Cases reported "Alzheimer Disease"

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1/18. Glial intranuclear inclusion bodies in a patient with Alzheimer's disease.

    We report a case of dementia in an elderly woman with the pathological findings of Alzheimer's disease and numerous intranuclear inclusions in astrocytes and occasionally in neurons. These inclusions were seen in the cerebral cortex, limbic areas, basal ganglia, thalamus, brain stem and cerebellum. They expressed ubiquitin and were ultrastructurally composed of haphazardly arranged straight filaments. The presence of similar intranuclear inclusions in previous cases of adult-onset dementia without other neuropathological changes suggests an important link between these kind of inclusions and dementia. To our knowledge, this type of intranuclear inclusions has not been previously described in association with Alzheimer pathology.
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2/18. Clasmatodendrosis correlating with periventricular hyperintensity in mixed dementia.

    We report a 79-year-old woman with possible Alzheimer's disease and confluent periventricular white matter hyperintensities on magnetic resonance imaging in whom postmortem analysis unexpectedly demonstrated no periventricular demyelination or cerebral arteriosclerosis. However, astrocytes in the periventricular white matter exhibited clasmatodendrosis, defined as cytoplasmic swelling and vacuolation of astroglia, with beading of their dendrites. This finding represents a previously unrecognized correlate of periventricular white matter hyperintensities. Ann Neurol 2002;52:378-381
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3/18. NACP/alpha-synuclein, NAC, and beta-amyloid pathology of familial Alzheimer's disease with the E184D presenilin-1 mutation: a clinicopathological study of two autopsy cases.

    Approximately 60% of familial and sporadic Alzheimer's disease (AD) cases manifest lewy bodies (LBs), of which a major component is alpha-synuclein. Although the pathogenic role of alpha-synuclein in AD remains unclear, LB formation might be associated with pathological beta-amyloid (Abeta) overproduction. Here, we present the clinical and pathological characteristics of two affected family members from a pedigree with the E184D mutation of presenilin-1. One case presented with typical clinical features of AD, but the other case also developed clinical characteristics of dementia with lewy bodies (DLB), including visual hallucinations, delusions, and parkinsonism. In both cases, neuropathological examination revealed numerous neurofibrillary tangles and severe Abeta deposition in senile plaques and amyloid angiopathy, in which Abeta42 rather than Abeta40 was predominant. Furthermore, remarkable alpha-synuclein pathology, including LBs and the accumulation of the non-Abeta component of AD amyloid (NAC) in plaques and astrocytes, was detected only in the case that presented with the symptoms of DLB. These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.
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4/18. autopsy case of aluminum encephalopathy.

    We report the case of a 59-year-old female aluminum encephalopathy patient who had chronic renal failure and took 3.0 g hydroxy-aluminum gel per day for the control of serum phosphorus level during a 15-year period. Nine months before her death she developed disorientation, memory disturbance, emotional incontinence, general convulsions and consciousness disturbance. Neuropathologically, the brain showed nerve cell atrophy and mild loss with stromal spongiosis, proliferation of astrocytes and microglia in the cerebral cortex, basal ganglia and thalamus. Some nerve cells were stained immunohistochemically by phosphorylated neurofilament, but apparent neurofibrillary tangles were not observed. aluminum was detected in the nerve cells of the cerebral cortex by X-ray microanalysis. Despite the long-term intake of aluminum, there were no neuropathological findings of Alzheimer's disease. The findings in our case suggested that aluminum alone might not develop Alzheimer's disease.
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5/18. Neuropathology of human alzheimer disease after immunization with amyloid-beta peptide: a case report.

    Amyloid-beta peptide (Abeta) has a key role in the pathogenesis of alzheimer disease (AD). immunization with Abeta in a transgenic mouse model of AD reduces both age-related accumulation of Abeta in the brain and associated cognitive impairment. Here we present the first analysis of human neuropathology after immunization with Abeta (AN-1792). Comparison with unimmunized cases of AD (n = 7) revealed the following unusual features in the immunized case, despite diagnostic neuropathological features of AD: (i) there were extensive areas of neocortex with very few Abeta plaques; (ii) those areas of cortex that were devoid of Abeta plaques contained densities of tangles, neuropil threads and cerebral amyloid angiopathy (CAA) similar to unimmunized AD, but lacked plaque-associated dystrophic neurites and astrocyte clusters; (iii) in some regions devoid of plaques, Abeta-immunoreactivity was associated with microglia; (iv) T-lymphocyte meningoencephalitis was present; and (v) cerebral white matter showed infiltration by macrophages. Findings (i)-(iii) strongly resemble the changes seen after Abeta immunotherapy in mouse models of AD and suggest that the immune response generated against the peptide elicited clearance of Abeta plaques in this patient. The T-lymphocyte meningoencephalitis is likely to correspond to the side effect seen in some other patients who received AN-1792 (refs. 7-9).
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6/18. Some immunohistochemical features of argyrophilic grain dementia with normal cortical choline acetyltransferase levels but extensive subcortical pathology and markedly reduced dopamine.

    Detailed immunohistochemical and biochemical studies are reported on two cases of progressive dementia showing no Alzheimer-type pathology but extensive argyrophilic grains as described previously by Braak and Braak. These cases had no specific clinical features, and the pathology of these brains showed subcortical gliosis (proliferation of astrocytes and microglia) without significant neuronal losses. Interesting novel immunohistochemical findings were the profuse appearance of complement-activated oligodendrocytes and oligodendroglial microtubular masses. Their appearance seems to indicate oligodendroglial reactions to widespread damage of myelinated axons. Cortical levels of choline acetyltransferase were normal, but striatal levels of dopamine and its metabolites were markedly reduced. This disease may be consistent with the criteria for progressive subcortical gliosis.
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7/18. Coexistence of paired helical filaments and glial filaments in astrocytic processes within ghost tangles.

    Ultrastructural examination of ghost tangles in an autopsy case of long-term Alzheimer's disease revealed, in addition to degenerate neurites containing paired helical filaments (PHF), astrocytic processes which included PHF. This finding suggests either that astrocytes in ghost tangles possess the capacity to produce PHF or that PHF are incorporated into astrocytes by endocytosis.
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8/18. An autopsy case of hereditary diffuse leukoencephalopathy with spheroids, clinically suspected of Alzheimer's disease.

    We report here a case of orthochromatic leukodystrophy with spheroids. A 40-year-old woman developed forgetfulness. About 1 year after the onset, clinical examination confirmed global intellectual deterioration with amnesia, spatiotemporal disorientation, and impairment of judgment. At age 43, she experienced tonic-clonic convulsions several times, and died of pneumonia at the age of 44. Alzheimer's disease was suspected clinically. Pathologically, there was severe diffuse demyelination of the deep white matter of the frontal, parietal and occipital lobes with relative preservation of the subcortical U fibers. In the central demyelinated areas, myelin loss was severe with diffuse gliosis, moderate loss of axons, and many axonal spheroids. At the periphery of the severely degenerated regions, there were a lot of macrophages and most had non-metachromatic lipid granules. The cerebral cortex was intact. The neuropathological findings of this case are consistent with hereditary diffuse leukoencephalopathy with spheroids (HDLS). Ten cases of HDLS were reviewed and presented many findings in common. The gray matter was intact and U fibers were well preserved in most cases. In white matter lesions, severe loss of myelin, moderate to severe axonal loss, much axonal swelling, and the presence of macrophages and hypertrophic astrocytes were common findings. In some cases with HDLS, dementia appeared without obvious neurological manifestations in the early stage. We should remember that some cases with HDLS show clinical symptoms similar to Alzheimer's disease, especially in the early stage.
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9/18. Paired helical filaments in astrocytes: electron microscopy and immunohistochemistry in a case of atypical Alzheimer's disease.

    A 54-year-old man who had cerebellar ataxia and pseudobulbar palsy at the age of 29 years, and soon developed dementia, myoclonus and convulsions, died after about 20 years in a vegetative state. Histological examination of the extensively atrophic and devastated brain (680 g) revealed the almost total loss of cerebral cortical neurons associated with numerous beta-protein amyloid plaques, many extracellular tangles and a large number of hypertrophic astrocytes, and prominent amyloid angiopathy. The astrocytes were frequently immunopositive for anti-human tau antibody (anti-htau) and anti-ubiquitin antibody (anti-ubi). Double immunostaining with anti-htau and anti-glial fibrillary acidic protein (GFAP) antibody clearly demonstrated htau-positive domains within the GFAP-positive perikarya/and processes of several astrocytes. Electron microscopy of the hippocampal CA1, which was completely devoid of pyramidal neurons, revealed, in astrocytes, abnormal filaments indistinguishable from the paired helical filaments (PHFs) seen in neurons. On immunoelectron microscopy, the filaments were observed to be labeled with anti-htau and anti-ubi, exhibiting the same immunohistochemical features as neuronal PHFs. This is the first demonstration of clearly constricted and both tau- and ubiquitin-positive PHFs in astrocytes, indicating that, in some special conditions like in our case, processes similar to those that attack neurons also affect astrocytes and ultimately make the latter form PHFs.
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10/18. glioblastoma multiforme of the hippocampus in advanced Alzheimer's disease.

    An 87-year-old woman suffered from Alzheimer's disease diagnosed 6 years prior to her death. autopsy showed in addition to far-advanced Alzheimer's disease, a large, partially necrotic glioblastoma occupying her right hippocampus. Occurrence of a glial neoplasm in Alzheimer's disease could well be coincidental, since both entities are fairly common in elderly individuals; it is however, uncommon for gliomas to centre on the hippocampus itself. For these reasons it is possible (although cannot be proven from a single case), that florid reactive gliosis commonly associated with Alzheimer's disease, may have played a role in eventually initiating neoplastic proliferation of astrocytes in this patient.
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