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Biomedical subjects

I Iraizoz

Publications and source records attributed to I Iraizoz.

4 recordsLinked to original sources

Calbindin immunoreactivity in normal human temporal neocortex.

Calbindin immunoreactivity in the temporal neocortex was examined in 4 subjects with no neurological, metabolic or malignant disease. The brains were obtained between 1 and 4 h after death and rapidly fixed by perfusion with 4% paraformaldehyde through the carotid arteries, cut into slabs, cryoprotected and stored at -80 degrees C. Sections of the whole left temporal lobe obtained with a freezing microtome were processed free-floating with a well known monoclonal antibody against calbindin according to the peroxidase-antiperoxidase (PAP) method. Calbindin-immunoreactive (CaBP-ir) neurons were found to be local-circuit neurons (interneurons) mainly distributed in the upper cortical layers (layers I, II and III), and were categorized as small multipolar neurons with ascending dendrites ramifying in the molecular layer, small bitufted cells, pyramid-like cells in layer II, horizontal neurons in the molecular layer, multipolar neurons with long descending dendrites, and large double-bouquet cells, some of them exhibiting a very long dendrite with claw-shaped terminals in layer V. Less than 10% of all CaBP-ir neurons were localized in the remaining cortical layers. Pyramidal cells were only very weakly or not stained at all. In addition, CaBP-ir fibres formed a dense plexus in the molecular layer, and vertical bundles 8-10 microns thick and 500-600 microns long, separated by blank spaces 20-40 microns wide were distributed in layers III and V/VI.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

Cell loss and nuclear hypertrophy in topographical subdivisions of the nucleus basalis of Meynert in Alzheimer's disease.

The nucleus basalis of Meynert was examined in six patients with Alzheimer's disease and five age-matched controls. A cytoarchitectonic study was followed by quantitative analysis of the population of neurons and by the determination of their nuclear area. Confirming previous neuropathological observations in Alzheimer's disease, a neuronal loss of 43% in the anterior, 25% in the intermediate and 30.5% in the posterior subdivisions of the nucleus basalis of Meynert was observed. Numerous surviving cells showed neurofibrillary tangles. In addition, we found that the nuclear area of the remaining nucleus basalis of Meynert neurons was significantly increased in all three subdivisions by at least 16%. The combined observation of cell loss and nuclear hypertrophy suggests that both regenerative and degenerative changes co-exist in the nucleus basalis in Alzheimer's disease.

Aged

Differential changes in cell size and number in topographic subdivisions of human basal nucleus in normal aging.

The age-related cell loss of the nucleus basalis of Meynert is of considerable importance because loss of its neurons may be followed by cognitive decline. Compared to the number found at ages 16-29 years, we found that 50% of the total population of neurons is lost by 90 years of age. This change in number is accompanied by modifications in the morphometric features, including a 17.3% increase in cell size by 60 years of age as compared with values at 16 years, and followed by a gradual decline. Topographic differences were seen both in the neuronal loss and in morphometry: in relation to the youngest group, the posterior subdivision is the most severely affected by 90 years (64.5% decrease in number and 10% reduction in neuronal size), followed by the intermediate subdivision (42% loss of neurons accompanied by 4% increase in cell size). In the anterior subdivision no significant decrease in the number of neurons could be detected, although a 15% increase in cell size occurred.

Aging