggest that serum cobalamin levels decrease in normal aging, but not in dementia or AD. A lower cobalamin concentration observed in AD sufferers still living in their own homes compared with institutionalized persons with AD seemed to be related to but not fully explained by eating habits. Patients with AD living in their own homes are at risk of developing cobalamin deficiency, and monitoring of serum cobalamin concentrations might be useful in this group.

Aged↗
PubMed1993

Cognitive functions and brain structures: a quantitative study of CSF volumes on Alzheimer patients and healthy control subjects.

In the present study we have investigated the connection between cerebrospinal fluid spaces and cognitive function in patients with senile dementia of Alzheimer type (SDAT) and in successfully aged control subjects. The cerebrospinal fluid (CSF) volumes were measured using a low field MRI technique, and the cognitive functions were assessed with a number of psychometric tests. We found that the SDAT patients showed significantly larger relative volumes in all examined CSF spaces. The largest differences between the groups were found in the volumes of the temporal horns. We also found a significant correlation between the relative CSF volumes in the basal parts of the brain, and episodic memory tests. Significant correlations were also detected between the relative volumes of the lateral ventricles, and degree of dementia as well as between the relative volumes of the lateral ventricles and episodic memory tests.

Aged↗