{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,13]],"date-time":"2026-08-13T19:35:38Z","timestamp":1786649738146,"version":"build-2736575974"},"reference-count":61,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","license":[{"start":{"date-parts":[[2025,4,30]],"date-time":"2025-04-30T00:00:00Z","timestamp":1745971200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,2]]},"abstract":"<jats:p>JOURNAL\/nrgr\/04.03\/01300535-202602000-00047\/figure1\/v\/2026-04-22T115157Z\/r\/image-tiff<\/jats:p>\n                  <jats:p>Alzheimer\u2019s disease is a multi-amyloidosis disease characterized by amyloid-\u03b2 deposits in brain blood vessels, microaneurysms, and senile plaques. How amyloid-\u03b2 deposition affects axon pathology has not been examined extensively. We used immunohistochemistry and immunofluorescence staining to analyze the forebrain tissue slices of Alzheimer\u2019s disease patients. Widespread axonal amyloidosis with distinctive axonal enlargement was observed in patients with Alzheimer\u2019s disease. On average, amyloid-\u03b2-positive axon diameters in Alzheimer\u2019s disease brains were 1.72 times those of control brain axons. Furthermore, axonal amyloidosis was associated with microtubule-associated protein 2 reduction, tau phosphorylation, lysosome destabilization, and several blood-related markers, such as apolipoprotein E, alpha-hemoglobin, glycosylated hemoglobin type A1C, and hemin. Lysosome destabilization in Alzheimer\u2019s disease was also clearly identified in the neuronal soma, where it was associated with the co-expression of amyloid-\u03b2, Cathepsin D, alpha-hemoglobin, actin alpha 2, and collagen type IV. This suggests that exogenous hemorrhagic protein intake influences neural lysosome stability. Additionally, the data showed that amyloid-\u03b2-containing lysosomes were 2.23 times larger than control lysosomes. Furthermore, under rare conditions, axonal breakages were observed, which likely resulted in Wallerian degeneration. In summary, axonal enlargement associated with amyloidosis, micro-bleeding, and lysosome destabilization is a major defect in patients with Alzheimer\u2019s disease. This finding suggests that, in addition to the well-documented neural soma and synaptic damage, axonal damage is a key component of neuronal defects in Alzheimer\u2019s disease.<\/jats:p>","DOI":"10.4103\/nrr.nrr-d-24-01440","type":"journal-article","created":{"date-parts":[[2025,5,6]],"date-time":"2025-05-06T11:01:55Z","timestamp":1746529315000},"page":"790-799","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":2,"title":["Pathological axonal enlargement in connection with amyloidosis, lysosome destabilization, and bleeding is a major defect in Alzheimer\u2019s disease"],"prefix":"10.4103","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0189-0282","authenticated-orcid":false,"given":"Hualin","family":"Fu","sequence":"first","affiliation":[{"name":"Institute of Nano Biomedicine and Engineering, School of Sensing Science and Engineering, School of Electronic Information and Electrical Engineering, Shanghai 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