Relationship of FDDNP-PET (amyloid and tau marker) to bmi, physical activity, and diet in older adults without dementia


      Exercise and diet impact body composition, but their age-related brain effects are unclear at the molecular imaging level. To determine whether body mass index (BMI), physical activity (PA), and Mediterranean diet (MD) relate to in vivo brain positron emission tomography (PET) of amyloid plaques and tau tangles using 2-(1-(6-[(2-[F-18]fluoroethyl)(methyl)amino]-2-naphthyl)ethylidene)malononitrile (FDDNP).


      Volunteers (n = 44, mean age = 62.6 + 10.7 years) with subjective memory impairment (SMI; n = 24) or mild cognitive impairment (MCI; n = 20) were recruited by soliciting for memory complaints. BMI > 25 defined being overweight or obese; PA and MD were self-reported. FDDNP-PET scans were used to quantify plaque/tangle binding in regions increased in Alzheimer’s disease (frontal, parietal, medial and lateral temporal, and posterior cingulate). Mixed models controlling for known covariates estimated BMI, PA, and MD relationships to FDDNP-PET.


      Overweight or obese MCI subjects had higher FDDNP-PET binding compared to those of normal weight (1.11(.03) vs 1.08(.03), ES=1.13, t(35)=-3.3, p=.002). Greater PA was associated with lower FDDNP-PET binding in MCI (1.07(.03) vs 1.11(.03), ES=1.04, t(35) =-3.1, p=.004) but not in SMI (1.07 (.03) vs 1.07(.03), ES=.02, t(35)=-0.1, p=.9). MD adherence was associated with lower FDDNP-PET binding, regardless of cognitive status (1.07(.03) vs 1.09(.02), ES=0.72, t(35)=-2.1, p = .04).


      These findings support a relationship between risk modifiers and in vivo measures of brain plaques and tangles. The results support maintaining normal body weight, regular physical activity, and greater adherence to a Mediterranean diet to protect brain health with aging to diminish AD neuropathology.