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Washington University Experience | NEURODEGENERATION | Alzheimer Disease | Gross Pathology | 10B Case 10 Denouement
Neuro Microscopic Description: Neuronal loss and gliosis are moderate. There are numerous diffuse beta amyloid plaques and a few cored plaques. Frequent neurofibrillary tangles and neuritic plaques are seen. No alpha-synuclein-positive inclusions (Lewy bodies, Lewy neurites or neuropil grains) are present. There are no TDP-43-immunoreactive neuronal cytoplasmic inclusions (NCIs) in the frontal lobe. There is only very modest cerebral amyloid angiopathy (CAA, defined here as immunoreactivity for amyloid beta peptide within vessel walls) and only very mild arteriolosclerosis. ---- Neuro Diagnosis Comment: There is neuropathological evidence of Alzheimer disease (AD). Frequent beta-amyloid plaques are seen in cortical and subcortical nuclei, and brainstem; they are sparse in the cerebellum. Neurofibrillary tangles and neuritic plaques are frequent in neocortical areas and medial temporal lobe structures. These changes fulfill the neuropathologic criteria for AD according to Khachaturian, CERAD, and NIA-Reagan Institute criteria. In the more recent National Institute on Aging-Alzheimer Association (NIA-AA) criteria, this case has neuropathological change consistent with AD (A3B3C3). Vascular pathology is also observed in this case. Arteriolosclerosis and CAA were generally mild and there were no infarcts. The parkinsonism may relate to the moderate to severe tauopathy in the midbrain but there was no significant loss of neurons from the substantia nigra. There was no evidence of any other neurodegenerative disease.