{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T06:05:54Z","timestamp":1791266754102,"version":"4.1.0"},"reference-count":36,"publisher":"Society for Neuroscience","issue":"5","license":[{"start":{"date-parts":[[2006,8,1]],"date-time":"2006-08-01T00:00:00Z","timestamp":1154390400000},"content-version":"vor","delay-in-days":181,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2006,2,1]]},"abstract":"<jats:p>Pathophysiologic hypotheses for Alzheimer\u2019s disease (AD) are centered on the role of the amyloid plaque A\u03b2 peptide and the mechanism of its derivation from the amyloid precursor protein (APP). As part of the disease process, an aberrant axonal sprouting response is known to occur near A\u03b2 deposits. A Nogo to Nogo-66 receptor (NgR) pathway contributes to determining the ability of adult CNS axons to extend after traumatic injuries. Here, we consider the potential role of NgR mechanisms in AD. Both Nogo and NgR are mislocalized in AD brain samples. APP physically associates with the NgR. Overexpression of NgR decreases A\u03b2 production in neuroblastoma culture, and targeted disruption of NgR expression increases transgenic mouse brain A\u03b2 levels, A\u03b2 plaque deposition, and dystrophic neurites. Infusion of a soluble NgR fragment reduces A\u03b2 levels, amyloid plaque deposits, and dystrophic neurites in a mouse transgenic AD model. Changes in NgR level produce parallel changes in secreted APP\u03b1 and A\u03b2, implicating NgR as a blocker of secretase processing of APP. The NgR provides a novel site for modifying the course of AD and highlights the role of axonal dysfunction in the disease.<\/jats:p>","DOI":"10.1523\/jneurosci.3291-05.2006","type":"journal-article","created":{"date-parts":[[2006,2,2]],"date-time":"2006-02-02T00:13:40Z","timestamp":1138839220000},"page":"1386-1395","source":"Crossref","is-referenced-by-count":106,"title":["Alzheimer Precursor Protein Interaction with the Nogo-66 Receptor Reduces Amyloid-\u03b2 Plaque Deposition"],"prefix":"10.1523","volume":"26","author":[{"given":"James H.","family":"Park","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David A.","family":"Gimbel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tadzia","family":"GrandPre","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jung-Kil","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ji-Eun","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weiwei","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel H. 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