Mid-life predictors of late-life cognitive impairment in type 2 diabetes: The Fremantle Diabetes Study — ASN Events
  1. Schedule
  2. ADS Clinical Orals - Outcomes
  3. Mid-life predictors of late-life cognitive impairment in type 2 diabetes: The Fremantle Diabetes Study

Mid-life predictors of late-life cognitive impairment in type 2 diabetes: The Fremantle Diabetes Study (#87)

David G Bruce 1 , Wendy A Davis 1 , Janet L Mace 1 , Melinda Nelson 1 , Timothy M Davis 1
  1. University of Western Australia, Fremantle, WA, Australia

Background: The pathophysiological causes of cognitive impairment and dementia in type 2 diabetes remain undetermined and long duration diabetes and/or cardiovascular risk factors during mid-life may be important.   

Aims: To investigate mid-life risk factors for late-life cognitive impairment in the Fremantle Diabetes Study (FDS).

Patients and methods: Type 2 survivors of the first FDS cohort (assessed in 1993/96) were recruited to Phase 2 of the FDS in 2008/11. Participants aged 50+ years completed the Mini-Mental State Examination and those with low scores (≤26/30) were rated using the Clinical Dementia Rating to diagnose dementia and cognitive impairment without dementia. Bivariate statistics and multivariate logistic regression were used. 

Results: Of 339 recruited survivors, 282 have completed the cognitive assessment. Risk factors were assessed at age 57.4±9.0 years when they had had diabetes for a median 2.4 years. Cognition was assessed at age 72.0±9.0 years, 14.6±1.1 years later, when 249 (88.3%) had normal cognition, 26 (9.2%) had cognitive impairment and 7 (2.5%) had dementia. Comparing normal with any cognitive impairment, there was no baseline difference in age, sex, diabetes duration, HbA1c, BMI, BP, dyslipidaemia, macrovascular disease or neuropathy. There were significant differences in education and proportions on insulin therapy and with retinopathy. With logistic regression and entering plausible variables with P<0.2, independent mid-life predictors of cognitive impairment were: education beyond primary school (odds ratio (95% CI): 0.18 (0.07-0.42), P<0.001), fasting plasma glucose (0.81, (0.69-0.95), P=0.009), insulin treatment (4.98 (1.63-15.24), P=0.005) and retinopathy (4.24 (1.45-12.38), P=0.008).

Conclusions: Cognitive impairment in type 2 diabetes is, i) not explained by mid-life cardiovascular risk factors, ii) probably related to cerebral microvascular disease, and iii) associated with early insulin treatment. The association with insulin and glycaemia has several possible explanations but may have important clinical implications.  Long-term longitudinal studies are helpful in clarifying this complex disease pathway.