The GRK2 Overexpression Is a Primary Hallmark of Mitochondrial Lesions during Early Alzheimer Disease
Figure 4
The subcellular features of the GRK2 immunoreactivity in the hippocampus of the rat subjected to 2-vessel occlusion. (a) Intact neurons show absence of any GRK2 immunopositive gold particles in their cytoplasmic matrix, X 15,000. (b) Neurons with the effect of chronic cellular hypoperfusion demonstrate the presence of a GRK2 overexpression (arrows) throughout the cell body, however, the intact mitochondria (M) were free from any GRK2 immunopositive gold particles, X 30,000. (c) “Hypoperfusion”-affected neuronal cell body show the presence of islands of GRK2 positive immunodecoration in the external membrane and in the matrix of damaged mitochondria and mitochondria-derived lysosomal structures (arrows), X 40,000. (d) Neurons with severe damage shows the presence of islands of GRK2 containing immunopositive gold particles that associated with the completely damaged (mitochondria-derived lysosomal structures) (arrows), but not with nondamaged mitochondria (intact and giant), X 40,000. (reprinted with permission of Neurotoxicity Research [8]).
