{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T03:49:01Z","timestamp":1788320941473,"version":"build-2803163510"},"reference-count":41,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2022,3,2]],"date-time":"2022-03-02T00:00:00Z","timestamp":1646179200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2022,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>SARS\u2010CoV\u20102 infection can damage the nervous system with multiple neurological manifestations described. However, there is limited understanding of the mechanisms underlying COVID\u201019 neurological injury. This is a cross\u2010sectional exploratory prospective biomarker cohort study of 21 patients with COVID\u201019 neurological syndromes (Guillain\u2013Barre Syndrome [GBS], encephalitis, encephalopathy, acute disseminated encephalomyelitis [ADEM], intracranial hypertension, and central pain syndrome) and 23 healthy COVID\u201019 negative controls. We measured cerebrospinal fluid (CSF) and serum biomarkers of amyloid processing, neuronal injury (neurofilament light), astrocyte activation (GFAp), and neuroinflammation (tissue necrosis factor [TNF] \u0251, interleukin [IL]\u20106, IL\u20101\u03b2, IL\u20108). Patients with COVID\u201019 neurological syndromes had significantly reduced CSF soluble amyloid precursor protein (sAPP)\u2010\u0251 (<jats:italic>p<\/jats:italic>\u00a0=\u00a00.004) and sAPP\u03b2 (<jats:italic>p<\/jats:italic>\u00a0=\u00a00.03) as well as amyloid \u03b2 (A\u03b2) 40 (<jats:italic>p<\/jats:italic>\u00a0=\u00a05.2\u00a0\u00d7\u00a010<jats:sup>\u22128<\/jats:sup>), A\u03b242 (<jats:italic>p<\/jats:italic>\u00a0=\u00a03.5\u00a0\u00d7\u00a010<jats:sup>\u22127<\/jats:sup>), and A\u03b242\/A\u03b240 ratio (<jats:italic>p<\/jats:italic>\u00a0=\u00a00.005) compared to controls. Patients with COVID\u201019 neurological syndromes showed significantly increased neurofilament light (NfL, <jats:italic>p<\/jats:italic>\u00a0=\u00a00.001) and this negatively correlated with sAPP\u0251 and sAPP\u03b2. Conversely, GFAp was significantly reduced in COVID\u201019 neurological syndromes (<jats:italic>p<\/jats:italic>\u00a0=\u00a00.0001) and this positively correlated with sAPP\u0251 and sAPP\u03b2. COVID\u201019 neurological patients also displayed significantly increased CSF proinflammatory cytokines and these negatively correlated with sAPP\u0251 and sAPP\u03b2. A sensitivity analysis of COVID\u201019\u2010associated GBS revealed a non\u2010significant trend toward greater impairment of amyloid processing in COVID\u201019 central than peripheral neurological syndromes. This pilot study raises the possibility that patients with COVID\u201019\u2010associated neurological syndromes exhibit impaired amyloid processing. Altered amyloid processing was linked to neuronal injury and neuroinflammation but reduced astrocyte activation.<\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc15585-fig-0005-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text>\n<\/jats:p><\/jats:sec>","DOI":"10.1111\/jnc.15585","type":"journal-article","created":{"date-parts":[[2022,2,9]],"date-time":"2022-02-09T06:13:48Z","timestamp":1644387228000},"page":"146-157","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":57,"title":["Amyloid processing in <scp>COVID<\/scp>\u201019\u2010associated neurological 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