Researchers here demonstrate a much reduced progression of the signs of Alzheimer's disease in mice by altering immune signaling:
Alzheimer's disease is one of the most common causes of dementia. [The] accumulation of particular abnormal proteins, including amyloid-ß (Aβ) among others, in patients' brains plays a central role in this disease. [Researchers] were able to show that turning off particular cytokines (immune system signal transmitters) reduced the Alzheimer's typical amyloid-ß deposits in mice with the disease. As a result, the strongest effects were demonstrated after reducing amyloid-ß by approximately 65 percent, when the immune molecule p40 was affected, which is a component of the cytokines interleukin (IL)-12 and -23.
Follow-up experiments [showed] that substantial improvements in behavioral testing resulted when mice were given the antibody blocking the immune molecule p40. This effect was also achieved when the mice were already showing symptoms of the disease. Based on the current [study], the level of p40 molecules is higher in Alzheimer's patients' brain fluid, which is in agreement with a recently published [study] demonstrating increased p40 levels in blood plasma of subjects with Alzheimer's disease.
The significance of the immune system in Alzheimer's research is the focus of current efforts. [Researchers] suspect that cytokines IL-12 and IL-23 themselves are not causative in the pathology, and that the mechanism of the immune molecule p40 in Alzheimer's requires additional clarification.