Pathological axonal enlargement in connection with amyloidosis, lysosome destabilization and hemorrhage is a major defect in Alzheimer’s disease

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Abstract Alzheimer’s disease (AD) is a multi-amyloidosis disease with Aβ deposits in the cerebral blood vessels, microaneurysms and senile plaques. How Aβ amyloidosis affects axon pathology is not well-examined. We studied Aβ-related axonal phenotypes with histochemistry, immunohistochemistry and fluorescence imaging methods. Widespread axonal amyloidosis with distinctive axonal enlargement was observed in AD. Aβ-positive axon diameters in AD brains were 1.72 times of control brain axons by average. Axonal amyloidosis also associated with MAP2 reduction, Tau phosphorylation, lysosome destabilization and hemorrhagic markers such as ApoE, HBA, HbA1C and Hemin. Lysosome destabilization in AD was also clearly identified in the neural soma, associating with the co-expression of Aβ and Cathepsin D, HBA, ACTA2 and ColIV, implicating exogeneous hemorrhagic protein intake might influence neural lysosome stability. The data showed that Aβ-containing lysosomes were 2.23 times as large as the control lysosomes. Furthermore, under rare conditions, axon breakages were observed, which likely resulted in Wallerian degeneration. In summary, axonal enlargement associated with amyloidosis, chronic microhemorrhage and lysosome destabilization is a major defect in Alzheimer’s disease.

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