Abstract

Introduction and Purpose: Cerebral amyloid angiopathy (CAA) can be observed in patients with progressive supranuclear palsy (PSP), though to a lesser degree than in Alzheimer’s disease. The present post-mortem 7.0-tesla magnetic resonance imaging (MRI) evaluates whether CAA has an influence on the degree of hippocampal atrophy (HA) and on the incidence of associated micro-infarcts (HMIs) and cortical micro-bleeds (HMBs). Material and Methods: Eight brains with PSP-CAA were compared to 20 PSP brains without CAA. In addition to the neuropathological examination, the hippocampus was evaluated on the most representative coronal section with T2 and T2*-weighted MRI sequences. The average degree of HA was determined in both groups. The incidence of HMIs and HMBs was also compared as well as the frequency of cortical micro-infarcts (CoMIs) and cortical micro-bleeds (CoMBs) in the hemispheric neocortex. Results: The neuropathological examination showed a higher incidence of lacunar infarcts in the PSP-CAA brains compared to the PSP ones. With magnetic resonance imaging (MRI), the severity of HA and the incidence of HMIs and HMBs was similar between both groups. Additionally, the frequency of CoMIs and CoMBs in the neocortex was comparable. Conclusions: The association of CAA in PSP brains has no influence on the degree of HA and on the incidence of the small cerebrovascular lesions in the hippocampus as well as in the neocortex.

Highlights

  • Introduction and PurposeCerebral amyloid angiopathy (CAA) can be observed in patients with progressive supranuclear palsy (PSP), though to a lesser degree than in Alzheimer’s disease.The present post-mortem 7.0-tesla magnetic resonance imaging (MRI) evaluates whether CAA has an influence on the degree of hippocampal atrophy (HA) and on the incidence of associated micro-infarcts (HMIs) and cortical micro-bleeds (HMBs)

  • TDP-43 pathology can be observed in PSP, some other studies suggest a lack of TDP-43 pathology [3]

  • There was no difference between the average age at death of the PSP brains with and without

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Summary

Introduction

Progressive supranuclear palsy (PSP) is a sporadic disorder with tau pathology [1]. The isoforms of four-repeat tau due to splicing of exon 10 define the tau filantous aggregates [2]. There are only a few studies concerning the hippocampal involvement in the pathology of PSP. In one study with magnetic resonance imaging (MRI), bilateral atrophy of both hippocampi together with the severe involvement of the thalami, the pallidum, and the brainstem is described [4]. Cerebral amyloid angiopathy (CAA) is absent in the normal aging brain [6]. Hippocampal atrophy (HA) in PSP is much less severe than in Alzheimer’s disease and frontotemporal lobar degeneration [8]. The present post-mortem 7.0-tesla MRI study investigates whether the presence of CAA in PSP brains influences the degree of HA and the incidence of hippocampal micro-infarcts (HMIs) and hippocampal micro-bleeds (HMBs). The frequency of cortical micro-infarcts (CoMIs) and cortical micro-bleeds (CoMBs) in the cerebral neocortex is compared between PSP-CAA and PSP brains

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