Could Aβ from the blood contribute to Alzheimer’s disease? It is believed that Aβ deposited in the brain originates from the brain tissue itself. However, Aβ is generated in both brain and peripheral tissues. Whether circulating Aβ contributes to brain AD-type pathologies remains largely unknown.
In a study led by Yan-Jiang Wang at Daping Hospital, Third Military Medical University in Chongqing, China, and Weihong Song at the University of British Columbia, Vancouver, Canada, researchers used a model of parabiosis between transgenic AD mice and their wild-type littermates. The reseachers found that the human Aβ originated from transgenic AD model mice entered the circulation and accumulated in the brains of wild-type mice, and formed cerebral amyloid angiopathy and Aβ plaques after a 12-month period of parabiosis. The finding implies that peripheral Aβ might contribute to the development of Alzheimer’s.
The researchers surgically joined AD model mice to wild-type mice such that the animals shared a blood supply, a technique known as parabiosis. Over several months, circulating human Aβ42 entered the brains of the wild-types. It accumulated there and formed plaques, though it did not appear to seed deposits with endogenous mouse Aβ. Plaque deposition in turn kicked off tau phosphorylation, inflammation, and degeneration. “This suggests that periphery-derived Aβ would be an important target for the prevention and treatment of AD. Alzheimer’s might be a whole-body disease,” according to Wang and Song.
- Wild-type mice shared a blood supply with AD mice for several months.
- The wild-types developed amyloid plaques and other signs of AD.
- This suggests peripheral Aβ could contribute to Alzheimer’s
Source: Alzforum | 11 November 2017