Accumulation of Exogenous Amyloid-Beta Peptide in Hippocampal Mitochondria Causes Their Dysfunction: A Protective Role for Melatonin
Figure 1
Aβ-induced axonal damage. Following the intracerebral injection of fAβ into the hippocampus, small blocks of tissue brain containing the lesion area were postfixed in osmium tetroxide 2%, embedded for 48 hours in Embed 812, cut into 70–90 nm ultrathin sections, and then subjected to immunohistochemical procedures using an anti-Aβ antibody. Binding sites of the primary antibody were then revealed by incubating with a gold-labeled secondary antibody. Finally, sections were counterstained with uranyl acetate and lead citrate and observed in an electron microscope. (a) Amyloid tangles within the concentric layers of myelin sheath of axons (white arrows) and a widening of the myelin sheath, corresponding to accumulations of Aβ from a primary pole, are observed. Electrodense spots sparse within the axon (black arrowheads), also seem to enter into the lumen from the primary pole (white arrowhead) (16,700x). (b) Aβ electrodense spots penetrating into the axons from widening onion bulb-like structures (white arrows) (10,000x). (c) Onion bulb detail (35,750x) showing abundant electrodense material corresponding to gold revealed Aβ (white arrow) and the detachment zone (black arrow). Amyloid tangles seem to be granulated once crossing the myelin sheath (black arrowheads). (d) Myelin sheath as observed in PBS-injected rat brain (magnification at 2156x).
