Of great interest is the fact that these cells are associated with amyloid plaques and they're able to prevent the formation or eliminate the presence of amyloid deposits in mice that develop the major hallmark of Alzheimer's Disease (AD).

AD is a neurodegenerative disorder that represents the most important cause of dementia in humans. Extracellular deposits of beta-amyloid peptides, often termed senile plaques, and formation of intracellular neurofibrillary tangles of hyperphosphorylated tau protein are the two principal marks of this disease.

A-beta aggregates are known to induce synaptic dysfunction and thus, are linked with learning and memory deficits both in human and in mouse models of AD, making A-beta deposits a target for prevention or treatment against this disorder.

"It's possible that stimulating the haematopoietic system may be a new therapeutic approach for the treatment of AD," says Serge Rivest. "In this regard, low macrophage colony-stimulating factor (M-CSF) levels were recently found in patients with presymptomatic AD or mild cognitive impairment, which together with low levels of other haematopoietic cytokines predicted the rapid development of the disease toward a dementia state two to six years later."

Exposure of mouse microglia to M-CSF in vitro enables the acidification of their lysosomes and subsequently, the degradation of internalized A-beta. Treatment of transgenic mice that spontaneously develop AD with M-CSF on a weekly basis prior to the appearance of learning and memory deficits prevented cognitive loss.

The treatment also increased the number of microglia in the parenchyma and greatly decreased Abeta levels in the brain. In addition, M-CSF treatment resulted in the stabilization of the cognitive decline state in transgenic mice that already had A-beta-mediated pathology.

The Canadian Institutes of Health Research supports this research.

Source: Centre Hospitalier de l'Universite Laval and the Society for Neuroscience