Figure 2
From: High Resolution Dissection of Reactive Glial Nets in Alzheimer’s Disease
Exposing macro- and microscopic AD pathology in post-mortem brain samples.
(a) Maximum projection of a vertical column of cortical tissue (5.1 mm X 0.468 mm and 40 μm thick) from an AD patient brain samples (female, 85 years old) and labeled with an AT8 antibody (Phospho-PHF-tau pSer202+Thr205) and Thiazine-red (TR) that reveal Aβ plaques, PHF and NFTs. (b,c) Individual maximum projections of image fields from panel (a). (d) Maximum projection showing a 4.6 mm2 (x: 2.35 mm, y: 1.95 mm) of temporal cortex from an AD sample (male, 87 years old) with a 30 μm imaging depth and labeled for Iba1 (microglia; magenta), GFAP (astrocytes; green) and Thiazine-Red (plaques, cyan). TR staining reveals the presence of subgroups of plaques/aggregates. The dense-core Aβ plaques (C, dashed white hexagons) are the most numerous while larger fibrillar amyloid plaques (F, dashed yellow squares) are found in older patients. PHF aggregates are also frequently observed (P, dashed orange triangles). Iba1+ cell clusters are detected around dense-core and fibrillar plaques but are absent around PHF aggregates. Coronas of reactive astrocytes are observed around the 3 types of plaques/aggregates. (e,f) General distribution of Iba1+ microglia in control and AD brain tissue (1 mm2). Topological density of Iba1-positive microglia before and after Voronoi segmentation, in which individual microglia territories are color-coded according to their surface area. The homogeneity of microglial cell distribution that we have measured in the healthy brain (left) is disrupted by the presence of plaques (right) in AD brain with individual microglial territories becoming smaller near plaques (darker areas) and larger in adjacent areas (lighter areas), suggest microglial cell aggregation near deposits and their depletion from adjacent areas. Scale bars: 200 µm (a) 20 µm (b,c).
