The deposition of amyloid beta (Abeta) protein is a neuropathological change that characterizes Alzheimer's disease. Animals with the osteopetrosis (op/op) mutation suffer from a general skeletal sclerosis, a significantly reduced number of macrophages and osteoclasts in various tissues, and have no systemic macrophage colony stimulating factor (M-CSF). This study examined the effect that M-CSF injections had on Abeta deposition and microglial cell distribution in the brains of normal and op/op mice. Abeta-positive plaques were detected in the cerebral cortex of op/op mice, but not in normal mice. M-CSF reduced the numbers of Abeta-positive plaques in op/op mice. The microglial cell population was reduced in op/op mice compared with normal mice, and M-CSF increased the numbers to 65.8% of that observed in normal mice. Our results suggest that a clearer understanding of the role that microglial cells play in Abeta deposition may help determine the mechanisms involved in the pathogenesis of Alzheimer's disease.

Amyloid beta-Peptides↗

PubMedDate not supplied

Calcium transport and release by the sarcoplasmic reticulum.

The slow rate of calcium transport by cardiac sarcoplasmic reticulum vesicles, compared to those prepared from skeletal muscle, is due mainly to a lesser density of transport sites and a lower Ca2+ affinity. Because the turnover rate of the cardiac sarcoplasmic reticulum calcium pump is similar to that of comparable skeletal muscle preparations, the cardiac sarcoplasmic reticulum seems able to effect the slower relaxation of the heart. Calcium permeability of skeletal sarcoplasmic reticulum vesicles is increased when the Ca2+ concentration outside the vesicles is increased, or when that inside the vesicle is decreased.

Adenosine Triphosphatases↗