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June 14, 2006
Inositol compounds prevent Alzheimer's disease in mouse model
A report published online in the journal Nature Medicine on June 11, 2006 revealed that a type of sugar known as cyclohexanehexol or inositol prevents the accumulation of amyloid beta deposits in the brains of mice bred to develop them. Amyloid beta deposits aggregate into plaques in the brains of humans with Alzheimer's disease, causing inflammation and the death of neurons.
Researchers led by Peter St George-Hyslop at Toronto Western Hospital Research Institute gave epi-inositol or scyllo-inositol to mice with human genes that predispose them to Alzheimer's-type disease as well as to normal mice. Some of the animals received the compounds before the onset of the disease at six weeks of age and continued to receive them until 4 or 6 months of age. Other mice received one of the two compounds at the age of 5 months, when the disease was well established. Control groups of both strains received neither compound.
Administration of either compound to the transgenic mice at 5 weeks resulted in improved cognitive function compared to the untreated transgenic mice at 4 and 6 months. Additionally, mice who received the inositol compounds experienced a reduction in brain amyloid beta levels and pathology, less synaptic loss and inflammation, and lowered mortality. Scyllo-inositol was responsible for a larger and more sustained effect than epi-inositol, and worked when given before as well as after disease onset.
Dr St George-Hsylop noted that the forms of inositol used in the study were not the same as myo-inositol, which is available as a nutritional supplement.
“Alzheimer's disease is probably going to be treated by a ****tail of drugs,” he concluded. “Some of them might be this compound, or one like it, that blocks the toxicity and aggregation of amyloid.”
Inositol compounds prevent Alzheimer's disease in mouse model
A report published online in the journal Nature Medicine on June 11, 2006 revealed that a type of sugar known as cyclohexanehexol or inositol prevents the accumulation of amyloid beta deposits in the brains of mice bred to develop them. Amyloid beta deposits aggregate into plaques in the brains of humans with Alzheimer's disease, causing inflammation and the death of neurons.
Researchers led by Peter St George-Hyslop at Toronto Western Hospital Research Institute gave epi-inositol or scyllo-inositol to mice with human genes that predispose them to Alzheimer's-type disease as well as to normal mice. Some of the animals received the compounds before the onset of the disease at six weeks of age and continued to receive them until 4 or 6 months of age. Other mice received one of the two compounds at the age of 5 months, when the disease was well established. Control groups of both strains received neither compound.
Administration of either compound to the transgenic mice at 5 weeks resulted in improved cognitive function compared to the untreated transgenic mice at 4 and 6 months. Additionally, mice who received the inositol compounds experienced a reduction in brain amyloid beta levels and pathology, less synaptic loss and inflammation, and lowered mortality. Scyllo-inositol was responsible for a larger and more sustained effect than epi-inositol, and worked when given before as well as after disease onset.
Dr St George-Hsylop noted that the forms of inositol used in the study were not the same as myo-inositol, which is available as a nutritional supplement.
“Alzheimer's disease is probably going to be treated by a ****tail of drugs,” he concluded. “Some of them might be this compound, or one like it, that blocks the toxicity and aggregation of amyloid.”
