Blocking New Blood Vessel Formation Cures Alzheimer's Disease in Mouse Model

Vaccination of mice with a syndrome that mimics human Alzheimer's disease (AD) with amyloid-beta protein normalized the production of bloods vessels in the brains of the animals and eliminated the accumulation of amyloid plaque.

Investigators at the University of British Columbia (Vancouver, Canada) worked with the Tg2576 mouse AD model. In addition to the characteristic amyloid-beta (A-beta) plaques that characterize the brain in AD, these animals displayed an abnormal number of brain blood vessels. Some of these blood vessels were incomplete and caused leakiness in the blood-brain barrier (BBB).

The investigators immunized a group of Tg2576 mice with peptides derived from the amyloid-beta protein. They reported in the February 28, 2013, online edition of the journal Scientific Reports that immunization with A-beta peptides neutralized the amyloid trigger leading to formation of new blood vessels and reversed the abnormal number of these vessels in the Tg2576 AD mice. Reduction in number of blood vessels resolved the animals' plaque burden, suggesting that formation of new blood vessels (neoangiogenesis) was a key mechanism underlying plaque formation.

“The discovery provides further evidence of the role that an overabundance of brain blood vessels plays in AD, as well as the potential efficacy of amyloid-beta as basis for an AD vaccine,” said senior author Dr.Wilfred Jefferies, professor of medical genetics at the University of British Columbia. “Now that we know blood vessel growth is a factor in AD, if follows that drugs targeting blood vessels may be good candidates as an AD treatment.”

Related Links:
University of British Columbia