Title | Preclinical Amyloid-β and Axonal Degeneration Pathology in Delirium. |
Publication Type | Journal Article |
Year of Publication | 2017 |
Authors | Idland, 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 |
Journal | J Alzheimers Dis |
Volume | 55 |
Issue | 1 |
Pagination | 371-379 |
Date Published | 2017 |
ISSN | 1875-8908 |
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. |
DOI | 10.3233/JAD-160461 |
Alternate Journal | J. Alzheimers Dis. |
PubMed ID | 27662296 |