Glucose Hypometabolism, Neuropsychiatric Symptoms Associated With Mild Cognitive Impairment

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The researchers concluded that risk for MCI was associated with neurodegeneration and neuropsychiatric symptoms among adults aged 50 years and older, and that an abnormal FDG-PET was a stronger driving force for cognitive decline.

Mild cognitive impairment (MCI) risk may be elevated among individuals with a combination of regional glucose hypometabolism and baseline neuropsychiatric symptoms (NPS), according to findings from a prospective cohort study published in The American Journal of Geriatric Psychiatry.

This study was derived from the Mayo Clinic Study of Aging, which was a longitudinal, population-based study of cognitive aging conducted in Rochester, Minnesota. Cognitively unimpaired adults (N=1363; 52.8% men) aged 50 years and older were followed for a median of 4.8 years.

Glucose was measured by fluorodeoxyglucose positron emission tomography (FDG-PET) in regions associated with Alzheimer disease, and hypometabolism was defined as a standardized uptake value ratio ≤1.47. The Beck Depression and Anxiety Inventories (BDI-II; BAI) and Neuropsychiatric Inventory Questionnaire were used to assess mental health and NPS, including delusion, anxiety, apathy, aberrant motor behavior, and sleep. All reported hazard ratios (HR) were adjusted for age, sex, education, and APOE ε4 status.

Individuals who had high anxiety (BAI ≥10) and regional glucose hypometabolism had an increased risk for MCI (HR, 7.21; 95% CI, 3.54-14.7; P <.001) as did those who were depressed (BDI-II ≥13) and with glucose hypometabolism (HR, 3.66; 95% CI, 1.75-7.65; P <.001) when compared with individuals with no depression and normal regional glucose metabolism.

Among individuals with a single symptom, an increased risk for MCI was observed for those with apathy (HR, 4.29; 95% CI, 2.57-7.16; P <.001), appetite change (HR, 2.46; 95% CI, 1.33-4.55; P =.004), anxiety (HR, 2.40; 95% CI, 1.33-4.33; P =.004), nighttime behavior (HR, 2.36; 95% CI, 1.47-3.78; P <.001), and glucose hypometabolism (HR, 2.35; 95% CI, 1.74-3.18; P <.001).

Individuals with comorbid depression and apathy (HR, 5.99; 95% CI, 3.11-11.53; P <.001) or apathy and irritability (HR, 3.18; 95% CI, 1.40-7.24; P =.006) had a higher level of risk than those with a single symptom. The overall number of NPS in combination with glucose hypometabolism increased risk for MCI in a dose-dependent manner: ≥1 NPS (HR, 3.74; 95% CI, 2.40-5.82; P <.001), ≥2 NPS (HR, 3.89; 95% CI, 2.20-6.86; P <.001), and ≥3 NPS (HR, 4.12; 95% CI, 2.03-8.37; P <.001).

A limitation of this study was the observational design, which did not allow the investigators to draw conclusions about the effect of glucose hypometabolism or NPS on the incidence of MCI.

The researchers noted that risk for MCI was associated with neurodegeneration and NPS among adults aged 50 years and older, and that an abnormal fluorodeoxyglucose positron emission tomography was a stronger driving force for cognitive decline. They concluded, “Our study suggests that combining information about brain regional glucose metabolism and NPS may be meaningful in predicting the risk of incident MCI.”

Disclosure: Multiple authors declared affiliations with industry. Please refer to the original article for a full list of disclosures.


Krell-Roesch J, Syrjanen J A, Vassilaki M, et al. Brain regional glucose metabolism, neuropsychiatric symptoms and the risk of incident mild cognitive impairment: the Mayo Clinic study of aging [published online June 17, 2020]. Am J Geriat Psychiat. doi:10.1016/j.jagp.2020.06.006.