[Pathogenesis and pathology of Alzheimer's disease].
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Alzheimer Disease↗
Biomedical subjects
M Tomonaga
Publications and source records attributed to M Tomonaga.
Papillary meningioma with pulmonary metastasis. Case report.
Successful surgical treatment by extirpation of remote metastases is extremely rare. A patient was admitted in whom multiple metastases to the lung occurred 8 years after extirpation of a papillary meningioma of the posterior fossa. The meningioma did not recur at the original site. The pulmonary metastases were surgically removed. The histological and electron microscopic findings of this case are presented.
Adult↗
[Study on pathophysiology of the myelodysplastic syndromes (MDS)--pattern of dysmegakaryopoiesis related to leukemic transformation].
A series of 116 patients with MDS consisted of 74 cases of RA, 10 cases of RARS, 14 cases of RAEB, 9 cases of RAEB-T and 9 cases of CMML, were studied on the quantity and morphological abnormalities of megakaryocytes in relation to over all survival and leukemic change. The amount of megakaryocytes was graded into four groups; marked hypoplasia (O), moderate hypoplasia (L), normoplasia (N) and hyperplasia (H), RA cases showed heterogeneous pattern; containing 14 cases (18.9%) of group (O), 18 cases (24.3%) of group (L), 31 cases (41.9%) of group (N) and 11 cases (14.9%) of group (H). RARS, RAEB, RAEB-T and CMML cases were classified into group (N) or group (H). The heterogeneous pattern of RA did not relate to leukemic change, but over all survival tended to be shorter in group (N) cases. A significant number of young female cases of RA were involved in group (O). Morphological abnormalities of MDS megakaryocytes were classified into five types; I, mononuclear micromegakaryocytes, II, binuclear micromegakaryocytes, III, mononuclear small megakaryocytes, IV, multiseparated-nuclear megakaryocytes and V, megakaryocytes with bizzare nuclei. RAEB and RAEB-T cases uniformly showed marked dysmegakaryopoiesis ranging from type I to V. whereas RA, RARS and CMML cases showed mild dysmegakaryopoiesis. Only five cases (6.4%) of RA cases had type I micromegakaryocytes. Eight RA cases with type I on diagnosis or obtaining it during the clinical course tended to develop acute myeloid leukemia (5 cases) or to transform to RAEB sooner or later. In two cases of RAEB in which hematological improvement was obtained with low dose cytosine arabinoside regimen, disappearance of type I micromegakaryocytes was noted. A female case with 5q-anomaly surviving more than 10 years showed marked megakaryocyte hyperplasia and almost exclusively type III and IV megakaryocytes. These findings indicated that pattern of dysmegakaryopoiesis, especially appearance of type I, was closely related to leukemic change in MDS. Thus quantitative and qualitative evaluations of MDS megakaryocytopoiesis seemed important to understand the further heterogeneity of pathophysiology in MDS subtypes.
Aged↗
Multiple intracerebral arteriovenous malformations: report of two cases.
We report the cases of two patients, each of whom had two separate angiographically demonstrable intracerebral arteriovenous malformations (AVMs). One patient had an intraventricular hemorrhage with AVMs in the basal ganglia and the insula on the left side, and the other had a pontine hemorrhage with AVMs in the pons and the occipital lobe on the right side. The AVMs in the former patient were removed totally without residual neurological deficit. We discuss the diagnostic problems of multiple intracerebral AVMs and stress the need for thorough neuroradiological evaluation so as not to miss an occult AVM. We also stress the necessity of total excision of all the lesions and point out several problems faced in surgery for AVMs.
Adult↗
[Aneurysm at the PCA posterior temporal artery junction: a case report].
A case of saccular aneurysm located at the PCA posterior temporal artery junction (E portion of PCA) was reported. A 35-year-old man was referred to us for surgical treatment of intracerebral hematoma in the right temporo-parietal lobes. On admission, the patient was somnolent and there was right oculomotor palsy, left homonymous hemianopsia and left hemiparesis. Left vertebral angiograms revealed a saccular aneurysm at the quadrigeminal segment of the posterior cerebral artery on the right. The hematoma was immediately evacuated by temporal corticotomy, and three weeks later, trapping of the aneurysm was performed through subtemporal approach. Postoperative course was uneventful. However, the left homonymous hemianopsia persisted. This was the only symptom which did persist. The incidence of PCA aneurysm is 1% in all cerebral aneurysms, or 15% in aneurysms of the posterior circulation. The majority of those are located at the junction proximal to the PCA-anterior temporal artery, or proximal to the PCA-posterior lateral choroidal artery junction. In the present case, the aneurysm was located more distally at the PCA-posterior temporal artery junction, and aneurysm at this site has been reported only six times in the literature. In addition to the present case, we reviewed 41 cases (42 aneurysms) in the literature, concerning the operative method and postoperative neurological deficits for the aneurysms of PCA. Neck clipping was performed in 23 cases without any further neurological deficits and trapping or proximal clipping of the aneurysms was performed in 16 cases, in which new neurological deficits developed in 3 cases.
Adult↗
[New topics of Alzheimer's disease research].
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Acetylcholine↗
[Approach to the dementia research].
Main causes of dementia in the elderly are vascular dementia and Alzheimer's dementia. Vascular dementia is related to both amounts and localization of lesions. Recently incidence of diffuse vascular leukoencephalopathy (Binswanger type, leukoaraiosis) and amyloid angiopathy are increasing. In Alzheimer's protein chemistry of amyloid (beta protein, A4 protein) revealed its precursor APP and its gene (chromosome 21), which produces protease inhibitor in the brain of Alzheimer and Down's brains. APP is considered as an membrane protein (receptor) and appears abundantly in the cerebral cortex. Immunohistochemical study showed that beta protein is observed also in normal aged brain. On the other hand, tau protein (main component of Alzheimer's neurofibrillary tangle, PHF) appeared as abnormal sprouting of neurites in Alzheimer's brain. The latter may related to dementia and neural death. In Alzheimer's dementia, several neurotransmitters, including acetylcholine, are reduced in the brain and related structural changes are observed. Recently olfactory bulb and mucosal changes are remarked as one of pathogenesis of this disease. Delayed neuronal death is a new phenomenon of nerve cell death of vascular origin and should be studied in human vascular dementia.
Aged↗
[Marked dysmyelopoiesis after induction chemotherapy in a case of acute myelomonocytic leukemia (M 4) with t(6; 11)].
A case of AML (M 4) with t(6; 11) showed recovery to myelodysplastic syndrome (MDS)-like bone marrow after one course of DCMP regimen. Dysplastic changes of three cell-lineages were observed and micromegakaryocytes were markedly increased in number. Recovering hematopoiesis was incomplete. During MDS-like phase, t(6; 11) disappeared, reverting to normal karyotypes. Low dose ara-C regimen did not show any effect. AML soon relapsed with reappearance of t(6; 11). MDS-like abnormal hematopoiesis has recently been reported to occur after remission induction therapy or at the time of relapse. G-6PD isozyme study revealed in a remission case of AML that hematopoiesis still consisted of abnormal clone in spite of karyotypic normalization. The abnormal hematopoiesis observed in our case can be referred to such a clonal disorder predominating after disappearance of blastic component of AML. It seems important to reveal what proportion of de novo AMLs shows such an abnormal hematopoiesis and to establish suitable therapeutic approach.
Antineoplastic Combined Chemotherapy Protocols↗
CML-T1: a cell line derived from T-lymphocyte acute phase of chronic myelogenous leukemia.
Most data suggest that malignant transformation in chronic myelogenous leukemia (CML) occurs in hematopoietic stem cell that is the progenitor of myelopoiesis and of B but not T lymphopoiesis. We established a T-lymphoid cell line (CML-T1) from a person with Ph-chromosome-negative CML in acute phase. Evidence of its T-lymphocyte origin includes the pattern cytochemical reactivity, reactivity with anti-T-cell monoclonal antibodies (MoAbs), and rearrangement of the beta-T-cell receptor (TCRB) gene. CML-T1 cells have features of type IV thymocytes. Cytogenetic analyses indicate a 47,XX, del(11), t(6;7)(q23;q24), +mar karyotype. CML-T1 cells exhibit molecular changes typical of CML, including translocation of the ABL protooncogene from chromosome 9 to 22, rearrangement of the BCR gene, and transcription of a chimeric BCR-ABL messenger RNA (mRNA). The ABL insertion on chromosome 22 appears interstitial, similar to other cases of Ph-chromosome-negative CML. These data clearly indicate that T cells can be involved in acute-phase CML. CML-T1 should be useful in studying this process as well as that underlying Ph-chromosome-negative CML.
Adult↗
[A trial for prolongation of chronic phase of chronic myeloid leukemia--maintenance of leukocyte counts within normal range with busulfan].
To prolong the survival of patients with chronic myeloid leukemia (CML), 19 patients were treated with busulfan to keep their leukocyte counts within normal range by controlling bone marrow hyperplasia. The duration of chronic phase in these patients was significantly longer than that in historical controls who were treated conventionally with busulfan. This prolongation was not ascribable to the difference in such prognostic factors between the two therapy groups as splenomegaly, leukocyte count and percentage of peripheral blasts. There was a significant difference again in the duration of chronic phase between the two therapy group even when restricted to each 11 patients with intermediate relative risk (0.7-1.5) according to Sokal et al. Four patients showed thrombocytopenia less than 5 x 10(4)/microliters, but all these patients recovered within 4 months and there was no further critical side effect except subcutaneous bleeding. This study suggests that maintenance of leukocyte count within normal range and suppression of granuloid hyperplasia in bone marrow with busulfan may prolong chronic phase of CML. Probability of clonal evolution may be decreased by reducing the total leukemic cell mass and suppressing cellular turnover of primitive CML stem cells. Another possibility is that prolongation of chronic phase might be dependent on the appearance of normal karyotype clone after long-term bone marrow suppression just like after intensive chemotherapy or alpha-interferon therapy.
Adolescent↗
[Effects of low dose Ara-C regimen in acute leukemias and RAEB].
Recent increase of leukemia among elderly patients prompted us to investigate the types of leukemia which can be induced into remission by low-dose Ara-C (LDAC) regimen. LDAC regimen was performed in 30 cases with overt acute leukemia (A), hypoplastic leukemia (B), and RAEB (C); Group A consists of M1 (1 case), M2 (4 cases), M3 (1 case), M4 (4 cases), M6 (1 case), and ALL (2 cases), Group B AML (8 cases), ALL (2 cases), and null (1 case), Group C RAEB (2 cases), and RAEB-T (4 cases). Complete remission (CR) rate was 23% (3/13) in group A, 64% (7/11) in group B, 0% (0/6) in group C. Partial remission rate was 33% (2/6) in group C. In group A, patients with M2 were induced into CR. In group B, both AML and ALL were induced into CR. Hypocellular marrow indicating low leukemic burden related to good sensitivity to Ara-C. Duration of CR was rather short; mean duration being 5.3 months. In group C, 2 PR cases of RAEB showed partial hematological recovery. LDAC regimen is effective especially for most of hypoplastic leukemia and some of M2. Side effects were tolerable, but all CR cases passed through bone marrow hypoplasia and needed supportive cares.
Acute Disease↗
[Difference of antibody profile for human T-lymphotropic virus type-I (HTLV-I) among individuals].
Healthy carriers, patients with ATL and HTLV-I associated myelopathy (HAM) were examined for HTLV-I antibodies of IgG and IgM classes and anti-p 40x antibodies, using ELISA, western blot (WB) and particle agglutination (PA) techniques. IgG antibodies were almost always detectable in sera from all of patients with ATL and HAM and healthy carriers with high titer in the PA test (normal carriers), and the average value of OD 405 was 2.0 +/- 0.3, 1.6 +/- 0.6 and 1.3 +/- 0.7, respectively. In anti-p 40x antibodies, the detectable incidence of HAM, ATL, normal carriers and carriers with low titer of the PA (low-PA group) was 90%, 67%, 44%, and 3%; and, the average value of OD 405 of the antibodies was 2.3 +/- 1.0, 0.7 +/- 0.5, and 0.7 +/- 0.7, respectively. On the other hand, the incidence of IgM antibodies demonstrated in HAM, ATL, normal carriers and low-PA group was 90%, 41%, 33%, and 53%, respectively. Furthermore, the follow-up observation of these antibodies revealed that the antibody profile of individuals for a long time was constant, i.e. in each carrier the value with high OD remained high and the presence of anti-p 40x and/or IgM antibodies remained present. These data has demonstrated that there are considerably differences among individuals in responsivilities for HTLV-I. Then, the antibody profile is mainly classified into 3 groups; hyper-, common- and hypo-immune patterns.
Aged↗
[Acute encephalopathy with symmetrical, widespread, edematous and necrotic lesions--an autopsy case report].
A 67-year-old, non-alcoholic Japanese female case with liver cirrhosis, in the course of admission due to ascites and rupture of the rectal varix, was affected by an unusual type of acute progressive encephalopathy, presenting inattentiveness and slurred speech as initial symptoms. Her consciousness was increasingly clouded. Variable symptoms such as saccadic eye movement, nystagmus, weakness, hyperreflexia, dysmetria, adiadochokinesis and painful dysesthesia were also noted. Laboratory examination disclosed abnormal liver functions, hyponatremia, respiratory alkalosis and normal blood ammonia. Cerebrospinal fluid was xanthochromic and contained slightly increased protein. On CT scan, bilateral symmetrical low density areas were demonstrated in the diencephalon, brainstem and cerebellum. A week after the onset, she was comatose with rigidity of the extremities. Hyperbilirubinemia and severe hyponatremia developed. On the second CT, low density areas extended to the cerebral deep white matter. Her respiration became irregular, and she expired 16 days after the onset. Autopsy disclosed edematous lesions with dark brown discoloration in the medial basal ganglia, ventral diencephalon and mesencephalic tegmentum. Less severely affected lesions with pale yellow discoloration extended into the cerebral white matter, pontine and medullar tegmentum and cerebellar dentate nuclei. In the central lesions, diapedesis of erythrocytes and serum-plasma was marked, with necrosis of the neurons. In the peripheral lesions, diapedesis of less proteinaceous fluid was noted, with less severe neuronal damages. Neither capillary prominence nor gliosis was remarkable. The clinical and pathological features of the present case bore some similarity to those of Wernicke's and Leigh's encephalopathies. However, the patient's age, habitus or clinical course was atypical for the latter.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗
Alzheimer's disease brain extract stimulates the survival of cerebral cortical neurons from neonatal rats.
Cell cultures of neonatal rat cerebral cortex in a serum-free medium were used to investigate a lack of neuronotrophic factors in Alzheimer's disease (AD) brain. A few neurons survived in the absence of brain extract. The addition of normal brain extract resulted in a 2.5-fold increase in neuronal survival. AD brain extract contained 4-fold neuronotrophic activity of normal brain extract. These findings are in contrary to the previous hypothesis of a lacking neuronotrophic factors in AD brain. These new results may change the concept of mechanism of neuronal death in AD.
Aged↗
Creatine kinase immunoreactivity: localization in nerve terminals in the hypothalamic area and superior colliculus of the mouse brain.
Immunoperoxidase studies of mouse brain using antibody to creatine kinase (CK) revealed the presence of immunoreactive neuronal varicosities in the zona incerta, lateral hypothalamic area, arcuate nucleus and superior colliculus. In the zona incerta and lateral hypothalamic area, the varicosities were distributed among the distinctive CK-immunoreactive neurons and some varicosities apparently emerged from these neurons. In the arcuate nucleus, the varicosities were concentrated in the periventricular region and occasionally clustered around unstained neurons. In serial sections, a portion of varicosities could be traced from the lateral hypothalamic area to the arcuate nucleus. In the superior colliculus, CK immunoreactivity formed a network pattern, which was mainly confined to the stratum zonale and stratum griseum superficiale.
Animals↗
Unilateral hemispheric cerebral changes similar to Creutzfeldt-Jakob disease in a case of hemiconvulsion.
A 77-year-old man suffered intermittent hemiconvulsions of unknown etiology on the left side for a period of about 5 weeks. At the autopsy, there was marked neuronal loss, severe proliferation of astrocytes and spongiform changes in the right cerebral cortex. The cerebral white matter showed loosening with astroglial proliferation in areas on the same side. These neuropathological changes were slight or absent in the left cerebral hemisphere. Histopathological changes were similar to those seen in unilateral Creutzfeldt-Jakob disease (CJD). Although unilateral CJD can not be ruled out, these unilateral hemispheric changes might be induced by intermittent hemiconvulsions.
Aged↗
Choroidal epithelial cyst of the prepontine region: case report and ultrastructural study.
A case of choroidal epithelial cyst of the prepontine region is reported. The cyst wall was studied using light and electron microscopy. Electron microscopy revealed that the lining of the cyst consisted of a single layer of epithelial cells resting on a basement membrane. The epithelial cells contained numerous club-shaped microvilli and occasional cilia. There were no coating materials on the surface of the microvilli. Tight junctions and interdigitations were present between contiguous cells. The blood vessels were fenestrated. These ultrastructural findings suggest that the epithelial cyst was derived from the choroidal epithelium rather than ependyma or endodermal tissue.
Adult↗
[A quantitative study of cerebral atrophy in senile dementia of Alzheimer type].
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Aged↗