"Plasma concentrations of p-tau181 and p-tau231 are elevated in patients with DLB and further elevated in patients with DLB with confirmed AD (Alzheimer disease) comorbid pathologic characteristics," Dr. Maria C. Gonzalez of the Norwegian Centre for Movement Disorders of Stavanger University Hospital and her colleagues write in JAMA Neurology.
"Plasma p-tau represents a promising biomarker to identify AD pathologic characteristics and a faster cognitive decline in individuals with this neurologic disorder," they add.
They researchers studied participants enrolled in the European-DLB (E-DLB) Consortium cohort at 10 medical centers. The patients were diagnosed over a 19-year period and followed for up to five years.
After excluding people with acute delirium or terminal illness and those with other previous major psychiatric or neurologic disorders, the researchers focused on 371 participants with probable DLB, 204 with Parkinson disease, 207 with AD, as well as 205 healthy controls. The overall mean age was 70 years.
Patients with DLB were similar to those in the AD group with respect to age, sex and years of education. The DLB group was older than the HC group and contained more men than the AD and HC groups.
The researchers compared the concentrations of plasma p-tau181 and p-tau231 with cognitive decline in individuals with probable DLB. The proteins were measured with in-house single-molecule-array assays, and cognition was assessed by the Mini-Mental State Examination (MMSE).
Baseline concentrations of plasma p-tau181 and p-tau231 in patients with DLB were significantly higher than those in the healthy controls, but they were lower than the AD group and similar to the Parkinson disease group.
Higher plasma levels of both markers were detected in patients with DLB and abnormal cerebrospinal fluid (CSF) amyloid-beta 42 levels compared with patients with normal levels of amyloid-beta 42 (difference in groups in p-tau181, -3.61 pg/mL; P=0.049; difference in groups in p-tau231, -2.51 pg/mL; P=0.02).
Plasma p-tau181 and p-tau231 levels were significantly associated with cognitive impairment at baseline and with faster cognitive decline during follow-up after adjustments for age and sex.
DLB patients with higher baseline plasma p-tau181 and p-tau231 levels tended to have lower baseline MMSE scores (for p-tau181, -0.092 MMSE points; P=0.001; for p-tau231, -0.16 MMSE points; P<0.001), and faster MMSE decline. Plasma p-tau181 level was linked with -0.094 MMSE points per year (P=0.02), and plasma p-tau231 level was linked with -0.130 0MMSE points per year (P=0.02), after adjusting for sex and age.
Dr. Michelle M. Mielke, a professor of neurology and epidemiology at Mayo Clinic in Rochester, Minnesota, told Reuters Health by email, "The current clinical method of obtaining information on AD pathology in patients with suspected comorbid pathology is via a lumbar puncture to collect CSF with subsequent measure of CSF amyloid-beta and phosphorylated tau."
"The study demonstrates that plasma phosphorylated-tau is a good predictor of AD pathology and of faster cognitive decline among DLB patients," added Dr. Mielke, who was not involved in the study. "This is exciting because a plasma marker is more feasible, less invasive, and generally less costly than a lumbar puncture, and will result in a more easily obtainable tool for diagnostic and prognostic information in DLB patients."
Dr. Ian C. Neel, an associate clinical professor and medical director of the geriatric medicine consult service at the University of California, San Diego, said, "It is unclear how useful this will be in clinical practice. The diagnosis of dementia is based on a constellation of symptoms and pattern of cognitive test scores."
"The test results alone cannot be used to make the diagnosis," Dr. Neel, who also was not part of the study, told Reuters Health by email.
Dr. Jonathan L. Haines, a professor of genomic sciences and chair of the Department of Population and Quantitative Health Sciences at Case Western Reserve University School of Medicine in Cleveland, Ohio, echoed Dr. Neel, noting, "It is not likely that this will impact treatment in the short term, other than helping patients and their families anticipate coming changes in behavior and cognitive decline."
"The comparison of AD, DLB, and cognitively normal individuals is well done and sets the stage for better diagnoses," Dr. Haines told Reuters Health by email. "However, the MMSE is not a very sensitive measure of cognitive decline, so the longitudinal analyses are not compelling. Predicting the rate of decline needs further study."
The study did not receive commercial funding.
Dr. Gonzlez did not reply to requests for comment.
SOURCE: https://bit.ly/3dcfxsw JAMA Neurology, online November 22, 2021.
By Lorraine L. Janeczko
Posted on
site created by:
© 2024 Medicom Medical Publishers. All rights reserved. Terms and Conditions | Privacy Policy