30.: Quantifying abnormal eating behavior and metabolic changes in frontotemporal dementia and motor neuron disease

Abstract

Abnormal eating behavior is a core diagnostic feature for behavioral frontotemporal dementia (bvFTD). We aimed to define the patterns of eating behavior and intake in bvFTD and semantic dementia (SD) compared to Alzheimer’s disease (AD) and controls. We hypothesized that these changes are not the result of increased hunger/decreased satiety, but may relate to disinhibition and dysfunction of hypothalamic pathways that control appetite. We examined the association between eating behaviors and metabolic health of FTD compared with motor neuron disease (MND), which shares a common pathology with FTD, and where the metabolic profile has been hypothesized to affect disease progression. Carers of 75 dementia patients (21 bvFTD, 26 SD, 28 AD) and 18 healthy control subjects completed validated questionnaires on appetite and eating behavior. All participants completed surveys on their hunger and satiety. Body mass index (BMI), and blood samples measuring cholesterol and insulin levels were prospectively collected. BMI measurements were compared to a cohort of 100 MND (bulbar and limb) and FTD/ MND patients. bvFTD patients displayed significant abnormalities in all domains of eating compared to AD patients. bvFTD patients had significantly increased carbohydrate intake and SD patients significantly increased sugar intake. Despite increased intake in the FTD groups, their hunger/satiety scores did not differ from the control group. BMI measurements were significantly higher in the FTD and FTD/MND groups than in the MND (bulbar and limb) and control groups. Increased BMI in the bvFTD and SD groups was also significantly associated with abnormal eating behavior. BvFTD patients had significantly increased insulin levels, triglyceride, cholesterol ratios, and lower high-density lipoprotein cholesterol levels compared to controls. Abnormal eating behavior is prominent in bvFTD and SD patients, and is associated with increased sugar and carbohydrate intake, and is not the result of increased hunger and lower satiety. Similar findings have been shown in obese patients, attributed to disinhibition, orbitofrontal pathology and dysfunction of hypothalamic pathways that control appetite, suggesting similar pathways may be affected in FTD. Abnormal eating behavior in FTD is associated with changes in BMI, and a blood metabolic profile similar to that seen in MND. Despite similar pathology however, BMI in all forms of MND appears lower than in FTD.