PubMed Health⌕ Search

Biomedical subjects

C G Gottfries

Publications and source records attributed to C G Gottfries.

222 records · Page 13Linked to original sources
PubMedDate not supplied

The neurochemistry of vascular dementia.

Vascular dementia (VAD) is cognitive impairment caused by changes in the blood circulation of the brain. It is not synonymous with multi-infarct dementia. The latter is a subgroup of VAD. Neurochemical investigations of noninfarcted brain tissue from patients with VAD show general changes in VAD brains. The serotonin metabolism is severely reduced and so is the activity of choline acetyltransferase. Monamine oxidase B is significantly increased in the white matter. A severe decrease in myelin components indicates white matter disturbances of such a degree that they must be considered to be of pathogenetic importance. The levels of some neuropeptides in the hypothalamus are increased. This is a finding which is in agreement with clinical findings of a high activity in the hypothalamic-pituitary-adrenal axis in patients with VAD. This high activity is possibly due to a loss of serotonergic inhibitory tone on the hypothalamus in VAD brains.

Brain↗
PubMedDate not supplied

Relationship between mental impairment and HPA axis activity in dementia disorders.

In 40 patients with Alzheimer's disease (AD, < 65 years), 56 patients with senile dementia of the Alzheimer type (SDAT, > or = 65 years) and 45 patients with vascular dementia (VAD), basal cortisol levels were estimated and the dexamethasone test (DST) was performed. The degree of dementia was assessed according to DSM-III-R and the GBS scale was used for quantitative measures of functional impairment. There were no significant differences in basal cortisol levels. Especially in the VAD group, scores on functional impairment correlated significantly with post-DST cortisol levels. The results indicate hypothalamic overactivity in demented patients which can be correlated to the degree of dementia. In VAD, and to a certain extent also in SDAT, there appears to be a disconnection between cortical areas, including the hippocampus and the hypothalamus.

Aged↗
PubMedDate not supplied

Diagnosis of dementias using partial least squares discriminant analysis.

Twenty patients with Alzheimer's disease (AD), 34 with senile dementia of the Alzheimer type (SDAT) and 12 with vascular dementia (VAD) were carefully investigated. The diagnoses were made according to the DSM-III-R criteria and for AD/SDAT also according to the NINCDS-ADRDA criteria. The data set consisted of 29 descriptor variables obtained at the examination, and the data were fitted to a partial least squares model using dummy variables for the response variables (i.e. clinical diagnoses). The distribution of the scores over the descriptor variable space revealed adequate classification regarding all three diagnoses, with some overlap between SDAT and AD and between VAD and SDAT. The study demonstrates a clear difference in symptomatology between AD and SDAT with no influence of age per se or the severity of dementia.

Aged↗
PubMedDate not supplied

The growth-associated protein GAP-43 is increased in the hippocampus and in the gyrus cinguli in schizophrenia.

Schizophrenia is a common and severe psychiatric disorder of unknown etiology. Numerous neuropathological studies have found subtle structural changes in limbic structures, especially medial temporal lobe structures and the gyrus cinguli. To test the hypothesis that synaptic disturbances are involved in the pathogenesis of schizophrenia, we studied the growth-associated protein 43 (GAP-43), a protein localized to presynaptic terminals, suggested to be involved in establishment and remodeling of synaptic connections, in postmortem brain tissue, using quantitative Western blotting immunohistochemistry. The material consisted of brain tissue from 17 schizophrenics (80 +/- 11 yr), diagnosed according to the DSM-III-R criteria, and 20 age-matched controls (75 +/- 13 yr). Quantitative analyses showed increased GAP-43 protein levels in schizophrenic compared to control brains, both in the hippocampus (2.43 +/- 0.78 vs 1.00 +/- 0.29; p < 0.0001) and in the gyrus cinguli (1.52 +/- 0.21 vs 1.00 +/- 0.35; p < 0.0001). Also by immunohistochemistry, increased GAP-43 staining was found in schizophrenic compared with control brains, throughout all layers of the gyrus cinguli and the hippocampus. Anomalous synaptic sprouting and reorganization, with resultant "miswiring," as well as a defect in synaptic pruning have been hypothesized to be pathogenetic factors in schizophrenia. We suggest that a decreased synaptic density, whether caused by disturbed development or damage/degeneration, may elicit a reactive synaptogenesis (reflected by an increase in GAP-43), which may be functional or anomalous. Synaptic pathology in the limbic system may be of importance in the development of psychotic symptoms in schizophrenia.

Aged↗
PubMedDate not supplied

Therapy options in Alzheimer's disease.

The aetiology of Alzheimer's disease and senile dementia of the Alzheimer type (AD/SDAT) are unknown, and primary prevention is thus infeasible. As overactivity in the hypothalamic-pituitary-adrenal axis (possibly indicating maladaptation to stress) and vitamin B12 deficiency are common, secondary prevention should focus on stress and dietary factors. Nerve growth factors and ganglioside GM1 have been used to inhibit progression of the disorder, but this treatment is still at an experimental stage, as are efforts to prevent the formation of amyloid. Breakthroughs in AD/SDAT treatment have been seen in trials with supplementation of neurotransmitter deficits. Tacrine, a drug that inhibits acetylcholinesterase, has proved to have a cognitive-enhancing effect, but this is limited in time and the drug has side-effects. Selective serotonin reuptake inhibitors have a proven effect on the emotional disturbances seen in AD/SDAT.

Alzheimer Disease↗