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Biomedical subjects

B Winblad

Publications and source records attributed to B Winblad.

At least 307 records · Page 17Linked to original sources
PubMed1994

[Care of demented patients with severe communication problems].

Two time-studies and an interview study were carried out at a geriatric clinic. The aim was to elucidate how much time caregivers use for direct patient care in their contact with severely demented patients compared with non-demented patients as well as how they experience the care of demented patients in a task assignment care system. The analysis showed that more time was used to help non-demented patients than demented patients with the same ADL-performance. Five types of patient reactions to communicative attempts made by the caregivers were described: the patient seems to enjoy contact, he avoids contact, contact leads to aggression, he reacts only sporadically to contact and he does not show any reactions to it. The caregivers described negative reactions to demented patients with communication problems. Communication problems seem to be a threat to caregivers' commitment.

Activities of Daily Living↗
PubMed1994

[Early stimulation--good memory in old age?].

For better or worse, the importance of neonatal stimulation has attracted increasing attention in recent years. Results from animal studies provide a hint of possible beneficial consequences for humans, even in a geriatric context.

Aged↗
PubMed1994

[Acute confusional states in patients with hip fractures can be prevented and treated].

Acute confusional states among the elderly constitute a manifest problem in most medical specialties. All too often the disoriented patient is deemed to be suffering from dementia, and no investigation is made of the background factors. Intervention studies have clearly shown that confusional states are both reversible and preventable.

Adrenocortical Hyperfunction↗
PubMed1993

Alzheimer's disease: molecular genetics and transgenic animal models.

Disease-causing mutations in the amyloid precursor protein (APP) gene have been found on chromosome 21 during the last 2 years in some early onset Alzheimer's disease (AD) families. Genetic evidence shows that other genes than the APP are also involved in the aetiology of AD. Linkage to a loci on chromosome 14 has been found in early onset disease. The identification of APP mutation has led to the realization that APP mismetabolism is a central event in the aetiology and pathogenesis of the disease. Experiments to test this in transgenic mice have so far met with little success. There are many possible explanations for the problems to generate transgenic mice. These include the possibilities that mice are incapable of developing AD for reasons dependent on their APP sequence; and that appropriate regulation of APP gene is required for pathology to develop. Current attempts that seem promising to model the disease pathology are the use of homologous recombination to insert the pathogenic mutation and transfection of YACs into transgenic animals.

Aged↗
PubMed1993

Decrease of somatostatin receptor binding in the rat cerebral cortex after ibotenic acid lesion of the nucleus basalis magnocellularis: a quantitative autoradiographic study.

The specific binding of 125I-Tyr11-somatostatin-14 (125I-Tyr11-SS-14) was measured in different cortical regions after unilateral ibotenic acid lesion of the rat nucleus basalis magnocellularis (NBM). A marked loss of acetylcholinesterase-positive fibers was observed in the frontal, parietal, temporal and occipital cortices ipsilateral to the lesion. The loss of cholinergic cell bodies in the NBM was further investigated with choline-acetyltransferase (ChAT) immunohistochemistry which indeed demonstrated a loss of ChAT-positive magnocellular perikarya. Autoradiographic analyses of specific binding of 125I-Tyr11-SS-14 demonstrated a significant reduction in binding density in the denervated parts of the neocortex. The decrease in specific binding was most pronounced (40-50%) in the superficial layers (I-III) of the frontal, parietal and temporal cortices 2 and 4 weeks after lesion. A significant loss in 125I-Tyr11-SS-14 binding in the deeper layers was only observed in the frontal cortex after 2 and 4 weeks. In the occipital cortex a significant decrease was measured in the superficial layers only after 4 weeks. The specific binding in all cortical regions returned to normal after 6 weeks. The results suggested that 125I-Tyr11-SS-14 binding sites are localized on cholinergic afferents in the rat neocortex and that an up-regulation of number of binding sites, alternatively an increased binding affinity occurred with time after lesion.

Animals↗
PubMed1993

Environmental influence on somatostatin levels and gene expression in the rat brain.

In the present study we have quantified preprosomatostatin-mRNA and somatostatin levels in rat brain following environmental stimulation. Animals were housed for 30 days in an enriched or impoverished environment prior to analysis. After 30 days of housing half of the rats from each environment were behaviourally tested for 3 days. Housing in enriched environment improved performance in a spatial learning situation. The open-field behaviour of these animals was characterized by initially higher rearing scores and a more rapid habituation to novel environment as measured by spontaneous locomotor activity. We found significantly elevated somatostatin levels in the cortex following enriched environment, compared with impoverished environment. Exposure to behavioural testing of impoverished animals led to increased cortical somatostatin levels. Hypothalamic somatostatin levels increased significantly after housing in enriched environment, while the testing procedure had no influence. Our data shows that the somatostatin system in the rat brain was activated in association with cognitive changes, that were induced by housing in an enriched environment.

Animals↗
PubMed1993

Muscarinic and nicotinic receptor changes in the cortex and thalamus of brains of chronic alcoholics.

The cholinergic system was studied in the cortical and thalamic brain tissues obtained at autopsy from 21 chronic alcoholics and 20 controls. The age related decrease in choline acetyltransferase (ChAT) activity observed in the thalamus of control brains was not found in the corresponding brain areas of chronic alcoholics. A significant decrease in the number of muscarinic receptor binding sites was observed with age in the frontal cortex of both controls and chronic alcoholics when analysed with the nonselective muscarinic antagonist [3H]quinuclidinyl benzilate ([3H]QNB). A significant increase in the number of muscarinic receptor binding sites was observed in the thalamus of controls but not in chronic alcoholics. When the subjects were divided into young (19-57) years, and old (59-84 years) chronic alcoholics marked losses in the total number of muscarinic receptors as well as M1 and M2 receptor subtypes were found in the thalamus of the old group of alcoholics compared to age-matched controls. A coupling of muscarinic receptors to G proteins was observed in thalamic tissues from both controls and chronic alcoholics. Guanylyl-imidodiphosphate (Gpp(NH)p) induced a steepening and rightward shift of the carbachol/[3H]QNB displacement curves performed in membrane preparations of the thalamus from both controls and chronic alcoholics. The number of high affinity nicotinic binding sites in the frontal cortex and thalamus did not differ significantly between controls and chronic alcoholics.

Adult↗
PubMed1993

Subchronic MK-801 treatment to juvenile rats attenuates environmental effects on adult spatial learning.

Treatment with the non-competitive NMDA receptor blocker MK-801 (0.16 mg/kg), given to juvenile rats before and after the exposure to an enriched environment on alternate days for 4 weeks, attenuated the improvements in spatial learning and open field adaptation which resulted from such environmental stimulation. Drug treatment affected the consolidation of experiences as an injection given after exposure to the enriched environment was needed to demonstrate this effect. In addition, MK-801 administration diminished the adverse effect of stimulus deprivation-the slow learning rate normally seen in rats housed in impoverished environment. Radioligand binding studies showed that drug treatment decreased [3H]MK-801 binding sites in cortex. The learning, activity and receptor binding effects were measured 4 months from cessation of the drug treatment and environmental manipulation. The results support the role of NMDA receptors in mediating cognitive changes associated with environmental stimulation.

Animals↗
PubMed1993

Disrupted beta 1-adrenoceptor-G protein coupling in the temporal cortex of patients with Alzheimer's disease.

The efficacy of beta 1-adrenoceptor-G protein coupling was studied in postmortem temporal cortex synaptic membranes from a series of control and Alzheimer's disease subjects. For the control cases, the non-hydrolysable GTP analogue 5'-guanylylimidodiphosphate (Gpp[NH]p) gave a significant reduction in the affinity of the agonist isoprenaline to displace binding of the radiolabelled antagonist (+/)-4-(3-t-butylamino-2-hydroxypropoxy)[5,7-3H]benzimidazol-2-one ([3H]CGP-12177). This effect was attributed to the conversion of high agonist-affinity sites to a lower-affinity state and was not found for the Alzheimer's disease cases. These data indicate that a disruption of beta 1-adrenoceptor-G protein coupling occurs in the temporal cortex of Alzheimer's disease patients.

Aged↗
PubMed1993

Low frequency of the APP 670/671 mutation in familial Alzheimer's disease in Sweden.

Molecular genetic studies have identified disease-causing mutations at codon 717 of the amyloid protein precursor gene in families with early-onset Alzheimer's disease. Recently, we reported a new mutation at codon 670/671 in a large Swedish family with Alzheimer's disease. The mutation results in two amino acid changes at the N-terminal of the beta-amyloid region. In the present study, we screened for the APP 670/671 mutation in sufferers from 31 other Swedish families with Alzheimer's disease using PCR and restriction enzyme digestion. The mutation was found only in the family previously reported and not in any other family. It is concluded that this mutation is a rare cause of familial Alzheimer's disease in Sweden.

Alzheimer Disease↗
PubMed1993

Differential diagnosis in dementia. Principal components analysis of clinical data from a population survey.

OBJECTIVE: To reduce all the clinical data, collected from an unselected group of subjects, to a small set of factors and to see how these factors correspond to standard clinical diagnosis of dementing disorders. DESIGN: Population survey. SETTING: General community: elderly older than 74 years, from an area in Stockholm, Sweden. SUBJECTS: Population-based sample including (1) all the screened positive subjects using the Mini-Mental State examination; and (2) a random sample of the screened negative subjects, matched by age and sex. A clinical examination and an informant interview were carried out. Cases were identified using Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition diagnostic criteria for Alzheimer's disease (AD) and other dementias. MAIN OUTCOME MEASURE: Independently from the clinical diagnosis, a principal components factor analysis was carried out to investigate groupings among the clinical data (factors). Factor scores, calculated as a weighted sum of the symptom variables and converted to a standard score form. RESULTS: Four major factors were found: cognitive impairment, cerebrovascular disease, disturbed behavior, and depressive symptoms. The comparison of these factors with the clinical diagnoses showed that (1) the cognitive impairment factor discriminated demented cases from nondemented; (2) the cerebrovascular disease factor discriminated vascular dementia from AD cases and nondemented; (3) the disturbed behavior factor discriminated AD cases from vascular dementia cases and nondemented, indicating behavioral changes characteristic of AD. CONCLUSIONS: This finding, if replicated, would have implications for the construction of diagnostic criteria for AD.

Aged↗
PubMed1993

Risk factors for late-onset Alzheimer's disease: a population-based, case-control study.

Our current knowledge of risk factors for Alzheimer's disease is limited and primarily addresses early-onset disease. This study aimed to determine the risk factors for late-onset Alzheimer's disease using a case-control approach. Ninety-eight cases and 216 controls were gathered from an ongoing population survey on aging and dementia in Stockholm (the Kungsholmen Project). We found a high relative risk (3.2; 95% confidence interval, 1.8-5.7) with the presence of at least one first-degree relative affected by dementia. Among all the other risk factors, alcohol abuse (relative risk, 4.4; 95% confidence interval, 1.4-13.8) and manual work (relative risk for men of 5.3; 95% confidence interval, 1.1-25.5) emerged as positively associated. No clear association was found with a family history of Parkinson disease, advanced parental age at index delivery, season of birth, or previous head trauma. In conclusion, our data suggest that the main risk factor for late-onset Alzheimer's disease is a family history of dementia, as has been previously reported for early-onset disease. Moreover, alcohol abuse and occupational exposure might play a specific role for this form of the disease.

Age Factors↗
PubMed1993

Effects of nucleus basalis lesion on muscarinic receptor subtypes.

The cholinergic system in the central nervous system is an important component of the neural circuitry of learning, memory and cognition. A decline of cholinergic innervation in the human brain is a characteristic feature of dementia of Alzheimer's type. In this study, changes in cholinergic markers were studied after a unilateral lesion of the nucleus basalis magnocellularis (nbM). Acetylcholinesterase (AChE) histochemistry showed a loss of cortical AChE-containing neurons, and choline acetyltransferase (ChAT) immunohistochemistry demonstrated a loss of cholinergic cells in nbM. The localizations of muscarinic M1 and M2 receptors using [3H]pirenzepine ([3H]PZ) and [3H]AF-DX 384, respectively, were studied by quantitative autoradiography 1, 2, 4 and 6 weeks following unilateral ibotenic acid lesion of nbM. A significant decrease in [3H]PZ binding sites was observed at postlesion week 1 in the parietal and temporal cortices. The decrease in [3H]AF-DX 384 binding sites on the lesioned side was observed throughout frontal, parietal and temporal cortices after postlesion week 1, with a significant increase after 6 weeks, possibly as result of loss of presynaptic receptors and upregulation of postsynaptic ones. Moreover, laminar distribution after nbM lesion shows that M1 and M2 receptor binding sites are more affected in superficial layers (I,II,III) than in the deep layers (IV,V,VI), depending on ligand, postlesion period and cortical region. Furthermore, nbM lesion causes a higher deficit of M2 receptors than of M1 receptors. These data suggest the existence of a presynaptic population as well as a postsynaptic population of M1 and M2 receptors which are differently affected after unilateral nbM lesion.

Acetylcholinesterase↗
PubMed1993

Screening of amyloid precursor protein gene mutation (APP 717 Val-->Ile) in Swedish families with Alzheimer's disease.

Screening for the APP 717 Val-->Ile mutation in the amyloid precursor protein (APP) gene in 34 Swedish families with familial Alzheimer's disease (FAD), 16 sporadic cases of Alzheimer's disease and five patients with Down's syndrome (DS) failed to identify further cases of the mutation. These results suggests that the mutation is rare among Swedish families with Alzheimer's disease. In addition, we summarize present reports of the frequency of the mutation.

Aged↗
PubMed1993

Predicting dementia from the Mini-Mental State Examination in an elderly population: the role of education.

Our study aimed to assess whether education affects the positive predictive value of the MMSE when it is used as a screening test for dementia. The MMSE has been consistently found to correlate with education and, at the same time, education is regarded by some researchers as being of potential etiological significance for dementia. In the present study, results on the MMSE from a community-based study in Sweden were compared with two standards: the clinical diagnosis of dementia and the Katz index of daily living activities. For both these comparisons, education did not substantially change the predictive ability of the MMSE. Our data, when compared with previous studies, show that the influence of education on the predictive ability of the MMSE varies in different populations. We conclude that differential MMSE cut-off points for different educational levels or adjustment techniques for education are not universally applicable.

Aged↗
PubMed1993

Prior knowledge and face recognition in a community-based sample of healthy, very old adults.

This experiment addressed the effects of prior knowledge on episodic face recognition in a community-based sample of healthy older adults from 75 to 96 years of age (N = 228). Subjects were presented with photographs of public Swedish individuals who attained their fame during the 1930s and 1940s, or during the 1980s. Results indicated an overall deterioration of face recognition performance across age. However, performance was higher with the dated than with the contemporary faces across the entire age range, suggesting that the ability to utilize prior knowledge in the context of face recognition is well preserved in very old age. Finally, a multiple regression analysis indicated that, among a variety of demographic, psychometric, and biological variables, age was the best predictor of face recognition performance.

Aged↗