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Home > Preclinical Amyloid-β and Axonal Degeneration Pathology in Delirium.

TitlePreclinical Amyloid-β and Axonal Degeneration Pathology in Delirium.
Publication TypeJournal Article
Year of Publication2017
AuthorsIdland, A-V, Wyller, TBruun, Støen, R, Eri, LMagne, Frihagen, F, Ræder, J, Chaudhry, FAbbas, Hansson, O, Zetterberg, H, Blennow, K, Bogdanovic, N, Brækhus, A, Watne, LOtto
JournalJ Alzheimers Dis
Volume55
Issue1
Pagination371-379
Date Published2017
ISSN1875-8908
Abstract

BACKGROUND: The clinical relevance of brain β-amyloidosis in older adults without dementia is not established. As delirium and dementia are strongly related, studies on patients with delirium may give pathophysiological clues.

OBJECTIVE: To determine whether the Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarkers amyloid-β 1-42 (Aβ42), total tau (T-tau), and phosphorylated tau (P-tau) are associated with delirium in hip fracture patients with and without dementia.

METHODS: CSF was collected in conjunction to spinal anesthesia in 129 patients. Delirium was assessed using the Confusion Assessment Method once daily in all patients, both pre- and postoperatively. The diagnosis of dementia at admission was based upon clinical consensus. CSF levels of Aβ42, T-tau, and P-tau were analyzed.

RESULTS: In patients without dementia, we found lower CSF Aβ42 levels (median, 310 ng/L versus 489 ng/L, p = 0.006), higher T-tau levels (median, 505 ng/L versus 351 ng/L, p = 0.02), but no change in P-tau in patients who developed delirium (n = 16) compared to those who remained lucid (n = 49). Delirious patients also had lower ratios of Aβ42 to T-tau (p 

CONCLUSION: The reduction in CSF Aβ42, indicating β-amyloidosis, and increase in T-tau, indicating neurodegeneration, in hip fracture patients without dementia developing delirium indicates that preclinical AD brain pathology is clinically relevant and possibly plays a role in delirium pathophysiology.

DOI10.3233/JAD-160461
Alternate JournalJ. Alzheimers Dis.
PubMed ID27662296
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