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Biomedical subjects

F C Stam

Publications and source records attributed to F C Stam.

At least 55 records · Page 3Linked to original sources

Visual evoked response in senile and presenile dementia.

The visual cortical evoked response was studied in 19 patients suffering from a condition diagnosed as senile or presenile (type Alzheimer) dementia. When compared with a group of normal subjects used as reference group, the latencies of waves II through VI were increased or markedly increased in these patients, and the amplitudes of waves III and VI (and, less consistently, those of waves II and IV) were increased. This corroborates the sparse data on other types of dementia available in the literature.

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Some cerebral proteins and enzyme systems in Alzheimer's presenile and senile dementia.

The water-soluble proteins of the cerebral gray matter and some enzyme systems (cholinesterase, acetylcholinesterase, lactate dehydrogenase, malate dehydrogenase, acid phosphatase) were studied in 9 autopsy cases of Alzheimer's presenile or senile dementia, 1 case of Pick's disease and 1 case of cerebral arteriosclerosis. The proteins and enzyme patterns were visualized on polyacrylamide gradient gels after electrophoresis. In all patients studied, the profiles of cerebral gray-matter proteins were normal. In the patients with advanced dementia, the enzyme patterns usually were abnormal. Particularly in Alzheimer's disease, the activity of malate dehydrogenase was markedly increased.

Acetylcholinesterase↗

Lack of evidence for dysfunction of the blood-brain barrier in Alzheimer's disease: an immunohistochemical study.

With immunohistoperoxidase techniques the presence of plasma (serum) proteins was investigated in senile plaques, congophilic angiopathy, neurons and glial cells in brains of patients with Alzheimer's dementia. Other investigators have found plasma proteins in brain parenchyma and suggested that blood-brain barrier dysfunction might be a primary factor in the pathogenesis of Alzheimer's dementia. These studies were performed on formol-fixed brains of patients with Alzheimer's dementia. In the present study we investigated both frozen and formol-fixed brain tissues. The influence of post-mortem delay, prolonged formol fixation and differences in clinical course on detection of plasma proteins by immunocytochemical techniques was also studied. Findings in cases with Alzheimer's dementia were compared with findings in nondemented controls with or without neurological disorders. Plasma proteins could not be demonstrated in the neuropil of a number of patients with Alzheimer's dementia. Moreover, plasma proteins were also found in neuronal cells and astrocytes in brains of nondemented controls. We discussed whether or not cytochemical detection of plasma proteins in the neuropil of post-mortem obtained brains is a reliable technique to investigate blood-brain barrier dysfunction. In our opinion there are, at the moment, no convincing arguments for blood-brain barrier dysfunction in Alzheimer's dementia.

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