Publications by authors named "William G Ellis"

Background And Purpose: Some studies have reported associations between intracranial atherosclerosis and Alzheimer disease pathology. We aimed to correlate severity of cerebral atherosclerosis, arteriolosclerosis, and cerebral amyloid angiopathy with neurofibrillary tangles, neuritic plaques, and cerebral infarcts.

Methods: This autopsy study (n=163) was drawn from a longitudinal study of subcortical ischemic vascular disease, Alzheimer disease, and normal aging.

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Hippocampal sclerosis (HS) is a common and often asymmetric neuropathological finding among elderly persons who experience progressive memory loss, but its cause is unknown and it is rarely diagnosed during life. In order to improve both understanding and diagnosis of late-life HS, bilateral hippocampi and cerebral hemispheres were reviewed in 130 consecutive autopsy cases drawn from a longitudinal study of subjects with subcortical ischemic vascular dementia (IVD), Alzheimer disease (AD) and normal aging. HS was found in 31 of 130 cases (24.

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Objective: To investigate loss of neurons in the nucleus basalis (NB) of Meynert in patients with subcortical ischemic vascular disease (SIVD) compared with healthy controls, patients with Alzheimer disease (AD), and patients with mixed AD and SIVD.

Design: Autopsied cases drawn from a longitudinal observational study of patients with SIVD, patients with AD, and healthy controls.

Setting: Multi center, university-affiliated, program project neuropathology core.

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Article Synopsis
  • The Alzheimer Disease Genetics Consortium (ADGC) conducted a thorough genome-wide association study on late-onset Alzheimer's disease, featuring a three-stage design that included both discovery and replication phases.
  • The study identified significant genetic associations with several genes, notably MS4A4A, CD2AP, EPHA1, and CD33, showing strong statistical significance across all stages.
  • Additionally, the research confirmed previous associations with other genes like CR1, CLU, BIN1, and PICALM as being linked to Alzheimer's susceptibility, while finding no association with the gene EXOC3L2.
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Merkel cell carcinoma (MCC) is a rare cutaneous neuroendocrine neoplasm of possible viral origin and is known for its aggressive behavior. The incidence of MCC has increased in the last 15 years. Merkel cell carcinoma has the potential to metastasize, but rarely involves the central nervous system.

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Article Synopsis
  • Frontotemporal lobar degeneration (FTLD) is a leading cause of early-onset dementia, with FTLD-TDP being the most common type linked to TDP-43 protein inclusions.
  • Researchers conducted a genome-wide association study with 515 FTLD-TDP patients and identified significant genetic links on chromosome 7p21, particularly related to the TMEM106B gene.
  • Variants in TMEM106B may increase the risk of developing FTLD-TDP, especially in those with GRN mutations, indicating a potential genetic mechanism for this form of dementia.*
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Background: Neurofibrillary tangles and beta-amyloid plaques have been observed in the amygdala in Alzheimer disease. A disproportionate abundance of this abnormality in the amygdala may cause behavioral symptoms similar to Klüver-Bucy syndrome.

Objectives: To describe an atypical behavioral presentation of Alzheimer disease and to review the literature on the subject.

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Objective: Magnetic resonance (MR) imaging is used widely for assessment of patients with cognitive impairment, but the pathological correlates are unclear, especially when multiple pathologies are present.

Methods: This report includes 93 subjects from a longitudinally followed cohort recruited for the study of Alzheimer's disease (AD) and subcortical cerebrovascular disease (CVD). MR images were analyzed to quantify cortical gray matter volume, hippocampal volume, white matter hyperintensities, and lacunes.

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Objective: To assess the interactions among three types of pathology (ie, cerebrovascular disease, hippocampal sclerosis [HS], and Alzheimer's disease [AD]), cognitive status, and apolipoprotein E genotype.

Methods: We report clinicopathological correlations from 79 autopsy cases derived from a prospective longitudinal study of subcortical ischemic vascular disease and AD.

Results: Thirty percent of the cases had significant cerebrovascular parenchymal pathology scores (CVDPS), 54% had significant AD pathology, and 18% had HS.

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The cornu ammonis 1 region of the hippocampus (CA1) sector of hippocampus is vulnerable to both Alzheimer's disease (AD)-type neurofibrillary degeneration and anoxia-ischemia. The objective of this article is to compare number and size of neurons in CA1 in AD versus ischemic vascular dementia. Unbiased stereological methods were used to estimate the number and volume of neurons in 28 autopsy-derived brain samples.

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A case of symptomatic Rathke's cleft cyst and growth hormone (GH) secreting pituitary adenoma is described. A patient presented with a visual field deficit and a brain magnetic resonance imaging (MRI) study demonstrated compression of the optic chiasm by a large suprasellar cyst and a small lesion in the sellar consistent with a microadenoma. Preoperative clinical evaluation revealed mild acromegalic features, glucose intolerance, hypertension, hypercholesterolemia, and carpel tunnel syndrome, and blood testing confirmed an elevated insulin-like growth factor-1 (IGF-1).

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Our previous studies found that experimental infection of BALB/c mice with the Gram-positive bacterium Nocardia asteroides induced a parkinsonian-type syndrome with levodopa-responsive movement abnormalities, loss of nigrostriatal dopaminergic neurons, depletion of striatal dopamine, and intraneuronal inclusions in the substantia nigra (SN) with an appearance similar to Lewy bodies. In the present study, an in situ hybridization technique was developed to detect nocardial 16S ribosomal RNA (rRNA), using a Nocardia-specific probe (B77). Cerebral cortical specimens from cynomolgus monkeys were examined for the presence of nocardial RNA 48 h, 3.

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Infection with the human immunodeficiency virus (HIV) is often associated with the acquired immunodeficiency syndrome (AIDS), and wasting is one of the defining clinical features of AIDS. Muscular weakness due to myopathy may develop at any stage of HIV infection. We report two illustrative cases of HIV-associated myopathies.

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