Article Figures & Data
Figures
- Figure 1.
Western blots of CB1 (lanes 1, 2), FAAH (lanes 3, 4), and CB2 (lanes 5, 6) immunoreactivities in human temporal cortex from an AD patient. Single bands of ∼50 kDa (CB1 and FAAH) or 60 kDa (CB2) were observed (lanes 1, 3, and 5, respectively). No immunoreactivities were detected when the primary antibodies were preincubated with the respective immunizing peptides (lanes 2, 4, and 6).
- Figure 2.
A-F, FAAH (A-C, E) and GFAP (D) immunoreactivities in parahippocampal cortex and FAAH activity in neuritic plaques (F). A, FAAH staining in a healthy individual sample. Note the neuronal pattern of staining (inset). B, Low and high (inset) magnifications of FAAH immunoreactivity in parahippocampal cortex of an AD case. Note the intense signal for FAAH in hypertrophied astrocytes surrounding neuritic plaques. C, Detail of FAAH immunoreactivity in hypertrophied astrocytes. D, Low and high (inset) magnification of GFAP immunoreactivity in an AD case. Note that the signal is detectable in both protoplasmic and fibrous (arrow) astrocytes. E, FAAH staining after preabsorption and coincubation of the antibody with the immunizing peptide. Note the absence of any detectable signal. F, FAAH activity. Individual plaques were dissected under microscope, homogenized, and assayed for FAAH activity using the conversion of [14C]AEA to [14C]ethanolamine during a 15 min incubation. Shown is the mean of five individual determinations; groups were significantly different using unpaired t tests with p < 0.05. Scale bars: A, B, D, 800 μm; E, inset in A, 400 μm; insets in B and D, 200 μm; C, 100 μm.
- Figure 3.
CB2 (A-C, E) and CD68 (D) stainings in parahippocampal cortex. A, CB2 staining in a healthy individual sample. No detectable signal could be seen. B, Low and high (inset) magnifications of CB2 immunoreactivity in parahippocampal cortex of an AD case. Note the intense signal for CB2 in microglial cells located on neuritic plaques. C, Detail of CB2 immunoreactivity in neuritic plaque-associated microglia. D, Low and high (inset) magnification of CD68 immunoreactivity in an AD case. E, CB2 staining after preabsorption and coincubation of the antibody with the immunizing peptide. Note the absence of any detectable signal. Scale bars: A, B, D, E, 800 μm; insets in B and D, 200 μm; C, 100 μm.
- Figure 4.
FAAH and CB2 are expressed in glial cells associated with β-amyloid-enriched neuritic plaques. A, B, FAAH (brown) and β-amyloid peptide (blue) stainings. Note that FAAH-positive cells are astrocytes surrounding β-amyloid-enriched plaques. C, D, CB2 (brown) and β-amyloid peptide (blue) stainings. CB2 immunostaining is limited to plaque-associated microglial cells.
- Figure 5.
CB1 staining in parahippocampal cortex. A, CB1 staining in a healthy individual sample. Pyramidal cortical cells showed moderate to intense staining level (inset). B, Low and high (inset) magnifications of CB1 immunoreactivity in parahippocampal cortex of an AD case. Note the general lower intensity of the signal for CB1 and how the neuritic plaques can be observed easily (arrows). C, Detail of CB1 immunoreactivity, showing no changes in the vicinity of neuritic plaques (arrows). D, CB1 staining after preabsorption and coincubation of the antibody with the immunizing peptide. Note the absence of any detectable signal. Scale bars: A, B, D, 800 μm; inset in B, 400 μm; inset in A, 200 μm; C, 100 μm.
