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Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: Contribution of rare homozygous and compound heterozygous VPS13C missense mutations to dementia with Lewy bodies and Parkinson’s disease

Fig. 4

Neuropathology of patient carriers P1 and P3. a Right hemisphere of patient P1 shows moderate frontotemporal atrophy, with the superior temporal gyrus more affected than the medial temporal gyrus. b Right hemisphere of patient P3 shows severe cortical atrophy, more pronounced in the frontal and temporal lobes. The pre- and post-central gyrus are relatively spared. c–e The lateral occipitotemporal gyrus of patient P1 shows (c) microspongiotic changes in the cortex (Hematoxylin–Eosin stain), (d) a relatively mild load of neurofibrillary tangles (arrow) and neuritic threads (arrowhead) (AT8 stain), and (e) severe α-synuclein pathology with Lewy bodies (arrow) and Lewy neurites (arrow head). f–h The frontal cortex of patient P3 shows (f) severe microspongiosis and neuronal loss (Hematoxylin–Eosin stain), (g) the abundance of hyperphosphorylated tau pathology with many neurofibrillary tangles (arrow) and neuritic threads (arrowhead) (AT8 stain), and (h) severe β-amyloid pathology with many classic (arrow) and diffuse senile plaques (4G8 stain). i–k α-synuclein pathology of patient P1 in (i) the frontal cortex, (j) the hippocampus (severe) and (k) the amygdala (severe). l–n α-synuclein pathology of patient P3 in (l) the frontal cortex, (m) the hippocampus (moderate) and (n) the amygdala (severe). Lewy bodies are marked with arrows, Lewy neurites with arrowheads

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