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Biomedical subjects

R D Terry

Publications and source records attributed to R D Terry.

At least 73 records · Page 4Linked to original sources
PubMed1989

The sense-making approach for audience assessment of adolescents.

The purpose of the research was to test the methodology used to identify how adolescents approach their nutrition concerns and questions. The methodology was based on Dervin's sense-making theory. Using a time-line interview technique, 305 adolescents 14 to 16 years of age detailed a situation involving their most important nutrition concerns. Other pertinent information was obtained. Cluster analysis was chosen as the appropriate analysis to identify groups of adolescents who responded similarly to the technique. Discriminant analysis was then used to determine which variables maximally separated the groups. Four groups were identified, two of which described action-oriented approaches to dealing with nutrition situations and differed in terms of how much outside help they wanted. The remaining two groups perceived barriers to dealing with situations and also differed in how much help they wanted. A fifth group indicated no nutrition concerns or questions. The results will be used to develop and test the effectiveness of nutrition education when it is focused on the different approaches.

Adolescent↗
PubMed1988

Decreased levels of protein kinase C in Alzheimer brain.

Protein kinase C (PK-C) levels were determined using [3H]phorbol-12,13-dibutyrate (PDB) binding and the in vitro phosphorylation of histone H I (III-S), in autopsied human frontal cortex of age- and postmortem time-matched normal and Alzheimer patients. PK-C levels in Alzheimer particulate fractions determined by both methods were about 50% of those in controls. PK-C levels in Alzheimer cytosol fractions were not significantly different from those in controls. In a parallel study, we measured the phosphorylation of a Mr 86,000 protein (P86), the major protein kinase C substrate in the cytosol fraction prepared from Alzheimer frontal cortex, and found it to be reduced to 43% of that in control brains. This reduction in P86 protein phosphorylation compared to controls was not detected in brain samples prepared from demented patients without Alzheimer's disease. We considered 3 extraneous factors (postmortem delay, age and sex) which may have affected the extent of P86 phosphorylation and concluded that the reduced P86 phosphorylation in the Alzheimer samples is not due to any of them. Reduced PK-C levels and Mr 86,000 protein phosphorylation may reflect a biochemical deficit related specifically to the pathogenesis of Alzheimer's disease.

Aged↗
PubMed1988

Increased Mr 60,000 protein phosphorylation is correlated with neocortical neurofibrillary tangles in Alzheimer's disease.

Increased Mr 60,000 protein phosphorylation has been found in the cytosol fraction of brain tissue from Alzheimer's disease patients. A correlation between this biochemical change and the morphologic abnormalities found in Alzheimer's disease was sought. Three neuropathologic features were studied: neurofibrillary tangles and neuritic plaques, findings characteristic of Alzheimer's disease, and gliosis, a non-specific change. The number of tangles correlated well with the extent of Mr 60,000 protein phosphorylation (p less than 0.001); but the number of plaques did not. To investigate the possibility that gliosis causes the increased Mr 60,000 protein phosphorylation, cases of Pick's disease and multi-infarct dementia were also studied. The levels of Mr 60,000 protein phosphorylation in these cases were comparable to those seen in normal controls. These findings suggest that the increased Mr 60,000 protein phosphorylation is closely related to diseased, tangle-bearing neurons and is not directly related to neuritic plaque formation or secondary gliosis.

Alzheimer Disease↗
PubMed1988

Alz-50, ubiquitin and tau immunoreactivity of neurofibrillary tangles, Pick bodies and Lewy bodies.

Immunocytochemical and quantitative immunochemical techniques were used to study the expression of Alz-50 antigen, ubiquitin and Tau in neurologic disorders characterized by the formation of filamentous neuronal inclusions. Alz-50, anti-ubiquitin and Tau-1 immunostained the intraneuronal neurofibrillary tangles and the neuritic component of plaques, both in Alzheimer's disease and in the brains of patients without dementia, but extraneuronal tangles were largely unstained. These antibodies also reacted with Pick bodies, and with the neurofibrillary tangles of Kufs' disease and Guam Parkinsonism-dementia. In sections from the brain of a patient with progressive supranuclear palsy, virtually all of the tangles were immunostained with Tau-1 but only a few with Alz-50 or anti-ubiquitin. Anti-ubiquitin also labelled Lewy bodies and the inclusions of granulovacuolar degeneration. Quantitative analysis of immunoblots of homogenized frontal cortex showed significantly more Alz-50 antigen in the brains of patients with Alzheimer's and Pick's disease than in controls. The level of this antigen was increased both in the crude homogenates and in the cytosolic fraction. Ubiquitin immunoreactivity was increased only in the brains of patients with Alzheimer's disease and then only in the crude homogenates. The finding that antigenic determinants for Alz-50, anti-ubiquitin and Tau-1 are shared by several filamentous neuronal inclusions occurring in diverse neurologic disorders may reflect common metabolic defects underlying the formation of these inclusions, or common metabolic responses to their presence.

Adult↗
PubMed1988

Neocortical morphometry, lesion counts, and choline acetyltransferase levels in the age spectrum of Alzheimer's disease.

We studied neocortical morphometry (cortical thickness, neurons, and glia), lesion counts (plaques and tangles), and choline acetyltransferase levels in up to 113 Alzheimer brains and 48 controls. Comparisons between young (under 65) and old (over 70) Alzheimer cases revealed more tangles in the former, but no other statistically significant differences in the measured variables. Differences in these parameters between young Alzheimer cases and young controls were similar to the differences found between old Alzheimer cases and old controls. Linear regression analyses correlating some of these variables with age in Alzheimer's disease, considered together with the effects of normal aging on the same parameters, reveal in Alzheimer's disease a spectrum of graded pathologic severity inversely proportional to age. Nevertheless, even in advanced old age (80 to 100), significant differences persist in these parameters between very elderly Alzheimer brains and controls.

Aged↗
PubMed1988

Neocortical morphometry and cholinergic neurochemistry in Pick's disease.

With a computerized image-analysis apparatus for neocortical morphometry and chemical methods for evaluation of the cholinergic system, five brain specimens of Pick's disease (PD) were studied and the results compared to those from specimens of age-matched normal subjects and Alzheimer's disease (AD). The PD specimens showed major reductions in brain weight, frontal and temporal cortical thickness, and large neuron populations, compared with controls. Lesser reductions were seen in small neurons and thickness of the inferior parietal cortex. The authors found no relationship between age of onset or disease duration and either the degree of cortical thinning or neuron loss or the number of Pick bodies in the neocortex and hippocampus. PD specimens were more atrophic than AD brains, having lower brain weights and more fronto-temporal thinning. Large neurons were comparably reduced in the two conditions in the frontal and temporal lobes, but small neuron losses were greater in the PD midfrontal area. Only the AD cases showed loss of large neurons in the inferior parietal region. Levels of choline acetyltransferase were normal in PD and reduced in AD, whereas muscarinic receptor binding was decreased in both.

Aged↗
PubMed1987

Response of septal cholinergic neurons to axotomy.

In the present study we employed quantitative morphometric techniques to assay the response of septal cholinergic neurons following unilateral transection of the fimbria/fornix and supracallosal stria. Analysis of 50-micron-thick tissue sections with a Quantimet 920 image analysis system demonstrated a reduction in ChAT immunoreactivity as early as 1 day following denervation. This decrease was associated with a drop in the number of labeled cells ipsilateral to the lesion and a decrease in the area of cholinergic perikarya on the lesioned and nonlesioned side of the septum. The response at 1 day, however, was transient, and at 4 days the number of labeled neurons was not significantly different from controls. By 8 days we observed a dramatic reduction in the number and size of ChAT-positive cells ipsilateral to the lesion and a reduction in the size of cholinergic perikarya on the contralateral (i.e., nonlesioned) side. These values persisted throughout the remainder of the study. To assess more completely the morphologic response of neurons to axotomy than can be determined in 50-micron-thick tissue sections, we embedded the adjacent immunolabeled tissue section in Epon and then serially sectioned it to a thickness of 0.75-1.0 micron. By using this method, we were able to measure the area, length, and width of the cell, the area of the nucleus and nucleolus, and the position of the nucleus (i.e., eccentricity). Measurements were performed on ChAT-labeled and nonlabeled cells. The results of our studies demonstrate that cholinergic and noncholinergic cells responded to axotomy in a characteristic yet different fashion from each other and that this response could be quantitatively assayed. In general, labeled and nonlabeled cells on the lesioned side of the septum shrink in response to denervation. This shrunken state was reflected in measurements of cellular area, length, width, and nuclear area. Moreover, other measurements of cellular morphology (i.e., area of the nucleolus, position of the nucleus) indicate that none of the neuronal populations examined in the present study displayed morphologic evidence of regeneration. Our results indicate a dramatic loss of cholinergic perikarya ipsilateral to the lesion. Moreover, although a few neurons do persist they do so in a shrunken state. These data provide an essential baseline for the second study in this series, which will evaluate the effect of nerve growth factor on the survival of denervated septal neurons.

Animals↗
PubMed1987

Neocortical cell counts in normal human adult aging.

Fifty-one brains from clinically and neuropathologically normal individuals ranging in age from 24 to 100 years were studied to determine what changes occur in neocortical neuroectodermal cell populations as a function of normal aging. Twenty-mu-thick sections from the midfrontal, superior temporal, and inferior parietal areas were examined with an image-analysis apparatus with combined manual and automatic editing capacity. Neuroectodermal cells were counted, measured, and assigned to one of ten categories, which were later summarized in three: large neurons (greater than 90 mu 2), small neurons (41 to 90 mu 2), and glia (5 to 40 mu 2). Determinations were also made of brain weight, cortical thickness, neuronal density, neuron-glia ratio, and percentage of cell area. The results showed statistically significant age-related decrements in the following values: brain weight, cortical thickness in the midfrontal and superior temporal areas, large neurons in all three areas, and the neuron-glia ratio in the midfrontal and inferior parietal areas. The total number of neurons, neuronal density, and percentage of cell area were all unchanged. Increasing with age were the number of small neurons in the midfrontal cortex and glia in the midfrontal and superior temporal areas. The following conclusions were drawn: Aging affects the frontal and temporal lobes more than the parietal; the salient change is shrinkage of large neurons with consequently increasing numbers of small neurons; constant neuronal density coupled with diminished cortical volume (decreased brain weight and cortical thinning) indicate that there is some neuronal loss with age, but it is of much lesser magnitude than previously supposed; and the number of glia increases with age.

Adult↗
PubMed1987

Senile dementia of the Alzheimer type without neocortical neurofibrillary tangles.

Senile dementia of the Alzheimer type (SDAT) is typified pathologically by neuritic plaques (NP) and neurofibrillary tangles (NFT) in the neocortex and hippocampus. However, in a large series of cases (60) over age 74 a significant minority (30%) lacked neocortical tangles. In order to determine if these latter cases (Group B) otherwise differ from the majority which have both neocortical plaques and tangles (Group A), various clinical and neuropathological parameters were measured for both groups and the results compared. The following indices were examined: degree of dementia, rate of progression of dementia, age at death, brain weight, cerebral hemispheric weight, cortical cell counts from the frontal, temporal, and parietal lobes, the number of neocortical NP, the number of hippocampal NP and NFT, and the levels of neocortical choline acetyltransferase and somatostatin. The two groups showed no statistically significant differences in any of these categories except for increased numbers of neocortical NP in Group A in midfrontal and superior temporal regions. However, cases in Group A showed greater pathologic abnormality in nearly every parameter, albeit without attaining statistical significance. We conclude that SDAT with neocortical NFT is the same disease as SDAT without them, although the presence of such tangles is associated with a tendency towards greater severity.

Aged↗
PubMed1987

Laminar and regional distributions of neurofibrillary tangles and neuritic plaques in Alzheimer's disease: a quantitative study of visual and auditory cortices.

The number of Thioflavine S-positive neurofibrillary tangles (NFT) and neuritic plaques (NP) was determined in visual and auditory cortical regions of 8 patients with Alzheimer's disease. On both a regional and laminar basis, NFT exhibited very distinctive and consistent distribution patterns. The mean (+/- SEM) number of NFT in a 250-micron-wide cortical traverse was very low in area 17, primary visual cortex (0.9 +/- 1.0), increased 20-fold in the immediately adjacent visual association cortex of area 18 (19.7 +/- 3.6), and showed a further doubling in area 20, the higher-order visual association cortex of the inferior temporal gyrus (35.5 +/- 8.8). Similar differences in NFT number were present between primary auditory (1.6 +/- 0.5) and auditory association (18.9 +/- 5.4) regions. On a laminar basis, NFT were predominantly present in layers III and V, although there were striking regional differences in the proportion of NFT in these 2 layers. Layer III contained 79% of the NFT in layers III and V in area 18, 41% in area 20, and only 27% in area 22. In contrast, NP showed different, and less specific, regional and laminar distribution patterns. Total NP number was similar in the 3 visual areas, although there were marked regional differences in the type of NP present. Nearly 80% of the NP in area 17 was of the NPc type (i.e., contained a dense, brightly fluorescent core), whereas over 70% of the NP in both areas 18 and 21 was of the NPnc type (i.e., lacked a dense, brightly fluorescent core). NP were present in every cortical layer but were most numerous in layers III and IV. The distinctive distribution patterns of NFT are very similar to the regional and laminar locations of long corticocortical projection neurons in homologous regions of monkey neocortex. This association suggests that NFT reside in the cell bodies of a subpopulation of pyramidal neurons, namely, those that furnish long corticocortical projections. In contrast, the distribution patterns of NP suggest that multiple neuronal systems contribute to their formation.

Aged↗
PubMed1987

Adolescents' beliefs about and reasons for using vitamin/mineral supplements.

Beliefs about and reasons for using vitamin/mineral supplements were investigated among 163 adolescents. Subjects' responses to belief statements about supplements and reasons cited for using supplements demonstrated both misconceptions and uncertainties. These results demonstrate the need for dietitians to routinely address the appropriate use of nutritional supplements with their adolescent clientele.

Adolescent↗
PubMed1986

Choline acetyltransferase immunoreactivity in neuritic plaques of Alzheimer brain.

We have observed dystrophic choline acetyltransferase (ChAT)-positive processes surrounding the amyloid core of neuritic plaques in human neocortex, amygdala and hippocampus, using a polyclonal anti-human ChAT antiserum. These data, and those from studies of the aged monkey by other investigators, provide a morphologic counterpart for the biochemical abnormality of the cholinergic system in Alzheimer's disease and senile dementia of the Alzheimer type.

Aged↗
PubMed1986

Klüver-Bucy syndrome and amyotrophic lateral sclerosis: a case report with biochemistry, morphometrics, and Golgi study.

We studied a patient with amyotrophic lateral sclerosis and the Klüver-Bucy syndrome. At autopsy there was extensive degeneration of the limbic system with the brunt of the changes in the medial temporal lobe, especially the entorhinal cortex and subiculum. Degenerative changes were also seen in the substantia nigra and lower motor neurons. Morphometric and biochemical studies implied a disease process that affected small, possibly somatostatinergic, cortical neurons. These latter findings and the lobar distribution of cortical atrophy were consistent with Pick's disease, but Pick bodies and ballooned neurons were not present.

Affective Symptoms↗
PubMed1985

Somatostatin-like immunoreactivity within neuritic plaques.

Alzheimer's disease or senile dementia of the Alzheimer type (SDAT) is a progressive neurodegenerative disease that is characterized pathologically by two types of microscopic lesions in the neocortex: the neurofibrillary tangle and neuritic plaque. The concentration of neuritic plaques is correlated with significant reductions in the level of specific neurotransmitter and neuropeptide systems in autopsied brains of patients with SDAT, including decreased amounts of the tetradecapeptide, somatostatin. The clinical effects of reduced cortical somatostatin activity in patients with SDAT is unclear, nor is it known whether somatostatinergic neurons participate in either lesion. In the present study we employed light microscopic immunocytochemistry to determine whether somatostatin-containing neurons participate in the formation of neuritic plaques. Examination of selected cortical regions from autopsied brains revealed 20-50% of all neuritic plaques contained somatostatin-positive profiles indicating that processes of somatostatinergic neurons are associated with neuritic plaque formation.

Aged↗
PubMed1985

Substance P immunoreactivity within neuritic plaques.

In the present immunocytochemical study we examined brain tissue of patients with Alzheimer's disease in order to determine the relationship of substance P (SP)-labeled processes to neuritic plaques. Swollen neuropeptidergic processes were consistently observed within a relatively small percentage of the plaques. These data provide a morphologic correlate to the biochemical finding that SP levels are reduced in the brain tissue of patients with Alzheimer's disease, and further indicate that Alzheimer's disease affects multiple neurotransmitter and neuropeptide systems.

Aged↗