One exception may be the case of systemic amyloidosis related to transthyretin mutations, which produce peripheral neuropathy and cerebral changes in the white matter in some cases [75] and hematogenic pattern of vascular deposition following systemic amyloidosis in areas of the brain that lack tight blood-brain barrier such as small circumventricular areas around the third and fourth ventricles, the infundibulum, and area postrema [76]. The gene discussed is TTR; the disease is primary systemic amyloidosis.