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Washington University Experience | NEURODEGENERATION | Alzheimer Disease | Gross Pathology | 2B Case 2 Denouement
Microscopic Appearance (not shown): Neuronal loss and gliosis are severe in most areas with frequent diffuse and neuritic beta amyloid plaques accompanied by numerous pTau immunoreactive neurofibrillary tangles, pre-tangles (diffusely immunoreactive neurons) and neuritic plaques. No alpha-synuclein-positive inclusions (Lewy bodies, Lewy neurites and neuropil grains) are seen. No Pick bodies are present. There are no TDP-43-immunoreactive neuronal cytoplasmic inclusions (NCIs) in the frontal lobe. There is mild cerebral amyloid angiopathy (CAA, defined here as immunoreactivity for amyloid beta peptide within vessel walls). There is extensive white matter pallor, axon loss, and enlarged perivascular spaces consistent with subcortical arteriosclerotic leukoencephalopathy (SAL). Comment: There is neuropathological evidence of Alzheimer disease (AD). Frequent beta-amyloid plaques and numerous neuritic plaques and frequent neurofibrillary tangles are present which indicate the presence of AD by Khachaturian, CERAD, NIA-Reagan Institute criteria and National Institute on Aging- Alzheimer Association (NIA-AA, A3,B3,C3) criteria. This case also displayed alpha-synuclein-positive inclusions in the form of Lewy bodies and Lewy neurites only in the olfactory cortex and amygdala. The neocortex and brainstem were unaffected; so the two Lewy body entities, Parkinson's disease and dementia with Lewy bodies and other Lewy body diseases, are excluded. In the staging of Lewy body pathology in Parkinson’s disease according to Braak et al., this case is consistent with the earliest pathological change of Lewy body disease and may be ranked stage 1. There was no evidence of any other neurodegenerative disease. Changes in the white matter including extensive myelin pallor, gliosis, and focal calcification of blood vessel walls were evident. The most severe white matter changes are associated with those areas of overlying cortex most affected by Alzheimer-type changes. The white matter lesions are quite pronounced and are likely to have contributed to the cognitive symptoms. In conclusion, the cognitive deficits experienced during life may be explained largely by Alzheimer disease compounded by changes in the white matter.
