Introduction Type 2 diabetes (T2D) is increasingly recognised as being a risk factor for Parkinson’s disease (PD). One proposed mechanism is an interaction between amylin, a highly amyloidogenic pancre- atic hormone, and α-synuclein. Amylin accelerates α-synuclein aggregation in vitro and interacts with α-synuclein in the locus coeruleus, and neuronal, extracellular and vessel-associated amylin deposits have been reported in Alzheimer’s disease and control brains. However, the molecular link between amylin and PD and the role of T2D remains unclear.

Methods The burden of amylin accumulation in post mortem anterior cingulate and frontal gyrus tissue from PD and non-neurodegenerative control cases, with and without T2D, was investigated using immu- nohistochemistry and western immunoblotting.

Results Immunohistochemistry revealed very infrequent amylin labelling of senile plaques and neurofibril- lary tangles along with rare perivascular amylin deposits in PD and control brains, irrespective of T2D status. Although western immunoblotting revealed significantly increased amylin levels in PD cases compared to controls, there was no difference between diabetic and non-diabetic cases.

Conclusion Our results do not support the hypothesis that brain amylin accumulation is increased by T2D. Higher amylin levels in PD may result from blood-brain barrier dysfunction but further studies are needed to clarify the relevance to PD pathogenesis.