Researchers from Sweden may have uncovered a link between Alzheimer’s and type 2 diabetes through research on amyloidosis, backing up research that claims patients with type 2 diabetes have a near two-fold greater risk of developing Alzheimer’s disease.
The formation of fibril deposits occurs in both Alzheimer’s and type 2 diabetes (T2D). However, new research suggests that amyloid formation in the brain may stimulate the growth of fibrils in the murine pancreas. Additionally, pancreatic-related amyloid can be found along human brain senile plaques.
Focusing on how amyloid deposits spread within a tissue or from organ to organ, researchers injected transgenic mice that expressed human islet amyloid polypeptide (IAPP) with preformed fibrils of synthetic IAPP, proIAPP, or beta-amyloid. After 10 months, the number of islets with amyloid was significantly higher compared to controls of all three types of fibrils. Additionally, the amyloid consisted of IAPP across all groups, and no amyloid deposits were found in the spleen, kidney, liver, heart, or lungs.
Researchers then analyzed human tissue from the pancreas and brain, and found that sections of pancreas with islet amyloid in patients with T2D had no beta-amyloid immunoreactivity, while all samples were immunoreactive for IAPP. Researchers also analyzed samples of the temporal cortex from patients with Alzheimer’s and compared them to patients with frontotemporal dementia, progressive supranuclear palsy, or no neurologic disease. IAPP reactivity was found in all samples, and those from Alzheimer’s patients had 1.4 times higher concentrations of IAPP than non-Alzheimer’s patients.
While researchers aren’t yet clear on how or if IAPP is produced or derived from pancreatic beta-cells, cross-seeding by amyloid aggregates may be a possible mechanism for the initiation of amyloid formation.
The pathological process amyloidosis, in which misfolded proteins (amyloids) form insoluble fibril deposits, occurs in many diseases, including Alzheimer’s disease and type 2 diabetes mellitus (T2D). However, little is known about whether different forms of amyloid proteins interact or how amyloid formation begins in vivo.
A study published in The American Journal of Pathology has found evidence that amyloid from the brain can stimulate the growth of fibrils in the murine pancreas and pancreatic-related amyloid can be found along with brain-related amyloid in human brain senile plaques.