Abstract
Aluminium is known to accumulate in neuropathological hallmarks. However, such has only tentatively been suggested in Biondi ring tangles. Owing to their intracellular and filamentous structure rich in β-pleated sheets, Biondi ring tangles might attract the adventitious binding of aluminium in regions of the blood-cerebrospinal fluid barrier. The study's objective was to establish whether aluminium co-localises with Biondi ring tangles in the brains of Parkinson's disease donors versus a donor that went on to develop late-onset epilepsy. Herein, we have performed immunohistochemistry for phosphorylated tau, complemented with aluminium-specific fluorescence microscopy in the choroid plexus of Parkinson's disease donors and in a donor that developed late-onset epilepsy. Aluminium co-localises with lipid-rich Biondi ring tangles in the choroid plexus. While Biondi ring tangles are not composed of phosphorylated tau, the latter is identified in nuclei of choroidal cells where aluminium and Biondi ring tangles are co-located. Although Biondi ring tangles are considered artefacts in imaging studies using positron emission tomography, their ability to bind aluminium and then release it upon their subsequent rupture and escape from choroidal cells may allow for a mechanism that may propagate for aluminium toxicity in vivo.