In FBD, a C-terminal 34 amino acid (aa) peptide of BRI2 accumulates as amyloid, leading to severe amyloid angiopathy of the brain and spinal cord with perivascular amyloid plaque formation, parenchymal plaques affecting the limbic areas, cerebellum, cerebral cortex, neurofibrillary tangles of hippocampal neurons and periventricular white matter changes [11]. This evidence concerns the gene ITM2B and ABri amyloidosis.