There are a number of publications that have reported on protein abnormalities in the setting of gadolinium (Gd) toxicity. Specifically amyloid production, light chain protein disease, with implications for the development of abnormal protein-related dementias (eg: Alzheimer's) and malignant disease such as Multiple Myeloma (MM).
What is the genesis for this abnormal protein production? I am certainly not an expert on protein production, so I am standing on somewhat shaky ground, but my opinion is that in part this may reflect how GBCAs are handled in vivo by the host. Injected GBCAs retained in the body generally appear in some combination of 3 forms: 1) the intact chelate (macrocyclics retain this form almost exclusively), 2) as Gd salts with carbonates and phosphates being common combining molecules, and 3) bound to macromolecules. These macromolecules are frequently proteins. The creation and recruiting of these macromolecules may form the basis for these protein abnormalities. It may be that in some hosts (here I am referring to a number of the GDD sufferers) this protein production intended to bind the foreign Gd atoms is either too exuberant or loses regulatory control. This excessive protein production may then result in production of undesirable proteins, such as amyloid or light chain. The long term results of excess abnormal protein production may result in multiple organ systems being clogged with proteins, such as renal tubules, and may also lead to protein-related dementias and malignancies.
Of the topics I have written on in GDD, this is the most conjectural in nature, and hence may only be part of the story, or may be incorrect.