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Review
. 2019 May;53(3):159-163.
doi: 10.4132/jptm.2019.03.14. Epub 2019 Mar 19.

Primary Age-Related Tauopathy: An Elderly Brain Pathology Frequently Encountered during Autopsy

Affiliations
Review

Primary Age-Related Tauopathy: An Elderly Brain Pathology Frequently Encountered during Autopsy

Daru Kim et al. J Pathol Transl Med. 2019 May.

Abstract

Due to the progressive aging of Korean society and the introduction of brain banks to the Korean medical system, the possibility that pathologists will have access to healthy elderly brains has increased. The histopathological analysis of an elderly brain from a subject with relatively well-preserved cognition is quite different from that of a brain from a demented subject. Additionally, the histology of elderly brains differs from that of young brains. This brief review discusses primary age-related tauopathy; this term was coined to describe elderly brains with Alzheimer's diseasetype neurofibrillary tangles mainly confined to medial temporal structures, and no β-amyloid pathology.

Keywords: Amyloid beta-peptides; Autopsy; Cognition; Dementia; Tauopathies.

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Conflict of interest statement

Conflicts of Interest

The authors declare that they have no potential conflicts of interest.

Figures

Fig. 1.
Fig. 1.
Histopathological findings of primary age-related tauopathy (PART) in a 92-year-old woman (A, C, E, G) compared with those of high– Alzheimer’s disease (AD) neuropathologic change (ADNC) in an 82-year-old man (B, D, F, H). Tau immunohistochemistry analyses revealed marked tauopathy centered in the hippocampus and subiculum of the PART brain (A) and the extension of tauopathy into the temporal neocortex of the high-ADNC brain (B) (AT8 immunohistochemistry). At a higher magnification, the granule cells of the dentate gyrus (arrowheads) and the neurons of the CA4 subregion (arrows) exhibited tau involvement in the PART brain (C), as well as in the brain of the advanced AD case (D) (AT8 immunohistochemistry). Although the hippocampus in the PART brain did not reveal any β-amyloid (Aβ)–positive plaques (E, G) (Aβ immunohistochemistry), the high ADNC brain showed Aβ deposition in the temporal neocortex through the CA4 subregion (arrows) that corresponded to Thal Aβ phase 4 (F, H) (Aβ immunohistochemistry).

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