Journal
NEURODEGENERATIVE DISEASES
Volume 16, Issue 5-6, Pages 398-406Publisher
KARGER
DOI: 10.1159/000446283
Keywords
A beta oligomers; Alzheimer's disease; Amyloid plaques; Cerebellum; Cerebral cortex; Neuropathology; Synaptic loss; Tangles; Temporal cortex
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Background/Aims: Investigations of A beta oligomers in neuropathologically confirmed Alzheimer's disease (AD) are still scarce. We report neurohistopathological and biochemical analyses using antibodies against tau and amyloid beta (A beta) pathology. Methods: Thirty elderly AD patients and 43 age matched controls with or without deposition of amyloid plaques (AP) were analyzed by immunohistochemistry. In 21 cases with available fresh tissue, Western blots were also performed. Neuropathological analysis included quantitative assessment of neurofibrillary tangles (NFT), AP and A beta oligomer densities in the mesial temporal cortex (TC). Results: NFT, fibrillar amyloid and A beta oligomeric deposit densities were significantly higher in AD patients than in controls. There was no relationship between oligomeric A beta densities and Braak NFT staging scores. Furthermore, A beta oligomer expression was closely correlated with A beta plaques in the TC. By Western blot, A beta oligomers were observed in AD patients, in plaque-free controls, in 1 'tangle-only AD' case, as well as in the cerebellum. A band near 55 kDa was the only Western blot signal that was significantly increased in the TC of AD patients compared to controls as well as less expressed in the cerebellum. Conclusion: These results suggest that a putative dodecamer, near 55 kDa, may contribute to AD vulnerability of the TC. (C) 2016 S. Karger AG, Basel
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