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T Uchihara

Publications and source records attributed to T Uchihara.

At least 55 records · Page 3Linked to original sources
PubMed1996

Inconstant apolipoprotein E (ApoE)-like immunoreactivity in amyloid beta protein deposits: relationship with APOE genotype in aging brain and Alzheimer's disease.

The aim of this study was to analyze the relationship between apolipoprotein E (ApoE) and amyloid beta-protein (A beta) deposits in 29 brains from a series of elderly women, whose intellectual status had been prospectively assessed by the Blessed test score (BTS). In three cases the APOE genotype was epsilon 3/4, in one epsilon 2/2, in 25 epsilon 3/3. ApoE-like immunoreactive lesions resembling a classic senile plaque (ApoE-SP) or a diffuse deposit (ApoE-DD) were quantitatively assessed in the first temporal gyrus (Brodmann's area 22). The density of ApoE-positive deposits (ApoE-SP+ApoE-DD) was correlated with BTS (negative correlation R2 = 0.36, P = 0.0006). The correlation of the density of ApoE-DD with BTS (R2 = 0.26, P = 0.0051) was weaker than that of ApoE-SP (R2 = 0.50, P < 0.0001). The density of ApoE deposits was correlated with that of A beta-immunoreactive lesions (positive correlation R2 = 0.57, P < 0.0001). ApoE immunohistochemistry labeled fewer deposits than A beta immunohistochemistry but showed as many senile plaques (ApoE-SP) as tau immunohistochemistry and the Gallyas and Bodian techniques. Two of the three cases with the epsilon 3/4 allele had Alzheimer's disease (AD) with numerous ApoE-immunoreactive senile plaques. In contrast, the brain of the third epsilon 3/4 case, whose intellectual status was normal, contained numerous A beta deposits but lacked ApoE-like immunoreactivity. The presence of ApoE may, thus, not be a prerequisite for A beta deposition, even in cases with the epsilon 3/4 allele. The density of ApoE-SP peaked in layer III, whereas that of ApoE-DD was maximal in deeper cortical layers. This contrast in the laminar distribution indicates that only some ApoE-DD may evolve into ApoE-SP. ApoE deposition was linked to the intellectual decline and was constant in the most severely demented patients, in whom numerous ApoE-positive (and A beta-positive) neuritic plaques were surrounded by dystrophic neurites. ApoE may accumulate in neuritic senile plaques during the progression of AD.

Aged↗
PubMed1996

Widespread immunoreactivity of presenilin in neurons of normal and Alzheimer's disease brains: double-labeling immunohistochemical study.

The immunolocalization of presenilin in human brain was studied using two antibodies raised against different portions of presenilin 1 (S182) protein. A granular staining was found in the cytoplasm of neurons in cortical layers III and V. One of the antibodies, also reactive to presenilin 2 (E5-1) protein, additionally stained dendrites and axons. This was seen in normal brains as well as in brains affected by Alzheimer's disease. Less prominent immunolabeling was noted in some senile plaques. No relationship to neurofibrillary tangles was found in double-labeling experiments combined with anti-paired helical filament-tau antibody (AT8). The widespread expression of presenilin in normal brain suggests a physiological role of the protein.

Aged↗
PubMed1996

Successful treatment of atypical mycobacterial meningitis by fluoroquinolone.

We report a case of restricted meningeal infection by atypical mycobacteria, identified by the polymerase chain reaction, in a non-immunocompromised adult successfully treated by multiple antibiotics including fluoroquinolone. New quinolones should be considered as a therapeutic option for such mycobacterial meningitis.

Administration, Oral↗
PubMed1996

Pure progressive clumsiness due to parietal atrophy in a young adult.

Progressive clumsiness developed in the right hand of a 33-year-old man, became bilateral and evolved very slowly for ten years. Another neurological deficit was restricted to a slight impairment of superficial sensations. Magnetic resonance imaging verified an atrophy of bilateral parietal lobes. The cerebral blood flow was markedly decreased in the atrophic area. Pure clumsiness of a very slowly progressive course due to parietal atrophy has never been reported in such a young adult. This clinical picture may suggest another variety of degenerative process.

Adult↗
PubMed1996

[Alzheimer's disease lesions: from morphology to cell biology].

Four different approaches to Alzheimer disease changes have been successively applied, and allowed a permanent feed forward-feed back enrichment of knowledge: morphologists described neurofibrillary tangles, senile plaques, amyloid angiopathy; with the help of immunohistochemical and biochemical techniques, they recognised A beta- and tau-associated pathologies; this, in turn, allowed more precise analysis of the lesions, and permitted recognising new ones such as neuropil threads; molecular genetics and molecular biology provided new insights, allowing the discovery of additional pathologic proteins, the relevance of which to physiology and pathology of the nervous system has now to be settled down. The increasingly intricate complex of lesions of Alzheimer syndrome is reviewed. A more comprehensive understanding is urgently needed for initiating efficient therapeutic researches. It will require together continuing a multidisciplinary approach, and a renewal of research in neuropathology.

Alzheimer Disease↗
PubMed1995

ApoE immunoreactivity and microglial cells in Alzheimer's disease brain.

The spatial relationship of apolipoprotein E (apoE)-like immunoreactivity (IR) to amyloid beta-peptide (A beta), astrocytes and microglial cells in the brain of Alzheimer's disease was studied by double immunolabelling. Diffuse apoE-like IR was seen in A beta diffuse deposits, and markedly increased in the core of classic senile plaques. Microglial cells, sometimes immunoreactive for apoE, were frequent in areas of apoE-like IR, where they often grouped into clusters in the core of apoE-labelled senile plaques. Although astrocytic processes were seen within these senile plaques, the cell bodies were always at a distance from the core. None of these astrocytes expressed apoE-like IR. Microglial cells, some of them immunoreactive for apoE, were seen in the center of apoE-labelled senile plaques. These data suggest that microglial cells play a more significant role than astrocytes in apoE deposition in senile plaques of Alzheimer disease.

Aged↗
PubMed1995

White matter amyloid in Alzheimer's disease brain.

Amyloid beta-protein (A beta) deposits in the white matter were investigated by the double immunohistochemical staining for A beta and neuritic, glial or vascular components. Reactive astroglia and neurite abnormality were absent around A beta deposits in the white matter (w-A beta) even those with a core. The association of w-A beta with blood vessels was not consistent. Aggregates of activated microglia were found to be the sole but a consistent accompaniment of A beta deposits even in the absence of other components such as neuron, synapse, neurite abnormality and reactive astroglia, as observed in the white matter. This suggests that the aggregates of activated microglia most likely represent one of the factors promoting the process of A beta deposition.

Alzheimer Disease↗
PubMed1995

Alzheimer-type pathology in melanin-bleached sections of substantia nigra.

Bleaching of melanin prior to Gallyas staining enabled us to detect an unexpectedly large number of neurofibrillary tangles (NFTs; 62 and 50 NFTs in the upper and the lower substantia nigra, respectively, mostly in the neuronal cytoplasm of the medial zona compacta) in brains of patients who had had Alzheimer's disease. Amyloid-like deposits were quite scarce. In Alzheimer's disease it has been commonly observed that other subcortical nuclei projecting widely to the cerebral cortex also contain a large number of NFTs, although they have few amyloid deposits. In these subcortical nuclei retrograde degeneration may initially affect intraneuronal processes, leading to the preferential development of NFTs in the neuronal cytoplasm.

Aged↗
PubMed1995

Spastic tetraplegia as an initial manifestation of familial Alzheimer's disease.

Two sisters with familial Alzheimer's disease developed spastic gait disturbance as an initial manifestation. Their gait disturbance progressed gradually, followed by dementia a few years later. Post-mortem examination of one of the patients disclosed degeneration of the thalamus and corticospinal tract in addition to numerous senile plaques and neurofibrillary tangles in the neocortex, both of which were confirmed by immunohistochemistry. This is the first report in which clinicopathological evaluation is sufficient to establish a new variant of Alzheimer's disease presenting initially as spastic tetraplegia.

Alzheimer Disease↗
PubMed1995

Widespread appearance of Alz-50 immunoreactive neurons in the human brain with cerebral infarction.

BACKGROUND AND PURPOSE: Tau-like immunoreactivity is known to develop in neurons under some experimental conditions simulating ischemia. The purpose of this study is to investigate the expression of tau-like immunoreactivity in the human brain after ischemic insult. METHODS: A series of autopsied human brains with or without ischemic lesion were investigated with immunohistochemistry (Alz-50, anti-tau, and anti-ubiquitin) and with silver-staining methods (Gallyas and Bodian methods). RESULTS: Punctate immunoreactivity to Alz-50 was visualized in the cytoplasm not only of the neurons in and around the ischemic lesion but also of the neurons free from classic ischemic changes around the necrosis. Some of the neurons around the ischemic lesion were stained by the Gallyas method. Immunostaining with anti-tau and anti-ubiquitin antibodies and the conventional Bodian method failed to visualize these neurons. CONCLUSIONS: The widespread appearance of Alz-50 immunoreactive neurons during the ischemic process signifies that tau-related proteins may be related to ischemic necrosis, but the lack of neurofibrillary tangles morphologically distinguishes ischemic development of tau-related proteins from the neurofibrillary degeneration in Alzheimer's disease.

Antigens↗
PubMed1995

Single-laser three-color immunolabeling of a histological section by laser scanning microscopy: application to senile plaque-related structures in post-mortem human brain tissue.

We describe a method for observing three-color immunofluorescence simultaneously in a histological section under a confocal laser scanning microscope. In this study we investigated the spatial relationship of blood vessels, reactive microglia, and amyloid beta-protein (A beta) deposits in post-mortem brain tissue of patients with Alzheimer's disease. HLA-DR was employed as a marker for activated microglia and von Willebrand factor (vWF) as a marker for vascular endothelial cells. HLA-DR was labeled with R-phycoerythrin (R-PE) and vWF with fluorescein isothiocyanate. A beta-protein was immunostained with the tandem conjugate of R-PE and cyanin 5. Three images were obtained serially by scanning a tissue section with a 488-nm laser beam in combination with an appropriate emission filter for each fluorochrome. Overlaying of these three images permitted simultaneous observation of three distinct structures: activated microglia, blood vessels, and A beta deposits. This technique provides an improved way to study the localization of three different antigens in a single tissue section.

Alzheimer Disease↗
PubMed1995

Spontaneous resolution of an acute spontaneous spinal epidural hematoma without neurological deficits.

A 46-year-old woman presented with sudden severe pain in the interscapular region. Physical examination, including detailed neurological evaluation, did not disclose any abnormalities. However, magnetic resonance imaging revealed an epidural hematoma anterior to the thoracic spinal cord and its spontaneous resolution thirty days after onset. Her hospital course was uneventful. To our knowledge, this report documents the first case of a spontaneous spinal spidural hematoma without neurological deficits. Spinal epidural hematoma may be more common than previously thought because some cases have probably been misdiagnosed as transient back pain of unknown etiology.

Acute Disease↗
PubMed1994

Compression of brachial plexus as a diagnostic test of cervical cord lesion.

STUDY DESIGN: This study evaluated the clinical significance of radicular signs around the neck in relation to mechanical lesions of the cervical spine and cord. SUMMARY OF BACKGROUND DATA: Classical radicular signs around the neck, such as Jackson's sign or Spurling's sign, are not sensitive enough to detect corresponding lesions. OBJECTIVES: Compression of the brachial plexus elicits radiating pain (BP) in patients with cervical lesions. The clinical significance of this new sign as a potential indicator of the cervical lesion compared with other classical signs was evaluated. METHODS: Sixty-five patients who underwent magnetic resonance imaging of the cervical spine were prospectively evaluated for these clinical signs that elicit radiating pain around the neck. Clinical signs were correlated to deformity of the cervical spine and cord and to final diagnosis. RESULTS: Classical radicular signs often were lacking, even in patients with mechanical lesions around the cervical spine. However, BP was often observed in these patients. CONCLUSIONS: Compared with the classical radicular signs, BP is highly sensitive and reasonably specific in detecting mechanical lesions around the cervical spine, and suggests radicular involvement.

Brachial Plexus↗
PubMed1994

Paraneoplastic encephalo-myelo-ganglionitis: cellular binding sites of the antineuronal antibody.

The cellular binding sites of an antineuronal antibody were characterized in an autopsy case of the paraneoplastic encephalo-myelo-ganglionitis. A 61 year-old woman developed a subacute sensorimotor polyneuropathy and, later, multiple involvement of cranial nerves, disturbance of consciousness, and generalized seizure. An autopsy revealed a small cell lung carcinoma and neuropathological changes that included disseminated encephalitis, spinal anterior horn lesions, severe loss of dorsal root ganglion neurons, and secondary degeneration and loss of the nerve fibers in the spinal posterior column and peripheral nerves. The serum IgG from the patient contained antineuronal antibody(s) including an antibody to 35- to 37-kDa neuronal antigens called anti-Hu as demonstrated in Western blot. In immunohistochemical studies, the serum IgG immunostained neurons of the brains, spinal cords, and dorsal root ganglia of humans or rats. Confocal laser-scanning microscopy revealed binding of the patient's IgG in the neuronal nuclei and cytoplasm, but not in the nucleoli. In immunoelectron microscopic studies, immunolabelling with the IgG was found diffusely in the karyoplasm, excluding nucleoli, and in the cytoplasmic matrix between the cisternae of the reticulums, Golgi apparatus, and mitochondria. Encephalo-myeloganglionitis is a clinicopathological entity frequently associated with the presence of neoplasm and antineuronal antibody, however, the role of the antibody in the pathogenesis remains to be elucidated.

Autoantibodies↗
PubMed1994

Abnormal cytoskeletal pathology peculiar to corticobasal degeneration is different from that of Alzheimer's disease or progressive supranuclear palsy.

An autopsy case of clinically diagnosed "corticobasal degeneration (CBD)" was investigated. In addition to status spongiosus and neuronal achormasia around the central sulcus, cortical pyramidal neurons and thread-like structures were densely stained by Gallyas stain and tau immunohistochemistry, but apparent fibrillary structures like Alzheimer's disease neurofibrillary tangle were absent. Bodian, methenamine-Bodian, Congo red, thioflavin S, or Bielshowsky stains failed to visualize these structures. They were not stained by immunohistochemical stain with anti-ubiquitin antibody. The widespread cytoskeletal pathology, which is distinct from that in Alzheimer's disease or progressive supranuclear palsy, is suggestive of CBD.

Alzheimer Disease↗
PubMed1994

Marked elevation of carcinoembryonic antigen and carbohydrate antigen 19-9 in the peripheral blood as an initial manifestation of meningeal carcinomatosis.

Marked elevation of tumor markers in the peripheral blood was initially a sole manifestation of meningeal carcinomatosis in a man with gastric carcinoma. In addition to extensive meningeal carcinomatosis, no metastatic lesions were found at autopsy other than microscopic infiltration into a tiny paraaortic lymph node. Elevation of these markers in the peripheral blood is best explained by meningeal carcinomatosis. When elevation of these markers is otherwise unexplainable, meningeal carcinomatosis should be considered as a diagnostic possibility even in the absence of neurological symptoms.

CA-19-9 Antigen↗
PubMed1994

Cryptic arteriovenous malformation of the choroid plexus of the fourth ventricle--case report.

A 54-year-old female presented with a cryptic arteriovenous malformation (AVM) of the choroid plexus of the fourth ventricle causing intraventricular hemorrhage. Computed tomography and magnetic resonance imaging disclosed the lesion near the fourth ventricle, but bilateral vertebral angiograms showed no abnormalities. The preoperative diagnosis was cavernous angioma. The mass was removed completely, and histological examination demonstrated an AVM of the choroid plexus. Vascular malformations of the choroid plexus of the fourth ventricle are extremely rare. The possibility of this lesion being the cause of primary intraventricular hemorrhage of unknown origin should always be considered.

Cerebral Angiography↗