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Updated: Aug 11, 2026

Longitudinal In Vivo Imaging of the Cerebrovasculature: Relevance to CNS Diseases
Published on: December 6, 2016
Discontinuous distribution of senile plaques within striate cortex hypercolumns in Alzheimer's disease
1Department of Neurology, University of Miami, FL, USA. rkuljis@mednet.med.miami.edu
Abstract:
Tangential sections of the primary visual (striate) cerebral cortex from five patients with histopathologically verified Alzheimer's disease were used to study the laminar and tangential disposition of senile plaques. These lesions were visualized with thioflavin S or the modified Bielschowsky method, and classified into four different, purely morphological types: "classical", (predominantly) "neuritic", (primarily amyloid) "core" and "diffuse", which were charted and analyzed using computer-assisted three- and two-dimensional reconstruction and mapping methods. These analyses reveal a tendency for a selective laminar disposition of the lesions (preferentially in layers II/III and V) which is generally consistent with previous reports performed at lower resolution, yet the specific pattern is highly variable among patients, and among plaque subtypes within individual patients. In addition, we observed a clustering of senile plaques in the tangential domain (i.e. parallel to the pial surface) in layers II/III, that suggests a selective involvement of iterated circuits within the "units", "modules", or "hypercolumns" that some believe compose this region of the cortex. These findings also imply an intriguing relative sparing of immediately adjacent components of the modular circuitry of the cerebral cortex, in the same cytoarchitectonic layers. Taken together, these findings indicate that: (1) senile plaques may arise in functionally and anatomically distinct subsets of iterated neuronal circuits that cannot be reduced to schemes based on traditional cytoarchitectonic layers; and (2) that individual variability in the patterns of striate cortex involvement and clinical manifestations must be taken into consideration when addressing the specific mechanisms underlying visual dysfunction in Alzheimer's disease.
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