Amyloid beta monomers are soluble and contain short regions of beta sheet and polyproline II helix secondary structures in solution, though they are largely alpha helical in membranes; however, at sufficiently high concentration, they undergo a dramatic conformational change to form a beta sheet-rich tertiary structure that aggregates to form amyloid fibrils. These fibrils  deposit outside neurons in dense formations known as senile plaques or neuritic plaques, in less dense aggregates as diffuseplaques, and sometimes in the walls of small blood vessels in the brain in a process called cerebral amyloid angiopathy.
Amyloid beta monomers are soluble and contain short regions of beta sheet and polyproline II helix secondary structures in solution, though they are largely alpha helical in membranes; however, at sufficiently high concentration, they undergo a dramatic conformational change to form a beta sheet-rich tertiary structure that aggregates to form amyloid fibrils. These fibrils and oligomeric forms of Aβ deposit outside neurons in formations known as senile plaques . There are different types of plaques, including the diffuse, compact, cored or neuritic plaque types, as well as Aβ deposits in the walls of small blood vessel walls in the brain called cerebral amyloid angiopathy.
A
and oligomeric forms of Aβ
D
dense
R
or neuritic plaques, in less dense aggregates as diffuseplaques, and sometimes
. There are different types of plaques, including the diffuse, compact, cored or neuritic plaque types, as well as Aβ deposits
R
vessels
vessel walls
D
in a process