دورية أكاديمية

Psychosis in Alzheimer Disease and Elevations in Disease-Relevant Biomarkers.

التفاصيل البيبلوغرافية
العنوان: Psychosis in Alzheimer Disease and Elevations in Disease-Relevant Biomarkers.
المؤلفون: Gomar JJ; Feinstein Institutes for Medical Research, Manhasset, New York., Koppel J; Feinstein Institutes for Medical Research, Manhasset, New York.; Department of Psychiatry, Zucker Hillside Hospital, Northwell Health, Glen Oaks, New York.
المصدر: JAMA psychiatry [JAMA Psychiatry] 2024 Aug 01; Vol. 81 (8), pp. 834-839.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: American Medical Association Country of Publication: United States NLM ID: 101589550 Publication Model: Print Cited Medium: Internet ISSN: 2168-6238 (Electronic) Linking ISSN: 2168622X NLM ISO Abbreviation: JAMA Psychiatry Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Chicago, IL : American Medical Association, [2013]-
مواضيع طبية MeSH: Alzheimer Disease*/blood , Biomarkers*/blood , tau Proteins*/blood , Psychotic Disorders*/blood , Cognitive Dysfunction*/blood , Cognitive Dysfunction*/etiology, Humans ; Male ; Female ; Aged ; Longitudinal Studies ; Neurofilament Proteins/blood ; Hallucinations/blood ; Hallucinations/etiology ; Hallucinations/epidemiology ; Aged, 80 and over ; Delusions/blood ; Delusions/epidemiology ; Phosphorylation ; Cohort Studies
مستخلص: Importance: The emergence of psychotic symptoms in Alzheimer disease (AD) is associated with accelerated cognitive and functional decline that may be related to disease pathology.
Objective: To investigate the longitudinal dynamics of plasma tau phosphorylated at threonine 181 (p-tau181) and neurofilament light chain protein (NfL) levels in association with the emergence of psychotic symptoms (delusions and hallucinations) in the context of AD.
Design, Setting, and Participants: This cohort study used longitudinal data from the Alzheimer Disease Neuroimaging Initiative (ADNI). Baseline analyses compared patients with mild cognitive impairment (MCI) and AD (both with psychosis [AD+P] and without psychosis [AD-P]) and participants who were cognitively unimpaired (CU). For the longitudinal analysis, participants with MCI and AD were subdivided into patients with evidence of psychosis at baseline (AD+P baseline) and patients free of psychosis at baseline who showed incidence of psychosis over the course of the study (AD+P incident). Study data were analyzed between June and November 2023.
Exposures: Plasma p-tau181 and NfL measures in individuals with MCI and AD, both with and without psychosis.
Main Outcomes and Measures: Plasma p-tau181 and NfL quantifications up to 48 months and concurrent assessments of presence or absence of delusions and hallucinations via the Neuropsychiatric Inventory (NPI) questionnaire.
Results: The cohort included 752 participants with AD (mean [SD] age, 74.2 [7.7] years; 434 male [57.7%]). A total of 424 CU participants had a mean (SD) age of 75.4 (6.6) years of whom 222 were female (52.4%). In the longitudinal analysis of p-tau181 trajectories of the AD+P group, the group of patients who showed incidence of psychosis over the course of follow-up (AD+P incident) demonstrated an associated increase in plasma p-tau181 levels compared with the group of patients who had psychosis at baseline (AD+P baseline) and showed an associated decrease in plasma p-tau181 levels (F4, 117 = 3.24; P = .01). The mean slope of p-tau181 change was significantly different in AD+P incident and AD+P baseline groups (F5,746 = 86.76, P < .0001) and when only individuals with amyloid-β positivity (Aβ+), which was determined using positron emission tomography, were compared (F5,455 = 84.60, P < .001). Patients who experienced psychosis at any time had increased levels of NfL relative to those who never experienced psychosis.
Conclusions and Relevance: Results of this cohort study suggest that the emergence of psychosis in AD was associated with elevations in plasma levels of p-tau181, highlighting the potential utility of plasma p-tau181 as a biomarker of neuropsychiatric illness in AD, which could have implications for predictive and treatment response strategies.
التعليقات: Erratum in: JAMA Psychiatry. 2024 Aug 1;81(8):846. doi: 10.1001/jamapsychiatry.2024.2377. (PMID: 39110434)
المشرفين على المادة: 0 (Biomarkers)
0 (tau Proteins)
0 (Neurofilament Proteins)
0 (neurofilament protein L)
0 (MAPT protein, human)
تواريخ الأحداث: Date Created: 20240626 Date Completed: 20240807 Latest Revision: 20240807
رمز التحديث: 20240807
مُعرف محوري في PubMed: PMC11209195
DOI: 10.1001/jamapsychiatry.2024.1389
PMID: 38922609
قاعدة البيانات: MEDLINE
الوصف
تدمد:2168-6238
DOI:10.1001/jamapsychiatry.2024.1389