Cases reported "Alzheimer Disease"

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1/12. Alzheimer's disease pathology in motor cortex in dementia with lewy bodies clinically mimicking corticobasal degeneration.

    We report here a 70-year-old woman whose initial clinical presentation suggested corticobasal degeneration, but autopsy revealed dementia with lewy bodies (DLB) with severe Alzheimer's disease (AD)-type pathology accentuated in the motor cortex, in conjunction with a high burden of both cortical and brain stem LB. review of the literature disclosed four patients with AD whose peri-Rolandic region was particularly involved by the disease and who exhibited similar clinical and neuropathological findings as in our patient except they lacked LB. It appears that DLB if associated with severe AD-type pathology can, like some unusual cases of AD, mimic corticobasal degeneration.
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2/12. Mapping biochemistry to metabolism: FDG-PET and amyloid burden in Alzheimer's disease.

    We evaluated the relationship between amyloid-beta protein (A beta) concentration and the metabolic abnormality in an Alzheimer's disease (AD) patient as measured by [18F]fluorodeoxyglucose positron emission tomography (FDG-PET). Across most regions there were significant inverse correlations among FDG-PET intensity values and both insoluble. The temporal lobe samples showed no significant correlation between FDG-PET values and A beta deposition. Findings support A beta as contributing to the hypometabolism in regions of the AD brain that are still relatively viable metabolically; those regions with chronic pathologic damage, such as temporal cortex, may have other factors that contribute to metabolic deficits.
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3/12. Case manager-defined roles in the medicare Alzheimer's Disease Demonstration: relationship to client and caregiver outcomes.

    This study explores the different approaches to case management within, the medicare Alzheimer's Disease Demonstration. Eight sites from around the country were selected to participate in a survey of case managers (N = 57) that evaluated their professional background and experience and how certain tasks, functions, and goals of case management were prioritized at each site. Client and caregiver outcomes were collected on a site-by-site basis as part of the demonstration. The hypothesis was that the way in which case managers performed their work would vary by site. Furthermore it was hypothesized that these differences would be measurable and correlated with project outcomes. Case managers differed significantly by site in how they prioritized tasks, functions, and goals, viewing themselves along a continuum from a clinical approach to one that emphasizes service management. These differences in case management style are reflected in between-site differences in certain client and caregiver outcomes but not others. Specifically, variations in case management style are not related to client cognitive or functional status but to other outcomes including behavioral management, caregiver burden, and service use.
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4/12. Senile dementia associated with amyloid beta protein angiopathy and tau perivascular pathology but not neuritic plaques in patients homozygous for the APOE-epsilon4 allele.

    Amyloid beta protein deposition in cortical and leptomeningeal vessels, causing the most common type of cerebral amyloid angiopathy, is found in sporadic and familial Alzheimer's disease (AD) and is the principal feature in the hereditary cerebral hemorrhage with amyloidosis, Dutch type. The presence of the Apolipopriotein E (APOE)-epsilon4 allele has been implicated as a risk factor for AD and the development of cerebral amyloid angiopathy in AD. We report clinical, pathological and biochemical studies on two APOE-epsilon4 homozygous subjects, who had senile dementia and whose main neuropathological feature was a severe and diffuse amyloid angiopathy associated with perivascular tau neurofibrillary pathology. Amyloid beta protein and ApoE immunoreactivity were observed in leptomeningeal vessels as well as in medium-sized and small vessels and capillaries in the parenchyma of the neocortex, hippocampus, thalamus, cerebellum, midbrain, pons, and medulla. The predominant peptide form of amyloid beta protein was that terminating at residue Val40, as determined by immunohistochemistry, amino acid sequence and mass spectrometry analysis. A crown of tau-immunopositive cell processes was consistently present around blood vessels. dna sequence analysis of the Amyloid Precursor Protein gene and presenilin-1 (PS-1) gene revealed no mutations. In these APOE-epsilon4 homozygous patients, the pathological process differed from that typically seen in AD in that they showed a heavy burden of perivascular tau-immunopositive cell processes associated with severe amyloid beta protein angiopathy, neurofibrillary tangles, some cortical lewy bodies and an absence of neuritic plaques. These cases emphasize the concept that tau deposits may be pathogenetically related to amyloid beta protein deposition.
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5/12. The parent they knew and the "new" parent: daughters' perceptions of dementia of the Alzheimer's Type.

    Psychosocial death is a significant dimension of the dementia of the Alzheimer's Type disease process but poorly studied. This article explores three phases of psychosocial death that emerged from in-depth interviews with three daughters caring for a parent with this chronic illness. The phases discussed include: (1) daughters creating a new relationship with their parent; (2) daughters grieving chronically throughout the illness; (3) daughters negotiating coherence between the parent that once was and the parent that exists now. Daughters' narratives reveal that witnessing the deterioration of a mind was a burdensome grave learning process that encompassed many losses. These daughters lacked appropriate education and support. Future research in this area is required to develop strategies for informal caregivers that respond to this disease process.
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6/12. Coexistence of CJD and Alzheimer's disease: an autopsy case showing typical clinical features of CJD.

    The present report concerns an autopsy case of CJD showing typical clinical features of CJD. The patient was a Japanese woman without hereditary burden or dementing disorder anamnesis who was 70-years-old at the time of death. She developed gait disturbance at age 68, followed by memory impairment, visual disturbance, and myoclonus. A neurological examination approximately 2 months after the disease onset revealed akinetic mutism, in addition to periodic synchronous discharges on electroencephalogram. Serial neuroradiological examinations disclosed progressive atrophy of the brain. She died of bronchopneumonia 25 months after the disease onset. The brain weighed 560 g (cerebrum 490 g, brainstem with cerebellum 70 g). Macroscopically, neuropathological examination showed prominent atrophy of the cerebrum, caudate nucleus, and cerebellum, in addition to necrosis of the cerebral white matter, compatible with panencephalopathic CJD. Histologically, there was neuronal loss with or without spongiform change in the cerebral cortex, parahippocampal gyrus, amygdala, striatum, pallidum, thalamus, pontine nucleus, and cerebellar granule cells, in addition to diffuse synaptic-type prion staining in the cerebrum and cerebellum. Furthermore, senile plaques, compatible with definite Consortium to establish a registry for Alzheimer's disease rank Alzheimer's disease, and neurofibrillary changes of the limbic system, consistent with stage IV of Braak's classification, were found. Based on these clinicopathological findings and a review of the published literature, it is concluded that there were two forms of coexistence of CJD and Alzheimer's disease in the same patient.
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7/12. Familial alzheimer disease associated with A713T mutation in APP.

    Mutations in APP are associated with familial early-onset alzheimer disease (FAD). Examination of the genomic sequence in one patient with FAD revealed a change located in the axon 17 of the APP gene at position 275329G>A (GenBank accession number: D87675; GI: 2429080); cDNA sequence 2137G>A (GenBank accession number: X06989; GI: 28720). This corresponds to the mutation A713T in APP. AD stage VI of neurofibrillary degeneration and stage C of Abeta-amyloid burden was found at the post-mortem neuropathological examination. Previous studies have suggested that the mutation A713T in APP is a silent mutation or polymorphism. However, we have not found this change in APP in a control population analyzed by the amplification-refractory mutation system (ARMS). It is concluded that A713T in APP is implicated in the pathogenesis of AD. Since the immunohistochemical study indicates that A713T mutation is not likely to relate with Abeta-amyloid processing, the causative role of this rare mutation remains to be warranted.
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8/12. Antipsychotic dose-sparing effect with addition of memantine.

    OBJECTIVE: To describe a case of an antipsychotic-sparing effect achieved after the addition of memantine to the regimen of a patient with severe Alzheimer's disease and aggressive behavioral disturbances. CASE SUMMARY: A 78-year-old white man with severe Alzheimer's disease was receiving risperidone 2 mg 3 times daily for persistent aggressive and dangerous behavioral disturbances. memantine was initiated, and the dose was titrated to 10 mg twice daily. The patient's response included improvement in functional status and resolution of problematic behaviors, allowing repeated reduction of the risperidone dose and ultimate discontinuation. DISCUSSION: Antipsychotics are often employed to treat behavioral disturbances for patients with Alzheimer's disease; however, the adverse effect potential of these agents remains a significant concern. Adjunctive medications that maintain or improve behavioral symptoms yet allow an antipsychotic-sparing effect are attractive. Such experiences have previously been described with other drug classes, but clinical experience is evolving with memantine. For this patient, the effect of this agent on behavioral symptoms and risperidone requirements is one example of such an antipsychotic-sparing effect. CONCLUSIONS: Response to memantine therapy may include behavioral improvements allowing a dose-sparing effect of antipsychotic medication. Changes in psychoactive drug burden may be a valuable surrogate marker of memantine's effects on behavior.
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9/12. Presenile dementia mimicking Pick's disease: an autopsy case of localized amygdala degeneration with character change and emotional disorder.

    This report concerns an autopsy case showing localized amygdala degeneration. The patient was a Japanese single woman without hereditary burden who was 58 years old at the time of death. At the age of 55 years, the patient began to feel anxiety, agitation and depressive in mood. At age 58 years, she developed marked character changes and emotional disorders, although disorientation and memory disturbance were slight. We suspected her disease was a variant of presenile dementia, especially Pick's disease, and some neuroradiological examinations disclosed bilateral temporal involvements. We could not make a definitive diagnosis from the clinical findings. She choked to death 3 years after the disease onset. From the neuropathological examinations, the known neurodegenerative diseases causing dementia, including Pick's disease, were excluded and we diagnosed our case as having localized amygdala degeneration. Localized amygdala degeneration itself is very rare. Moreover, in this case, the amygdala degeneration was presumed to be idiopathic, without any apparent cause. To our knowledge, this is the first case of idiopathic localized amygdala degeneration. This case indicates that localized amygdala degeneration can cause presenile dementia, and that character changes and emotional disorders are predominant over memory disturbance and/or disorientation.
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10/12. diagnosis of Alzheimer's disease in an exhumed decomposed brain after twenty months of burial in a deep grave.

    After 20 months of interment in a deep grave, the decomposed body of the 81-year old testator of a will was exhumed to sustain the burden of proof that he lacked testamentary capacity when the will was rewritten two days prior to his death. The brain was mushy and pulverized with complete disappearance of the brainstem, cerebellum and subcortical ganglia. Small foci of relatively intact dorsal frontal neocortex were identified. Sections from these foci were stained with hematoxylin and eosin, bielchowsky silver stain and immunostains for beta amyloid peptide (betaA4), tau and alpha-synuclein. Despite severe autolysis and decomposition, the bielchowsky stain and the betaA4 immunostains showed preserved frequent neuritic amyloid plaques with very few residual neurofibrillary tangles. cerebral amyloid angiopathy was present. At the present time this case represents the first documented and reported case of direct tissue diagnosis of Alzheimer's Disease pathology in a decomposed brain following long term burial in a deep grave.
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