Interaction between amyloid-β pathology and cortical functional columnar organization.
Amyloid-β plaques are one of the major neuropathological features in Alzheimer's disease (AD). Plaques are found in the extracellular space of telencephalic structures, and have been shown to disrupt neuronal connectivity. Since the disruption of connectivity may underlie a number of the symptoms of AD, understanding the distribution of plaques in the neuropil in relation to the connectivity pattern of the neuronal network is crucial. We measured the distribution and clustering patterns of plaques in the vibrissae-receptive primary sensory cortex (barrel cortex), in which the cortical columnar structure is anatomically demarcated by boundaries in Layer IV. We found that the plaques are not distributed randomly with respect to the barrel structures in Layer IV; rather, they are more concentrated in the septal areas than in the barrels. This difference was not preserved in the supragranular extensions of the functional columns. When comparing the degree of clustering of plaques between primary sensory cortices, we found that the degree of plaques clustering is significantly higher in somatosensory cortex than in visual cortex, and these differences are preserved in Layers II/III. The degree of areal discontinuity is therefore correlated with the patterns of neuropathological deposits. The discontinuous anatomical structure of this area allows us to make predictions about the functional effects of plaques on specific patterns of computational disruption in the AD brain.
Brain Research Center, Faculty of Life Sciences, Bar-Ilan University, Ramat Gan, 52900 Israel.
Shlomit
S
Beker
Vered
V
Kellner
Lucia
L
Kerti
Edward A
EA
Stern
D000367:Age Factors; D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000704:Analysis of Variance; D000818:Animals; D052160:Benzothiazoles; D001931:Brain Mapping; D004195:Disease Models, Animal; D003576:Electron Transport Complex IV / Q000378:metabolism; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D008959:Models, Neurological; D009154:Mutation / Q000235:genetics; D009434:Neural Pathways / Q000473:pathology*; D058225:Plaque, Amyloid / Q000378:metabolism*; D053764:Presenilin-1 / Q000235:genetics; D013003:Somatosensory Cortex / Q000378:metabolism* / Q000473:pathology*; D013844:Thiazoles
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D052160:Benzothiazoles; C508853:PSEN1 protein, human; D053764:Presenilin-1; D013844:Thiazoles; C009462:thioflavin T; D003576:Electron Transport Complex IV