Laminar distribution of neuron degeneration in posterior cingulate cortex in Alzheimer's disease

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Abstract
The laminar distribution of neuron losses in posterior cingulate cortex were evaluated in 25 clinically and neuropathologically diagnosed cases of dementia of the Alzheimer type (DAT). The layer of maximal neuron loss in area 23a for each DAT case was determined by comparison with mean neuron densities for each layer of 17 neurologically intact control cases. The DAT cases were separated into five classes: class 1, 12% of all DAT cases, no or less than 40% neuron loss in any layer; class 2, 24%, maximal neuron losses in layers II or III; class 3, 28%, losses mainly in layer IV; class 4, 12%, losses mainly in layers V or VI; class 5, 24%, severe losses in all layers. An analysis of large and small neurons showed that in class 2 there was an equal loss of both in layer IIIa−b, in class 3 mostly small neurons were lost in layer IV, in class 4 mostly large neurons were lost in layers III, IV and V, while in class 5 there was no selectivity. The age of disease onset and length of the disease were the same for all classes, although classes 4 and 5 tended to have an earlier onset. No measures of thioflavin S-stained neuritic plaque (NP) or neurofibrillary tangle (NFT) density discriminated among these classes. In 64% of all DAT cases there was a progressive shift in NFT from ventral area 30 where most were in layer II to areas 23a−b where there was a balance between those in superficial and deep layers to dorsal area 23c where most were in layers V and VI. There were four cases with massive numbers of NFT in area 23a (1802±477 versus 261±44 for all other cases). Since one of these cases was in each of classes 1, 2, 3 and 5, it is unlikely that this form of amyloid deposition is related to laminar specificities in neuron degeneration. Finally, neuron and NFT densities in the hippocampal formation were the same for each class. In conclusion, differential laminar changes in neuron density provide a basis for neuropathological subtyping of DAT which is more sensitive than measures of thioflavin S-stained NP and NFT densities either in neocortex or the hippocampus.