Ented with unstable gait and was prone to falls. At the PET scan, he was bedridden as well as the MMSE score was 1 of 30. An MRI showed diffuse brain atrophy prominent in the correct anterior temporal, hippocampus, amygdala, and caudate nuclei. He died of aspiration pneumonia 79 days after PET scan.[18F]THK5351 and [11C]PiB PET scansBrain MAO-B levels had been quantified making use of a human MAO-B ELISA kit (Ab157393, Abcam, Cambridge, UK) with MAO-B common (M7441, Sigma-Aldrich Corp.). Extraction of MAO-B was performed in accordance with the manufacturer’s guidelines. For the quantification ofFigure 1 shows the [18F]THK5351 PET photos in the two subjects. Photos from a cognitively regular individual are shown for comparison in the bottom (Fig. 1). Topic 1 showed important [18F]THK5351 retention within the globus pallidus and midbrain. Mild PSMA Protein N-6His tracer retention was observed also in the other cortices, includingIshiki et al. Acta Neuropathologica Communications (2018) six:Web page four ofSubject 1 (PSP-RS)Topic two (PNFA)Cognitively normalFig. 1 [18F]THK5351 PET images from two study subjects in addition to a cognitively typical subject. The scale indicates SUVR range from 0 toparahippocampal and inferior temporal gyri. Subject two showed prominent [18F]THK5351 retention in the parahippocampal and inferior temporal gyri, as well as the globus pallidus and midbrain. No exceptional retention of [11C]PiB was observed within the neo cortex in both in the subjects (data not shown).Neuropathological examinationBrain weight in topic 1 was 1580 g. Autopsy revealed serious atrophy inside the midbrain tegmetum and pons, and subthalamic nucleus, and fairly mild atrophy inside the frontal cortex, but not inside the basal ganglia. Neuropathological examination revealed tau pathology in neuronal and glial cells constant with PSP. Globose tangles had been observed inside the midbrain, pons, medulla, subthalamic nucleus, and nucleus basalis of Meynert. Moderate numbers of tufted astrocytes had been observed also within the amygdala, motor cortex, and superior frontal gyrus. Neurofibrillary tangles have been observed inside the entorhinal cortex and subiculum, which corresponded to age-related Braak stage II [1]. The tau immunoreactivity density appeared greatest within the medial temporal regions, followed by the basal ganglia and frontal cortex. Modest cerebral infarctions were observed in the putamen as well as the cerebellum. Gliosis and neuronal loss have been observed also in the substantia nigra. Nonetheless, amyloid-, -synuclein, and TDP-43 pathology were absent in this case. These characteristics were constant with all the diagnosis of definite PSP. Brain weight in topic 2 was 920 g. Autopsy revealed extreme atrophy in bilateral temporal lobes, which includes the hippocampus and amygdala. Brain atrophy wasobviously observed in the tegmentum on the midbrain and pons. There was neuronal loss in the pigmented neurons of the substantia nigra and locus coeruleus. Brain atrophy was observed also in the globus pallidus, hypothalamic nucleus, and cerebellar dentate nucleus. AT8 immunostaining revealed abundant tau burden, such as neurofibrillary tangles, globose tangles, tufted astrocytes, coiled bodies, and neuropil threads within the temporal, cingulate, frontal, striatum, globus pallidus, and subthalamic nucleus. Moreover, thorn-shaped astrocytes, typical in aging-related tau astrogliopathy, were observed in the temporal lobe gray and white matter [21]. Sparse amyloid plaques had been observed in the cerebral cortex (Thal phase for any plaques: 2, CERAD: Sparse).
