Subfield- and layer-specific changes in parvalbumin, calretinin and calbindin-D28k immunoreactivity in the entorhinal cortex in Alzheimer's disease
Section snippets
Subjects and diagnosis of Alzheimer's disease
A total of 20 brains (14 from AD patients and six from control subjects) were used for the histological analyses. Age, sex, AD duration, mini-mental status (MMS), cause of death and post mortem delay are shown for each subject in Table 1, along with histopathological diagnoses using CERAD (the Consortium to Establish a Registry for Alzheimer's disease) criteria.44 The study was approved by the local Ethics Committee and all autopsies were performed at Kuopio University Hospital.
All AD patients
Histological analyses
The cytoarchitectonic characteristics of the eight entorhinal subfields have been previously described in detail on Thionin-stained sections by Insausti et al.33 In addition to the Thionin staining, we used the Bielschowsky stain to compare the extent of entorhinal degeneration between age-matched controls and AD cases. In only two of the control cases, occasional NFTs were observed in layer II of the lateral rostral (ELr), intermediate (EI), lateral caudal (ELc), caudal (EC) and caudal
Discussion
This is the first study to characterize in detail the AD pathology that occurs in the eight entorhinal subfields. Using two histological and three immunohistochemical stainings, we show that neurons in the entorhinal cortex are differentially vulnerable in AD in a subfield-, layer- and cell-specific manner.
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