Osteoarthritis Associated With Acceleration of Beta-Amyloid Accumulation

The accumulation of beta-amyloid (Aβ) is faster in the setting of osteoarthritis (OA), according to study findings published in the journal Neurology.

Previous research has found an association between OA and Alzheimer disease (AD) and accelerated Aβ pathology. For the study, researchers evaluated longitudinal changes in Aβ among patients with Aβ pathology.

The researchers sourced data for this study from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Longitudinal data from ¹⁸F-florbetapir (FBP) Aβ positron emission tomography (PET) scans were combined with apolipoprotein (APOE)-e4 and OA information to evaluate the association between OA and Aβ accumulation.

The study population comprised 374 individuals who were Aβ+ and were cognitively unimpaired (n=114), had mild cognitive impairment (MCI; n=212), and dementia (n=48).

The subset of individuals with (n=119) and without (n=255) OA were median age 76 (range, 61-93) and 75 (range, 55-92) years; 48.7% and 49.4% were women; 61.3% and 63.5% carried APOE-e4; and, they had obtained 16 (range, 6-20) and 16 (range, 8-20) years of education, respectively.

At baseline, Aβ deposition in the precentral cortex associated with a diagnosis of cognitive impairment (β, 0.051; P <.001) and in the postcentral cortex with a diagnosis of cognitive impairment (β, 0.053; P <.001) and male gender (β, -0.032; P =.002).

At follow-up, Aβ deposition in the precentral cortex associated with Aβ (β, 0.777; P <.001), the interaction between OA and APOE-e4 (β, 0.128; P =.011), OA (β, 0.098; P =.011), and male gender (β, -0.068; P =.021).

Predictors for deposition in the postcentral cortex associated with Aβ (β, 0.658; P <.001), the interaction between OA and APOE-e4 (β, 0.124; P =.021), OA (β, 0.105; P =.011), age (β, -0.005; P =.014), and male gender (β, -0.070; P =.014).

The longitudinal change in Aβ deposition in the precentral cortex associated with cognitive impairment (β, 0.051; P <.001) and time (β, 0.011; P <.001), whereas in the postcentral cortex, the change was associated with cognitive impairment (β, 0.049; P <.001), time (β, 0.008; P <.001), the interaction between time and OA (β, 0.005; P =.033), and male gender (β, -0.032; P =.005).

Future tau levels measured at a median of 5.4 years were not significantly predicted by any factors in the adjusted analyses; however, in the unadjusted analysis, future tau associated with OA in the precentral cortex (β, 0.688; P =.021) and the interaction between Aβ and OA in the precentral (β, 0.871; P =.009) and postcentral (β, 0.649; P =.032) cortices.

The major limitation of this study was that the OA history was self-reported by participants.

The researchers concluded, “[T]his longitudinal Aβ PET and follow-up tau PET imaging study suggest that OA diseases may accelerate faster Aβ accumulation and induce higher Aβ-related tau deposition in primary motor and somatosensory cortices in Aβ+ elderly adults.”