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Biomedical subjects

B Winblad

Publications and source records attributed to B Winblad.

At least 271 records · Page 15Linked to original sources
PubMed1995

Autonomic dysfunction in Alzheimer's disease.

Twenty-nine patients fitting the NINCDS-ADRDA criteria of Alzheimer's disease participated in a study of autonomic functions. A number of tests on parasympathetic and sympathetic functions were made. Eighteen of the patients were tested a second time one year later. Fifteen healthy subjects with no family history of dementia disorders served as controls. Compared to the controls, the patients showed signs suggesting autonomic dysfunction affecting parasympathetic, as well as vasomotor sympathetic, functions.

Age of Onset↗
PubMed1995

Prevalence and correlates of depression in a population of nonagenarians.

BACKGROUND: Clinicians see many more nonagenarian patients now and there is a need for epidemiological data relating to this group. The aim of the present study was to investigate the prevalence of depressive symptoms and syndromes in this age group. METHOD: The DSM-IV and the ICD-10 criteria for depression were used and correlated with physical health, disability in daily life, gender, use of drugs, social circumstances and cognitive dysfunction. Data were derived from 329 persons aged 90 and over, registered in a parish of Stockholm, who had been extensively examined by physicians and nurses. RESULTS/CONCLUSIONS: The prevalence of Major Depressive Episode as defined in DSM-IV was 7.9%; and of mild, moderate and severe Depressive Episode (combined); as defined in ICD-10 9.1%. No gender difference was found. Disability in daily life and the use of psychotropic drugs were found to correlate with depressive symptoms and syndromes.

Activities of Daily Living↗
PubMed1995

Dimensions and progression in the interaction between bilingual/monolingual caregivers and bilingual demented immigrants: analysis of video-recorded morning care sessions in institutions coded by means of the Erikson theory of "eight stages of man".

Seven demented Finnish immigrants were video-recorded during morning care together with bilingual and monolingual Swedish-speaking caregivers. A phenomenological-hermeneutic analysis of the video-recordings inspired by Ricoeur's philosophy was performed. The structural analysis was made by means of the Erikson theory of "eight stages of man." A statistical analysis was done in order to study dimensions and progression of interaction and compare the communication seen in relation to how caregivers supported the patients' integrity.

Adolescent↗
PubMed1995

Unexpected dental behavior in five Alzheimer patients. Differences between cognitive and functional capacity, graphic performance, and dental behavior.

The aim of the study was to analyze five patients with Alzheimer's disease in whom the degree of dementia assessed by cognitive and functional tests was at variance with the behavior in the dental setting and to relate these factors to the outcome of the graphic test. Possible reasons for the differences were discussed. The subjects were diagnosed as having Alzheimer's dementia on the basis of the DSM-III-R. Their cognitive and functional impairments were assessed with the Mini-Mental State Examination test and Katz's index of activities of daily living. Behavior in the dental office was registered in a structured form. The graphic function was assessed as Human Figure Drawing. Besides the stage of dementia, the patient's personality, social and medical background, and memories of previous dental care influence the demented patient's behavior in the dental office. To provide secure conditions for treating demented patients, the dentist must be able to interpret the patient's unique personality in the context of the dental situation.

Activities of Daily Living↗
PubMed1995

[Care of patients with dementia--a ticking cost bomb?].

Owing to the increasing number of elderly people, the prevalence of dementia will also increase. In 1990, there were about 101,000 people with moderate to severe dementia in Sweden, or 6.4 percent of the population over 65 years of age (65+ pop.). The figure will increase to about 121,000 by the year 2000 (7.7 percent of the 65+ pop.), and to 156,000 by 2025 (7.5 percent of the 65+ pop.). The corresponding health care costs, which were SEK 30 billion in 1991, are estimated to reach SEK 35 billion by 2000, and SEK 46 billion by 2025. Assuming comparable increases in the prevalence of dementia in the other Nordic countries, the overall number of dementia patients will increase from 247,000 in 1991 to 371,000 by 2025, and the respective costs from SEK 74 billion to SEK 110 billion.

Aged↗
PubMed1995

Early symptoms and neurological findings in demented subjects from a community survey.

The prevalence of the symptoms at disease onset reported by close informants, in an unselected group of demented elderly, is presented in this study. Of the 174 dementia cases, 98 were Alzheimer disease (AD), 41 were vascular dementia (VaD), and 35 were other dementias. In 42% of AD subjects, single memory deficit was the earliest problem, while in 56% of VaD cases, the tendency was to present two or more disturbances in the early stages. Slightly younger mean age at onset was reported in VaD than in AD cases. Our results support the hypothesis that the debut of the dementia is variable with any combination of symptoms. However, when memory problems start, assessment is needed. Among the neurological findings in the clinical examination, extrapyramidal signs were present in 25% of all dementia cases and in 20% of AD cases. A higher frequency of extrapyramidal signs was present in more severe cases, confirming previous reports of the unfavorable prognostic value of these signs.

Age Distribution↗
PubMed1994

Excessive production of amyloid beta-protein by peripheral cells of symptomatic and presymptomatic patients carrying the Swedish familial Alzheimer disease mutation.

The 39- to 43-amino acid amyloid beta-protein (A beta), which is progressively deposited in cerebral plaques and blood vessels in Alzheimer disease (AD), is secreted by cultured human cells during normal metabolism. In studies of cell lines transfected with beta-amyloid precursor protein (beta APP) cDNAs, the beta APP mutation K670N/M671L found in a Swedish familial AD (FAD) pedigree has previously been shown to cause a marked augmentation of A beta secretion. Here, we have conducted blinded analyses of beta APP metabolism in primary skin fibroblasts from affected members of the Swedish FAD pedigree and their unaffected siblings or spouses. These fibroblasts continuously secrete a homogenous population of A beta molecules starting at Asp-1 (D672 of beta APP). We found a consistent and significant approximately 3-fold elevation of A beta release from all biopsied skin fibroblasts bearing the FAD mutation. No significant alterations of other metabolic derivatives of beta APP were detected. The elevated A beta levels were found in cells from both patients with clinical AD and presymptomatic subjects. Thus, A beta overproduction in this FAD pedigree is not a secondary event but is consistent with a causal role in the development of the disease. Increased A beta secretion can begin many years prior to onset of symptoms, even in peripheral tissues, indicating that it does not require preexisting neural abnormalities.

Alzheimer Disease↗
PubMed1994

Loss of neurones after long-term adrenalectomy in the adult rat hippocampal formation.

The effects of long-term adrenalectomy (ADX) on hippocampal neurones were investigated 5 months after surgery in male Sprague-Dawley rats. Cells in Nissl-stained sections from ADX rats were counted and compared with those in sections from sham-operated rats. The ADX rats had a significantly reduced number of dentate granule cells. A novel finding was a significant reduction in the number of pyramidal cells in CA1, CA2, CA3 and CA4 regions of the hippocampus. Thus long-term adrenalectomy causes loss of dentate granule cells and pyramidal neurones of the hippocampus.

Adrenalectomy↗
PubMed1994

Increased beta-amyloid release and levels of amyloid precursor protein (APP) in fibroblast cell lines from family members with the Swedish Alzheimer's disease APP670/671 mutation.

Cell lines transfected with the Swedish Alzheimer's disease amyloid precursor protein APP670/671 mutation release significantly more beta-amyloid than wild-type cells. Citron et al. [Proc. Natl. Acad. Sci. USA (1994) in press] have recently shown that fibroblasts carrying the APP670/671 mutation also release more beta-amyloid than control cells [1]. The present study confirms a ca. threefold increase in beta-amyloid release from mutation-bearing fibroblasts. APP mRNA levels did not differ between mutation-bearing and control cells, although mutation-bearing fibroblasts contained significantly more APP751/770 than controls. Mild stress decreased beta-amyloid secretion and increased APP751/770 levels in all cell lines. In conclusion, the proportion of APP committed to amyloidogenic processing is increased in fibroblasts from family members with the APP670/671 mutation, and this mutation may also compromise the APP stress response.

Alzheimer Disease↗
PubMed1994

Relative abundance of Alzheimer A beta amyloid peptide variants in Alzheimer disease and normal aging.

The Alzheimer A beta amyloid peptide (A beta) is the principal proteinaceous component of amyloid associated with Alzheimer disease (AD). We have determined the relative abundance of A beta structural variants present in amyloid from brains of 10 individuals with sporadic AD, 2 individuals with familial AD carrying specific mutations in the Alzheimer amyloid precursor protein gene, and 5 nondemented elderly controls. A procedure of isolation based on the extreme insolubility of A beta amyloid was used. The purified, nondigested A beta was analyzed by N-terminal sequencing and electrospray-ionization mass spectrometry. Three principal A beta variants were detected--A beta-(1-40), A beta-(1-42), and A beta-(11-42)--in all brains analyzed. The predominant variant in sporadic AD was A beta-(1-40), whereas the principal A beta variant in nondemented elderly controls was A beta-(1-42). The ratio A beta-(1-40)/A beta-(1-42) differed by 10-fold between brains from nondemented controls and those with sporadic AD.

Aged↗
PubMed1994

Astrocytes associated with senile plaques possess muscarinic acetylcholine receptors.

AUTOPSY sections of the temporal and parahippocampal gyri were incubated with the monoclonal antibody M35 to label muscarinic acetylcholine receptors. Senile plaques were visualized either by counterstaining with Congo red or by Bielschowsky silver-stain of adjacent sections. The antibody labelled pyramidal and non-pyramidal cells in the grey matter, as well as fibrous astrocytes in the white matter and first cortical layer, of elderly control brains. In AD brains however, the grey matter was characterized by prominently labelled fibrous astrocytes and few or poorly labelled neurones. M35-immunoreactive astrocytes were often associated with senile plaques. These findings suggest that plaque-associated astrocytes may be responsive to acetylcholine or cholinergic drugs.

Aged↗
PubMed1994

Lack of association between apolipoprotein E allele epsilon 4 and sporadic Alzheimer's disease.

Apolipoprotein E (apoE) is a protein involved in the transport of lipids and a component of Alzheimer's disease (AD) plaques. There are three common alleles of the apoE gene, designated epsilon 2, epsilon 3 and epsilon 4. An association between familial and sporadic AD and the epsilon 4 allele was recently reported. We have investigated Swedish Alzheimer patients and controls. The epsilon 4 allele frequency in familial and sporadic cases and in controls was 47, 22 and 18%, respectively. There was no significant difference between sporadic AD and controls but in familial cases the increased epsilon 4 allele frequency previously reported was confirmed.

Aged↗
PubMed1994

Amyloid precursor protein mutation causes Alzheimer's disease in a Swedish family.

Since the report of a double mutation at codons 670 and 671 of the amyloid precursor protein (APP) gene identified in two Swedish families with clinically diagnosed Alzheimer's disease (AD), a carrier with dementia has died. Neuropathology confirmed the clinical diagnosis of AD. Genealogical investigations have confirmed that the two families are related to common founders. Two-point linkage analysis of the mutation versus the disease in the revised pedigree now gives a lod score of 7.62.

Aged↗
PubMed1994

Regionally selective alterations in G protein subunit levels in the Alzheimer's disease brain.

In the present study the relative densities of a number of G protein subunits were quantified in membranes prepared from the hippocampus, temporal cortex and angular gyrus of Alzheimer's disease and control post-mortem brain by immunoblotting with specific polyclonal antisera against Gs alpha, Gi alpha, Gi alpha-1, G(o) alpha and G beta protein subunits. In addition, basal, Gs-stimulated and Gi-inhibited adenylyl cyclase activities were measured in the same hippocampal membrane samples. Densitometric analysis of the immunoblot data revealed a 58% reduction in the levels of Gi alpha, and a 75% reduction in the levels of Gi alpha-1, in the Alzheimer's disease temporal cortex. Gi alpha levels were reduced, by 37% in the angular gyrus of the Alzheimer's disease cases. The ratio of large to small molecular weight isoforms of the Gs alpha subunit was significantly increased in both the hippocampus and the angular gyrus of the Alzheimer's disease samples when compared to control values, although the difference in individual Gs alpha isoform levels did not attain statistical significance when comparing groups. No statistically significant differences were observed in G(o) alpha or G beta levels when comparing control and Alzheimer's disease cases. Gs-stimulated adenylyl cyclase activity was significantly reduced in the Alzheimer's disease samples compared to controls, whereas Gi-inhibited adenylyl cyclase activity was unchanged. No significant differences were observed between the control and Alzheimer's disease samples for either basal or forskolin stimulated adenylyl cyclase activity. The ratio of hippocampal Gs-stimulated to basal adenylyl cyclase activity correlated significantly with the large to small Gs alpha subunit ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1994

beta-Amyloid related peptides exert differential effects on [3H]MK-801 binding to rat cortical membranes.

The effects of beta-amyloid protein 1-40 (beta AP 1-40), substance P (SP), and the amidated and carboxylic acid C-terminated forms of the SP homologous beta AP fragment 25-35 (beta AP 25-35-NH2 and beta AP 25-35-COOH) were studied on [3H]MK-801 binding to the rat brain NMDA receptor cation channel. All peptides gave dose-dependent enhancements of [3H]MK-801 binding stimulated by low glycine. beta AP 25-35-COOH, but not beta AP 25-35-NH2 produced an inhibition of [3H]MK-801 binding stimulated by high glycine in the presence of either low or high glutamate. Low glutamate-stimulated [3H]MK-801 binding was also inhibited by SP but not by beta AP 1-40. It is concluded that beta AP related peptides exert differential effects on the NMDA receptor complex at the glycine and possibly also the glutamate recognition sites.

Amyloid beta-Peptides↗
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↗