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Biomedical subjects

M Tarnawski

Publications and source records attributed to M Tarnawski.

At least 37 records · Page 2Linked to original sources
PubMed1997

Relationships between regional neuronal loss and neurofibrillary changes in the hippocampal formation and duration and severity of Alzheimer disease.

The total numbers of neurons with and without neurofibrillary changes in the hippocampal subdivisions were estimated in 16 subjects with Alzheimer disease (AD) and in 5 normal elderly controls. On the basis of clinical symptoms, AD patients were subdivided into relatively less (AD-1. Functional Assessment Staging [FAST] stages 7a to 7c) and more severely affected (AD-2, FAST stages 7e to 7f) patient groups. In the AD-1 group relative to controls, the total number of neurons was reduced only in CA1 and in the subiculum. In the AD-2 group, neuronal losses were found in all sectors of the cornu Ammonis and in the subiculum and ranged from 53% in CA3 to 86% in CA1. The dentate gyrus was the only hippocampal subdivision without significant neuronal loss. Within the combined AD patient groups, significant correlations were noted between both clinical stage and duration of AD and both the total number of neurons and the percentage of neurons with neurofibrillary changes in CA1, CA4, and the subiculum. Regression analyses predicted neuronal losses over the maximal observed duration of 22 years of 87% in CA1, 63% in CA4, and 77% in the subiculum. Our data suggest that over the course of AD, continuous neurofibrillary tangle formation and continuous neuronal loss occur in the hippocampal subdivisions. The rate of neuronal loss appears to be similar for CA1, CA4, and the subiculum.

Aged↗
PubMed1996

Subpopulation of dogs with severe brain parenchymal beta amyloidosis distinguished with cluster analysis.

A study of the brains of 30 dogs, mongrels from 6.5 to 26.5 years of age, revealed that all dogs older than 13 years of age develop amyloid-beta-positive plaques. Cluster analysis based on the age of the dogs and the numerical density of amyloid-positive plaques stained with monoclonal antibody 4G8 (17-24aa) revealed that the population of old dogs consists of two subpopulations: one with a very low (0.8/mm2 on average) and other with a high (19.2/mm2 on average) numerical density of plaques. These two groups (19.5 and 19.1 years of age, respectively) appear to emerge from the younger group (12.2 years of age on average), with moderate (2.2/mm2 on average) numerical density of 4G8-positive plaques. These data may indicate that only a portion of the mongrel population (43%) is susceptible to amyloidosis beta or that only this severely affected subpopulation was exposed to a factor or factors inducing this pathology and developed severe cortical amyloidosis that correlates with age. Dog plaques are only of the diffuse type, with nonfibrillar, thioflavin S-, and Congo red-negative amyloid in all groups distinguished by cluster analysis. Only from 10% of 4G8-positive plaques in the mildly affected group to 29% in the severely and 37% in the moderately affected group are Bielschowsky positive. In the younger, moderately affected group, 6E10 (1-17aa)-positive plaques prevail. In the two old groups with severe and weak changes, almost all 4G8-positive plaques are also 6E10-positive. Carboxy-terminal region immunocytochemistry reveals that BC42-positive plaques are numerous, whereas BC40-positive plaques are few or absent. The differences in the silver-positivity of plaques and their immunoreactivity in both the amino- and carboxy-terminal regions may reflect differences in amyloid-beta deposition and resolution. Dog parenchymal amyloidosis beta appears to be a model for the study of diffuse plaques.

Amyloid beta-Peptides↗
PubMed1996

New ways of performing in vivo flow velocity measurements in the basilar artery.

The basilar artery is the only large artery in which two flows merge, and this is reflected in the flow downstream. We report quantitative flow-velocity measurements with a phase-based MR technique, i.e. the Fourier velocity encoding method, in the basilar artery of a volunteer. To our knowledge, this has not previously been performed successfully. A comparison is made with the results of flow velocity measurements in the basilar artery with transcranial Doppler ultrasonography; the techniques agreed very well. Although Doppler ultrasonography is still most widely used, no information on the flow rate and the flow velocity distribution in the basilar artery can be provided. MR flow measurement techniques appear promising when detailed information on the flow velocity distribution and flow rate is needed.

Adult↗
PubMed1995

The origin of amyloid in cerebral vessels of aged dogs.

Our morphometric study of 30 dogs, mongrels, from 6.5 to 26.5 years of age, shows amyloid angiopathy in cortical and leptomeningeal vessels of all dogs older than 13.2 years of age, and the increase in the numerical density of amyloid-positive vessels correlated with age. Cluster analysis distinguished the group of six dogs (25%) to be relatively less affected, a large group of 13 animals (54%) to have moderate pathology, and five dogs (21%) to have severe amyloid angiopathy. Amyloid accumulation starts in large vessels, particularly in the tunica media of large arteries. Amyloid deposition appears to be associated with smooth muscle cells. Ultrastructural studies of samples from nine dogs are in agreement with in vitro studies suggesting that smooth muscle cells are the source of soluble amyloid beta. beta-protein polymerizes in the basal lamina of the tunica media. Muscle cells in the area of amyloid-beta accumulation degenerate and die. Thioflavin-positivity of only 24% of cortical and 66% of leptomeningeal beta-protein-positive vessels suggests that thioflavin-negative deposits contain soluble, not yet fibrillized protein and/or partially degraded and depolymerized amyloid.

Aging↗
PubMed1995

A quantitative immunocytochemical study of blood-brain barrier to endogenous albumin in cerebral cortex and hippocampus of senescence-accelerated mice (SAM).

The blood-brain barrier (BBB) to endogenous albumin was studied in the cerebral cortex and hippocampus of the senescence-accelerated prone (SAMP8) mouse and senescence-accelerated resistant (SAMR1) mouse strains in corresponding age groups by using a quantitative immunocytochemical procedure. Brain samples after immersion-fixation were embedded at low temperature in Lowicryl K4M and sectioned with an ultramicrotome. Thin sections were exposed to anti-mouse albumin antiserum followed by protein A-gold. Labeling density (gold particles per microns 2) was recorded over four compartments: vascular lumen, endothelium, subendothelial space, and brain parenchyma (neuropil). Morphometric analysis of the electron micrographs revealed that the barrier function of capillaries located in the cerebral cortex of SAMP8 mice was not significantly different from that in control (SAMR1) mice. Nevertheless, in SAMP8 mice, the percentage of leaking microvessels was higher than in control animals. In the older (11-month-old) group of control mice, the percentage of leaking microvessels was higher in the hippocampus than in the cerebral cortex. In SAMP8 mice, however, these differences were negligible. In contrast, in 4-month-old animals, the labeling density of the subendothelial space, which was considered an indicator of albumin escape, was significantly higher in SAMP8 than in SAMR1 mice. Also, the labeling density of the neuropil in the hippocampus of both groups of mice was significantly higher than that in the cerebral cortex. This finding suggests that albumin has an access to the parenchyma of the hippocampus in normal conditions, and that this phenomenon becomes more pronounced during the process of senescence.

Aging↗
PubMed1994

A quantitative immunocytochemical study of the osmotic opening of the blood-brain barrier to endogenous albumin.

The time sequence of the blood-brain barrier opening to endogenous albumin in rat brain after intracarotid infusion of hyperosmolar L(+)arabinose was studied using quantitative immunocytochemistry. Brain samples obtained 1, 5, and 30 min after insult were immersion-fixed in formaldehyde-glutaraldehyde mixture and embedded at low temperature in Lowicryl K4M. Untreated rats or rats exposed only to Ringer's solution were used as a control. Ultrathin sections were exposed to anti-rat albumin antiserum followed by protein A-gold. The density of immunosignals (gold particles per square micrometre) was recorded over four compartments: vascular lumen, endothelium, subendothelial (perivascular) space including basement membrane, and brain parenchyma (neuropil). The labelling density of the vessel lumen, containing blood plasma, was considered to represent 100% of the circulating albumin. Morphometric and statistical analysis indicated that in control animals only 0.4-0.6% of circulating albumin appears in the subendothelial space and in the basement membrane. As soon as one minute after L(+)arabinose infusion, this value increased to 3%, followed by a further increase to 25% and 56% after 5 and 30 min, respectively. A slow increase of the labelling density in the adjacent neuropil suggests that the basement membrane represents an obstacle for escaping albumin, which apparently sticks to or is trapped by this membrane. The results indicate that the applied procedure, although based on morphometric analysis of static electron micrographs can also be used for studying dynamic processes such as transvascular passage of albumin after disruption of the brain-blood barrier.

Animals↗
PubMed1994

Noninvasive determination of local wavespeed and distensibility of the femoral artery by comb-excited Fourier velocity-encoded magnetic resonance imaging: measurements on athletic and nonathletic human subjects.

The local distensibility of arteries is of interest because distensibility varies from artery to artery, may be altered by disease to different extents in different arteries, and may be modified by physiological or pharmacological means. Using magnetic resonance imaging (MRI) we have measured local arterial wavespeed in the femoral artery in healthy human subjects and calculated local arterial distensibility. We acquired 2-D coronal and sagittal MR phase contrast angiograms of the femoral artery. We used a novel imaging technique, comb-excited Fourier velocity-encoded MRI, to obtain simultaneous measurements of arterial blood velocity at two stations 14 cm apart on the femoral artery. The separation of the two stations divided by the delay between the onset of forward flow at the two stations was used to calculate the wavespeed. The measurements were made on 16 healthy men (8 athletes, 8 non-athletes) in the age range 20-30 years, who were scanned with the use of ECG gating and an extremity coil in a 1.5 Tesla scanner (GE Medical Systems, Milwaukee, WI). By systematically altering the delay between the R-wave and data acquisition, a temporal resolution of 2-4 ms was achieved. The onset of forward flow at each station was determined from a least-squares fit to the data for 30% of the maximum velocity during the cardiac cycle. Average femoral artery wavespeed was 7.7 m/s +/- 1.2 in the athletes and 11.5 m/s +/- 1.1 in the non-athletes (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Neurofibrillary pathology in brains of elderly schizophrenics treated with neuroleptics.

The clinical histories of 102 schizophrenics who died at 70 years of age or older were reviewed. The incidence of neurofibrillary tangles (NFTs) was two times higher in the patients who received (74%) than in those who did not receive (36%) treatment with neuroleptics. The development of NFTs started earlier in the treated group. Further studies comparing brains of nine schizophrenics (average age, 86 years) who did not receive treatment with neuroleptics and seven age-matched cases who received neuroleptics, both with neurofibrillary pathology and neuritic plaques, showed characteristic differences. The numerical density of NFTs was slightly greater in the cornu Ammonis (CA1 and CA2) and subiculum of treated patients. Significantly lower numerical density and lower percentage of pretangles (stage 0) and early and mature tangles (stages 1 and 2) and increased number of end-stage tangles (stage 3) were found in the CA, subicular complex, and cerebral cortex of the treated group. These changes suggest accelerated neurofibrillary degeneration in neurons. A significant increase in the numerical density of tau-1-positive plaques was observed in sector CA1 of the CA (from 0.15/mm2 to 17.36/mm2), subiculum (from 0/mm2 to 16.62/mm2), temporal cortex (from 0.14/mm2 to 9.46/mm2), and occipital cortex (from 0.08/mm2 to 0.39/mm2). The higher numerical density of tau-1-positive plaques, but not of 4G8-positive plaques, indicates acceleration of neurofibrillary changes in the plaques of patients treated with neuroleptics. The significant decrease (20-25%) in the numerical density of neurons in the pyramidal layer of sectors 2-4 in the CA appears to be associated with accelerated neurofibrillary changes in neurons and plaques in the treated group. This study demonstrates that chronic treatment with neuroleptics--not schizophrenia itself--significantly increases the risk of more frequent, earlier, and accelerated development of neurofibrillary pathology in the brains of elderly schizophrenics.

Aged↗
PubMed1990

The measurement of time-averaged flow by magnetic resonance imaging using continuous acquisition in the carotid arteries and its comparison with Doppler ultrasound.

A continuous acquisition method was used to measure the time-averaged flow in the carotid arteries of 10 normal volunteers, using an interleaved flow-sensitive and flow-compensated field echo sequence on a 1.5 T magnetic resonance (MR) system. Validation of the sequence and technique was performed using a pulsatile rotating phantom. The measured flow rates for the common carotid arteries were compared with Doppler ultrasound values obtained immediately after the MR measurement using a Duplex scanner. The correlation (r = 0.52, P less than 0.01) was significant with data spread accounted for by the inherent errors of both techniques. The difference between time-averaged flow measured by MR and Doppler ultrasound was 1.9%. Short-term reproducibility of each technique was assessed by consecutive measurements with values of 6.8% and 6.6% respectively for MR and Doppler; measurements after a 2 - 4 week interval gave a long-term reproducibility of 11.8% and 9.8% respectively. The advantages of continuous acquisition make the method suitable for non-invasive flow measurements, particularly for vessels that are not accessible to ultrasound.

Blood Flow Velocity↗
PubMedDate not supplied

Neurofibrillary pathology--correlation with hippocampal formation atrophy in Alzheimer disease.

The three-dimensionally reconstructed hippocampal formations in three patients with very severe, immobile Alzheimer disease (AD) and three age-matched nondemented individuals were examined for a correlation between atrophy of hippocampal formation subdivisions and neurofibrillary changes, neuronal loss, and extent of amyloid deposition in plaques and vessels. In AD, a similar severe volume loss was observed in both cellular layers and layers composed of fibers. A strong correlation between the decrease in the volume of hippocampal formation subdivisions and the decrease in the total number of neurons suggests a causative role for neuronal loss in hippocampal formation volumetric loss. Strong regional correlations between the relative decreases in the total number of neurons and the relative increases in the total number of neurofibrillary tangles implicates neurofibrillary pathology as a possible etiologic proximate factor in neuronal and volumetric loss in the hippocampal formation of AD patients.

Aged↗
PubMedDate not supplied

Neuronal loss and beta-amyloid removal in the amygdala of people with Down syndrome.

The decrease in the number of neurons free of neurofibrillary changes, neurons with neurofibrillary degeneration, and the total volume of beta-amyloid (A beta) deposits in the amygdala of people with Down syndrome and in late stages of Alzheimer disease were estimated by using morphometry and regression analysis. This model predicts that the duration of neurofibrillary changes from the pretangle stage to ghost tangles is approximately 4.7 years. The correlation between the decrease in the number of neurons and the decrease in the amount of A beta indicates that amyloid deposition is associated with neurons and that loss of neurons causes decrease in A beta deposition. The presence of neurons only with neurofibrillary tangles, and the absence of the amyloid deposits predicted by regression analysis suggest that neurons with tangles are not engaged in amyloid deposition. The disappearance of amyloid by approximately 2.2 years after loss of neurons free of neurofibrillary changes indicates that A beta deposits are degradable and removable and that even in severely atrophic amygdala, there are mechanisms of amyloid resolution. This study shows that in normal aging in the amygdala, extracellular A beta appears later than neurofibrillary changes.

Adult↗
PubMedDate not supplied

Dural sinus occlusion due to calvarial metastases: A CT blind spot.

Dural sinus thrombosis can be a difficult diagnosis to establish because it may present with nonspecific signs of raised intracranial pressure. Diagnosis by CT is well documented but signs may be subtle. Angiography is the "gold standard" but is invasive and requires a very high index of clinical suspicion to request. Magnetic resonance offers a method of demonstrating the dural sinuses in multiple planes and, furthermore, flow within the sinuses may be depicted by MR angiography. We report on three cases where the diagnosis of superior sagittal sinus thrombosis due to calvarial metastases was missed by CT, primarily due to their site over the convexity, but was demonstrated accurately using MR with MR angiography.

Cerebrospinal Fluid↗
PubMedDate not supplied

Simultaneous detection of multiple components of motion with MRI.

OBJECTIVE: Simultaneous detection of two or more components of motion using new magnetic resonance pulse sequences was investigated. MATERIALS AND METHODS: The technique employs Fourier phase encoding to encode the first component, and phase contrast detection to encode the second. Although the technique can be generalized to any number of spatial dimensions and motional orders, applications in which one or two spatial dimensions are obtained with a single Fourier velocity or acceleration dimension are most likely to be useful. For example, Fourier-encoded velocity and phase-contrasted acceleration information can be combined into the same image. RESULTS: Several variations of the pulse sequence were investigated in phantoms and human volunteers. The first variation acquired images having an appearance similar to that of Fourier velocity-encoded images in which signal displacement is proportional to velocity, but with pixel intensity determined by acceleration. In another variation two spatial dimensions were acquired with a third dimension that uses Fourier velocity encoding to measure axial velocity within a curved tube. Radial velocity components were determined simultaneously with a second velocity-encoding gradient pulse. CONCLUSION: The phantom and in vivo results presented here suggest that simultaneous detection of two or more components of motion is feasible.

Adult↗
PubMedDate not supplied

Differential susceptibility to neurofibrillary pathology among patients with Down syndrome.

Individual differences in the development of neurofibrillary changes were examined in eight cortical regions in the brains of 43 subjects with Down syndrome (DS; age range, 15-69 years) using sections stained with monoclonal antibodies (mAb) tau-1 and 3-39. Neurofibrillary pathology was found in 4 cases below 36 years of age and in all 20 cases above that age. In the 24 positive cases, numerical density of pretangles stained with tau-1 and 3-39, respectively, was 6.1/mm2 and 0/mm2; early tangles, 5.0/mm2 and 5.3/mm2; mature tangles, 4.0/mm2 and 5.0/mm2 (p < 0.01); and end-stage tangles, 0.04/mm2 and 2.5/mm2 (p < 0.001). Numerical density of pretangles stained with mAb tau-1 and tangles and plaques stained with mAb 3-39 correlates weakly with age (r = 0.43; p< 0.02), and together with the wide range of numerical densities suggested heterogeneity of the population examined. Cluster analysis based on two variables - i.e., numerical density of pretangles stained with mAb tau-1 and neurofibrillary tangles (NFTs) and plaques stained with mAB 3-39, distinguished three groups of subjects with severe, moderate and weak changes. The severely affected group of 5 subject (21%) had an average 54.6/mm2 of neurons and 13.9/mm/ plaques with neurofibrillary changes, whereas the moderately affected group (6 subjects; 25%) showed a significantly lower numerical density of neurons and plaques with neurofibrillary changes (25.7/mm2 and 8.1/mm2, respectively) as compared with the most affected group. Most of the subjects (13; 54%) belong to the third group with only 2.2/mm2 of neurons and 1.4/mm2 plaques with neurofibrillary pathology. Comparison of these three groups of Down syndrome subjects representing high, moderate, and low susceptibility to neurofibrillary changes with the general population suggests that the risk of Alzheimer disease is similar but the onset of pathological changes is earlier in DS.

Adolescent↗
PubMedDate not supplied

Atrophy of hippocampal formation subdivisions correlates with stage and duration of Alzheimer disease.

The hippocampal formations of 13 subjects with severe Alzheimer disease [AD; Global Deterioration Scale (GDS) stage 7] and of 5 age-matched subjects without symptoms of dementia were reconstructed from serial sections. Functional assessment staging (FAST) was used at the time of demise to assess 9 patients at stages 7a-c (incipient averbal and nonambulatory) and 4 patients at stages 7e-f (immobile). The duration of the disease from FAST stage 5 until demise ranged from 2 to 8 years in the first of these subgroups, and from 10 to 13 years in the second. The volumes of the entire hippocampal formation and of the cornu ammonis, its sectors and layers, the dentate gyrus, the subicular complex, and the entorhinal cortex were calculated. Hippocampal formation volume decreased by 36% in the incipient averbal and nonambulatory patients and by 60% in the severely functionally impaired immobile patients, in comparison with controls. In the final substages of AD, immobile patients exhibited significant atrophy, in comparison with controls, in the cornu ammonis and all of its sectors and layers except CA4, the subicular complex and all of its parts, and the entorhinal cortex (p < 0.05). Within the AD patient group, significant correlations were noted between both the magnitude of functional severity and the duration of AD and the volumes of most hippocampal formation subdivisions studied. For the cornu ammonis, subicular complex, and entorhinal cortex, volumetric loss correlations with FAST stage 7 ordinally enumerated substages were r = -0.71, -0.79, and -0.62, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗