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Biomedical subjects

C G Gottfries

Publications and source records attributed to C G Gottfries.

At least 127 records · Page 7Linked to original sources
PubMed1989

The home care patient. A comparison with the nursing home patient.

Forty-two patients receiving medical home care (MHC) were studied and compared with a group of 191 nursing home (NH) patients in the same area. Most MHC patients were over 65 years old. In both groups the illnesses that dominated were mainly circulatory and musculoskeletal diseases. The NH patients had significantly lower test results concerning intellectual, motor and ADL functions. The frequency of dementia was 3 times higher for both MHC and NH patients than for the average population in the same age groups. Depressed mood, anxiety, fear and panic were common symptoms for MHC as well as for NH patients. Both groups of patients investigated had frequent communication with relatives and friends. MHC patients took part in activities outside the home less frequently than NH patients. The results of this study indicate that MHC and NH patients constitute two different groups, that both NH and MHC care are needed, and that one form cannot replace the other. The high frequency of dementia in both groups stresses the point that mental impairment is a strong factor for the need of care.

Activities of Daily Living↗
PubMed1988

Dementia: classification and aspects of treatment.

The syndrome dementia is defined by evidence of a decline in memory, thinking, and emotional functions. In this article, dementia is delimited only by its symptoms; the etiology, the course, and the extensiveness of the disorder are not used as criteria of a dementia syndrome. In the descriptive diagnoses of dementia disorders, however, different aspects of the disorders are used. Descriptive diagnoses are (a) benign senile forgetfulness, (b) primary degenerative disorders, (c) secondary dementias, (d) cerebrovascular disorders with dementia, (e) reversible dementias, and (f) dementias with unknown etiology. Primary degenerative disorders include the subgroups (a) senile dementia of Alzheimer type (SDAT), (b) Alzheimer's disease (AD), (c) Pick's disease, and (d) Huntington's chorea. The question whether SDAT a nd AD should be included in one group is discussed. Very interesting and stimulating treatment research is going on in the field of dementias. Although there has still been no real breakthrough, some results indicate that dementia symptoms may be influenced by treatment. At present, treatment strategies go along the following lines: (a) pharmacological treatment, (b) control of sleep apneas and circulatory disturbances, (c) brain tissue transplantation, and (d) psychotherapy and mental activation. The pharmacologyical manipulation of dementia disorders focuses on substituting failing neurotransmitter systems. The use of nootropic drugs and gangliosides is still at an experimental level. Findings of vitamin B12 deficiency in late-onset dementia make vitamin B12 substitution relevant. White matter disturbances such as incomplete infarctions are reported in brains from demented patients. Coincident findings of increased sleep apneas with severe hypoxemia make studies of circulatory disturbances of interest.(ABSTRACT TRUNCATED AT 250 WORDS)

Dementia↗
PubMed1988

Immunocytochemical investigations on the presence of neuron-specific antibodies in the CSF of Parkinson's disease cases.

The CSF and sera of 7 patients with Parkinson's disease were investigated immunocytochemically, in order to see if antibodies were present which recognized DA-ergic cell bodies in glutaraldehyde fixed rat brain. In 2 patients a marked labeling of DA-ergic neurons in the substantia nigra was observed, identified by anti-DA antiserum and by 6-OHDA induced degeneration, but also other neurons in the ventral mesencephalon were recognized. The other patients were weakly positive or negative. Sera gave unspecific labelling of all neurons. In one patient the sub-classes of IgG were investigated and found to be of IgG3 (labeling nerve terminals) and of IgG1-2, low affinity type (recognizing perikarya). The epitopes recognized have not been identified, but are unlikely to be DA-like, since blocking experiments and ELISA-tests gave negative results. The possible clinical importance of the results are discussed.

Aged↗
PubMed1988

Low B12 levels related to high activity of platelet MAO in patients with dementia disorders. A retrospective study.

In 35 patients with Alzheimer's presenile disease (AD), 56 patients with senile dementia of the Alzheimer type (SDAT), 54 patients with vascular dementia (VD) and 10 patients with confusional states, age, vitamin B12 in serum, P-folate, B-folate and B-Hb were investigated. Platelet monoamine oxidase (MAO) and cerebrospinal fluid (CSF) levels of homovanillic acid (HVA), 5-hydroxyin-doleacetic acid and 3-methoxy-4-hydroxyphenylglycol were measured. Group differences showed that vitamin B12 levels were reduced in the group of patients with confusional states and SDAT. Five out of ten and 13 out of 56 (respectively) had vitamin B12 concentrations below the lower limit of the reference value (130 pmol/l). A negative correlation was found between B12 levels and platelet MAO activity. The findings indicate that there is a subgroup of patients with late-onset dementia that has low vitamin B12 blood concentrations. HVA levels in CSF, usually found to be reduced in AD patients, were normal in this subgroup.

Aged↗
PubMed1988

Alzheimer's disease. A critical review.

Clinical and neuropathological findings in a 51-year-old woman by Alois Alzheimer (1) led to a description of the disorder which Kraepelin (2) named Alzheimer's disease (AD). In this progressive dementia disorder the senile plaques and fibrillary tangles found at brain autopsy are the diagnostic hallmarks. As the same type of neuropathological changes are found in dementias of senile age, these disorders are named senile dementia of the Alzheimer type (SDAT). The two forms are often combined into one group, the Alzheimer dementias, (AD/SDAT) and, according to the DSM-III, classified as primary degenerative disorders (PDD). However, it must be emphasized that there is no scientific basis for sampling the two forms, the diagnoses of both AD and SDAT are exclusive. Several hypotheses are being proposed as to the etiology of AD/SDAT. Genetic factors, aluminium or other toxic factors, immunological disturbances, disturbed glucose metabolism, deficiency of essential nutrients, and stress, are some of the lines followed when seeking the etiology. The pathogenesis of the disorder involves not only structural changes but also neurochemical disturbances and neuroendocrine dysfunction, findings which are related to the behavioural disturbances seen in the disease. At present there are no reliable biological markers for AD/SDAT. Clinical investigations together with laboratory data and brain imaging support the assumption of several sub-groups within the Alzheimer type dementias. The neurochemical findings made in AD/SDAT have constituted the basis for formulating pharmacological treatment strategies. Drugs affecting the cholinergic and monoaminergic systems have been used, as well as neuropeptides and similar drugs. Gangliosides and phosphatidylserine have also been tested in clinical trials. Hitherto, this treatment has not been as successful as expected. Cholinergic drugs have given a marginal effect on memory functions. Emotional disturbances and disturbed motor performance have to some extent been influenced by the use of selective 5-hydroxytryptamine reuptake blockers and L-dopa. Whether this treatment is of clinical importance must be further investigated. Interesting neuropathological and neurochemical research is being conducted on AD/SDAT. However, clinical research aiming at delimiting homogeneous subgroups of dementia has not kept in step with neurobiological research. More effort must be put into clinical research if therapeutic progress is to be achieved.

Aged↗
PubMed1987

5-Hydroxytryptamine-sensitive [3H]imipramine binding of protein nature in the human brain. II. Effect of normal aging and dementia disorders.

Recently, a high-affinity [3H]imipramine binding site of protein nature that appeared related to the 5-hydroxytryptamine (5-HT, serotonin) uptake mechanism was demonstrated in the rat brain. In a preceding paper a similar [3H]imipramine binding site of protein nature and displaceable by 5-HT was demonstrated in the human brain. Most previous [3H]imipramine binding studies of the human brain have used desipramine-sensitive binding, which appears to contain a significant amount of additional binding not related to 5-HT neurons. Therefore this study of the human brain in the normal aging, in Alzheimer's disease/senile dementia of Alzheimer type (AD/SDAT) and in multiinfarction dementia (MID) presents data on 5-HT-sensitive [3H]imipramine binding. The influence of normal aging (17-100 years) was studied in the frontal and cingulate cortices, in the putamen, caudate nucleus, amygdala and in the hippocampus. An age-related change in 5-HT-sensitive [3H]imipramine binding was only noted in the cingulate cortex with a 50% loss in Bmax over the adult age range. In contrast, desipramine-sensitive [3H]imipramine binding studied in the frontal cortex and in the putamen showed marked increases in Bmax with age which correlated with increases in Kd. It is suggested that these increases are related to an increased binding to lipophilic membrane components not related to 5-HT neurons. The 5-HT-sensitive [3H]imipramine binding (Bmax) was reduced to 60% of control in the cingulate cortex and to 50% in the putamen in AD/SDAT. In MID there was a 50% loss of [3H]imipramine binding sites (Bmax) in the putamen, but a 30% loss in the cingulate cortex did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Increased affinity of choline acetyltransferase for choline in Alzheimer's disease: a steady-state kinetic study.

The steady-state kinetics of choline acetyltransferase (CAT) from autopsy samples of human caudate nucleus of aged controls and of patients with Alzheimer's disease was studied. In 10 samples from Alzheimer's disease-afflicted brains the affinity for the limiting substrate choline (Ch) was significantly higher: Michaelis constant KmCh was for these samples 1.93 +/- 0.72 mM while in the samples from 9 age-matched controls KmCh was 2.53 +/- 0.78 mM. The difference is statistically significant (P less than 0.05). Endogenous choline concentrations in the samples were 124 +/- 39 (n = 10) nmol/g wet wt. in the Alzheimer's disease-afflicted samples and 180 +/- 57 (n = 9) nmol/g wet weight (n = 9) in the control samples (P less than 0.05). The initial velocity at 70 microM acetyl co-enzyme (AcCoA) in Alzheimer's samples was 171.5 +/- 131.0 pmol [14C]acetyl choline [14C]ACh/mg protein/min as compared to the controls 422.1 +/- 231.0 pmol [14C]ACh/mg protein/min replicating many previous findings about decline of CAT activity in Alzheimer's disease. However, in the same samples the affinity for the other substrate acetyl-CoA (AcCoA) was significantly lower for the Alzheimer patients, KmAcCoA = 61 +/- 40 microM, than for the age-matched control patients, KmAcCoA = 28 +/- 8 microns (P less than 0.01). The data suggest some compensation of the loss of enzyme molecules via changed affinity for the limiting substrate, Ch.

Aged↗
PubMed1987

Antibodies in cerebrospinal fluid of some Alzheimer disease patients recognize cholinergic neurons in the rat central nervous system.

The etiology of Alzheimer disease is unclear. However, immunological aberrations have been suggested to be critical factors in the pathogenesis of this neurodegenerative disease. This study was carried out to investigate if cerebrospinal fluid (CSF) from Alzheimer disease patients contains antibodies that recognize specific neuronal populations in the rat central nervous system. The results indicate that in a subgroup of patients this is indeed the case. The antibodies reported in this study have the following properties: (i) they recognize neuronal populations and components in the medial septum and spinal motor neurons in rats perfused with a mixture that fixes small neurotransmitter molecules; (ii) adsorption of the patient CSF with staphylococcal protein A-Sepharose and using a polyclonal antiserum against human IgG3 indicates that the immunocytochemical reaction in these brain regions is mainly due to the subclass IgG3; and (iii) the CSF immunocytochemical reaction is blocked by preincubation of the sections with a rabbit anti-acetylcholine antiserum. These results provide evidence that antibodies in the CSF of some, but not all, Alzheimer disease patients recognize acetylcholine-like epitopes in cholinergic neurons in the rat central nervous system.

Acetylcholine↗
PubMed1987

A double-blind evaluation of electroconvulsive therapy in Parkinson's disease with "on-off" phenomena.

Eleven patients with severe Parkinson's disease and on-off-phenomena were included in a controlled double-blind study on the effect of electroconvulsive therapy (ECT). Pharmacological treatment was optimally adjusted before the trial. The severity of extrapyramidal symptoms was measured before, during and after the treatment. The patients were randomly allocated into one group, receiving active ECT and another, receiving sham treatment. The patients given active ECT showed significantly (P less than 0.05) prolonged duration of "on"-phases after ECT, in comparison to the sham-treated group. When collecting data from the controlled part of the study and the subsequent with open administration of ECT, the treatment was in addition found to significantly decrease the time and number of steps required to walk 10 meters. Moreover it reduced the severity of parkinsonian symptoms according to the Webster scale. The improvement induced by ECT was generally short-lasting. Lumbar punctures were performed before and after ECT. The concentrations of monoamine metabolites in cerebrospinal fluid were not affected by the treatment. The results indicate that ECT has an antiparkinsonian effect which probably is mediated via changed responsiveness of dopamine receptors and that further improvement is possible in patients, therapy resistant to the presently available medication.

Aged↗
PubMed1987

Monoamines and their metabolites in cerebrospinal fluid of patients with senile dementia of Alzheimer type using high performance liquid chromatography and gas chromatography-mass spectrometry.

Monoamines and their main metabolites were measured using HPLC-EC in the cerebrospinal fluid from age-matched elderly in-patients affected with senile dementia of Alzheimer type and chronic schizophrenia. Determination of the monoamine metabolites MHPG, HVA and 5-HIAA was also performed by means of gas chromatography-mass spectrometry. Significant differences were obtained with the two methods, the largest deviation being found for HVA, which was 15% higher in the HPLC method than in the GC-MS method, despite the correlation between the results of two measurements being consistent for all the three metabolites. The degrees of motor, intellectual and emotional deterioration were assessed using GBS rating scale. The results show a clear psychobehavioral and neurochemical differentiation of the two patient groups. HVA and 5-HIAA levels were significantly lower in SDAT patients, and showed a trend toward negative correlation with the degree of dementia.

Aged↗
PubMed1986

Multiple biochemical deficits in both gray and white matter of Alzheimer brains.

A biochemical investigation of 21 brains from patients with dementia of Alzheimer type (AD/SDAT) and 22 brains from controls was made. In the normal brains 5-hydroxytryptamine (5-HT), noradrenaline (NA) and dopamine (DA) were reduced with age while their metabolites were not reduced. In the brains from the Alzheimer patients the examination of gray matter (caudate nucleus and hippocampus) showed a significant reduced activity of choline-acetyl transferase (CAT) and a reduction of acetylcholinesterase (AChE) that bordered significance in the hippocampus. In the brains from the Alzheimer patients a disturbance was found in the 5-HT system in the form of reduced levels of 5-HT and 5-hydroxyindolacetic acid (5-HIAA). The catecholamine systems were also disturbed but to a less extent. In the 5-HT and DA systems the active amines as well as the metabolites were reduced in the brains from patients with AD/SDAT indicating not only a possible neuronal loss but also an incapacity of the remaining neurons to compensate for the loss by an increased turnover. The lipid content was slightly reduced in gray matter of the demented brains. In white matter there was a more severe reduction of the lipids and in this tissue also the cerebrosides and sulfatides were reduced. It is concluded that in brains from patients with AD/SDAT there are multiple biochemical deficits in gray as well as in white matter. The changes in white matter may be of pathogenetic importance in subgroups of AD/SDAT.

Age Factors↗
PubMed1986

Brain and brain monoamine oxidase in aging and in dementia of Alzheimer's type.

Brain MAO-B activity increases with age. The rate of increase varies in different brain regions. Brain MAO-A activity does not change with age in man and is decreased in the rat. Brain MAO-B activity in AD/SDAT is higher than in age-matched controls. The increased MAO-B activity in aging is due to an increased concentration of otherwise unchanged extrasynaptosomal MAO-B. The increase in brain MAO-B activity with age and in AD/SDAT is more pronounced in white matter than in gray matter. Platelet MAO is increased in patients with AD/SDAT.

Aging↗
PubMed1986

Pharmacokinetics of zimeldine in male alcoholics.

The pharmacokinetics of zimeldine, a 5-HT reuptake blocker with antidepressive effects, was studied after a single oral dose and after multiple oral administration in 19 alcoholic males, 10 with and 9 without chronic liver damage. The average plasma concentration of zimeldine as assessed by the AUC values (area under the plasma concentration-time curve) was significantly higher in the chronically liver damaged patients than in the patients without chronic liver damage. The plasma half-life of zimeldine was also significantly longer in the chronically liver damaged patients. There were no differences in the obtained pharmacokinetic parameters between the patients having nonchronic liver damage and healthy control subjects. The pharmacokinetics of the active metabolite norzimeldine (resulting from N-demethylation of zimeldine) showed no differences between the two groups of alcoholics and the healthy controls. The IgA values were significantly correlated to both the AUC and plasma half-life of zimeldine. No other correlation between clinical chemistry parameters and pharmacokinetic parameters of zimeldine and norzimeldine were found.

Adult↗