WEDNESDAY, April 25 (HealthDay News) -- In cognitively normal older individuals, amyloid-β (Aβ)-associated longitudinal cognitive decline only occurs in the presence of elevated phospho-tau 181 (p-tau181p) in the cerebrospinal fluid (CSF), according to a study published online April 23 in the Archives of Neurology.
To examine the relationship between CSF Aβ and p-tau181p and their association with clinical cognitive decline over time, Rahul S. Desikan, M.D., Ph.D., from the University of California San Diego in La Jolla, and colleagues studied 107 clinically and cognitively normal older individuals in a longitudinal cohort. Participants with a baseline Clinical Dementia Rating (CDR) of zero underwent lumbar puncture at baseline and longitudinal clinical assessments.
The researchers found that, in individuals with elevated p-tau181-p, decreased CSF Aβ1-42 was associated with a significant change in global CDR, CDR-Sum of Boxes, and the cognitive subscale of the Alzheimer's Disease Assessment Scale. CSF Aβ1-42 had no significant effect on longitudinal clinical decline in the absence of CSF p-tau181p.
"In cognitively normal older individuals, Aβ-associated clinical decline during a mean of three years may occur only in the presence of ongoing downstream neurodegeneration," the authors write.
Several authors disclosed financial ties to the pharmaceutical industry. Data were obtained from the Alzheimer's Disease Neuroimaging Initiative, which is funded by the pharmaceutical industry.
Abstract
Full Text (subscription or payment may be required)
Editorial (subscription or payment may be required)
