Alzheimer morphology is not increased in dialysis-associated encephalopathy and long-term hemodialysis
Autor: | Vera H. Koch, A. P. Harrison, B. Lindner, H. J. Friedrich, E. Reusche |
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Rok vydání: | 2001 |
Předmět: |
Adult
Male Aging Silver Staining Pathology medicine.medical_specialty medicine.medical_treatment Encephalopathy tau Proteins Autopsy Pathology and Forensic Medicine Diagnosis Differential Silver stain Amyloid beta-Protein Precursor Cellular and Molecular Neuroscience Degenerative disease Alzheimer Disease Renal Dialysis medicine Humans Aluminum Compounds Dialysis Aged Neurons business.industry Brain Neurofibrillary Tangles Middle Aged medicine.disease Nerve Degeneration Female Neurotoxicity Syndromes Choroid plexus Neurology (clinical) Hemodialysis Alzheimer's disease business |
Zdroj: | Acta Neuropathologica. 101:211-216 |
ISSN: | 1432-0533 0001-6322 |
Popis: | This study examines the role of aluminium in the etiology of Alzheimer's disease (AD). Brains taken at autopsy (n = 50) from patients with a history of long-term hemodialysis (HD) and intake of aluminium (Al)-containing drugs were examined by light microscopy. Using our modified silver stain we have been able to demonstrate and clearly discriminate between AD changes and dialysis-associated encephalopathy (DAE) on paraffin sections; evaluation was done with a 3-point scale. DAE morphology is characterized by lysosome-derived intracytoplasmic, Al-containing, pathognomonic, argyrophilic inclusions in choroid plexus epithelia, cortical glia and neurons. A statistically significant difference was found between the amounts of drug-related Al ingested and the degree of DAE-related morphological change (P0.001). On the other hand no apparent microscopical increase in AD morphology was found. No AD changes were seen whatsoever in patients under the age of 60, despite a history of long-term HD with ingestion of "pure" Al up to 2.5 kg. Patients over 60 years of age occasionally presented with sparse deposits of beta A4 amyloid (beta A4) and/or a low incidence of AD-type neurofibrillary tangles (NFT). In accordance with CERAD criteria these were identified as normal, age-related phenomena (P0.001 for beta A4; P0.001 for NFT). Rare, isolated cases from a group of 127 long-term hemodialyzed patients have been reported previously, who presented with intermingled, clearly distinguishable lesions of both age-related AD morphology and DAE changes. Comparison of AD morphology with an age-matched control group was not statistically significant (P0.6 for beta A4, P0.7 for NFT). In our experience, Al does not cause an increase in AD morphology, at least not in terms of bioavailable Al in drugs or as a result of long-term HD. |
Databáze: | OpenAIRE |
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