Comorbid Neurodegeneration in Primary Progressive Aphasia: Clinicopathological Correlations in a Single-Center Study

Figure 4

Overview of neuropathological findings in our cases, original magnification 200×. Alzheimer’s disease in case 1 ((a and b) similar findings in cases 2–6 and 8–9). Immunohistochemical deposits of amyloid beta-peptide in the form of extracellular plaques of different types and deposits in vessel walls in the form of cerebral amyloid angiopathy in the cerebellum meet the criteria for degree “A3” (a). Immunostaining for hyperphosphorylated tau protein reveals depositions in the occipital cortex–grade VI in the Braak scoring system, which is an example of degree “B3” (b). Prominent Lewy body pathology in case 1 was immunohistochemically positive with antibodies against the pathological form of alpha-synuclein (clone 5G4) in the amygdala ((c) similar findings were seen in cases 2 and 9). Hyperphosphorylated tau protein immunohistochemical depositions (clone AT8) in mesencephalic structures were characteristic of PSP in case 3 ((d) similar findings in case 8). The same immunohistochemical method revealed characteristic globular oligodendroglial inclusions typical for GGT type I in the subcortical white matter in case 7 ((e) similar findings of different degrees in cases 3 and 8). Tau deposits are pathognomonic for ARTAG in the amygdala of case 8 ((f) similar findings in case 3). Hyperphosphorylated TDP-43 protein inclusions in the temporal cortex are characteristic of FTLD-TDP type A in case 5 (g). Hyperphosphorylated TDP-43 protein inclusions in the sclerotic hippocampal region in LATE, case 7 ((h) similar findings in cases 4 and 8).

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