The Abnormally Phosphorylated Tau Lesion of Early Alzheimer’s Disease

摘要

The perirhinal cortex (area 35) is well-known locus for neurofibrillary tangles (NFT) in initial Alzheimer’s disease (AD) and fully developed AD and may contain tau alterations in non-demented elderly. The topography and location of this vulnerable cortex, however, is difficult to appreciate because of its variable architecture and to deviations imposed by temporal sulcal patterns. We have immunostained human brains with a short duration of dementia using antibody AT8, which recognize abnormally hyperphosphorylated tau, calcium binding protein-parvalbumin and other phenotype markers to more fully appreciate the extent of area 35 before it is obscured by pathology. We have observed in the mildly affected AD tau immunoreactive lesion that extends from the temporopolar/insular region anteriorly to the posterior parahippocampal cortex. In its anterior–posterior course, it covers the medial bank of the collateral sulcus. Although the tau lesion encroaches slightly into the temporopolar cortex (area TG) anteriorly and medially and the ectorhinal cortex (area 36) laterally, area 35 is unambiguously defined. Ventromedial temporal pathology as revealed by AT8 suggests the presence of a relatively large lesion early in AD involving all of the perirhinal cortex and other non-isocortical areas. The present study demonstrated that the early stage AD patients exhibited AT8 immunoreactive cells in the temporopolar, hippocampus, perirhinal, entorhinal, and insular cortices.