Anna Marseglia

Early Cognitive Deficits in Type 2 Diabetes : A Population-Based Study

Evidence links type 2 diabetes to dementia risk. However, our knowledge on the initial cognitive deficits in diabetic individuals and the factors that might promote such deficits is still limited. This study aimed to identify the cognitive domains initially impaired by diabetes and the factors that play a role in this first stage. Within the population-based Swedish National Study on Aging and Care–Kungsholmen, 2305 cognitively intact participants aged ≥60 y were identified. Attention/working memory, perceptual speed, category fluency, letter fluency, semantic memory, and episodic memory were assessed. Diabetes (controlled and uncontrolled) and prediabetes were ascertained by clinicians, who also collected information on vascular disorders (hypertension, heart diseases, and stroke) and vascular risk factors (VRFs, including smoking and overweight/obesity). Data were analyzed with linear regression models. Overall, 196 participants (8.5%) had diabetes, of which 144 (73.5%) had elevated glycaemia (uncontrolled diabetes); 571 (24.8%) persons had prediabetes. In addition, diabetes, mainly uncontrolled, was related to lower performance in perceptual speed (β – 1.10 [95% CI – 1.98, – 0.23]), category fluency (β – 1.27 [95% CI – 2.52, – 0.03]), and digit span forward (β – 0.35 [95% CI – 0.54, – 0.17]). Critically, these associations were present only among APOE ɛ4 non–carriers. The associations of diabetes with perceptual speed and category fluency were present only among participants with VRFs or vascular disorders. Diabetes, especially uncontrolled diabetes, is associated with poorer performance in perceptual speed, category fluency, and attention/primary memory. VRFs, vascular disorders, and APOE status play a role in these associations.

Cognitive functioning among patients with diabetic foot.

AIMS Using diabetic foot (DF) as an indicator of severe diabetes, we aimed to investigate the cognitive profile of DF patients and the relations between cognitive functioning and both diabetes complications and comorbidities. METHODS Dementia-free patients with DF aged 30-90 (n=153) were assessed through medical records and a cognitive battery. Information on diabetes complications and comorbidities was collected via interview; glycated hemoglobin (HbA1c) was tested. Data were analyzed using robust logistic or quantile regression adjusted for potential confounders. RESULTS The mean Mini-Mental Examination (MMSE) score of patients was 24.6 (SD=3.6), and 40% had global cognitive dysfunction (MMSE ≤24). Among elderly patients (aged ≥65), MMSE impairment was related to amputation (OR 3.59, 95% CI 1.07-12.11). Episodic memory impairment was associated with foot amputation (OR 4.13, 95% CI 1.11-15.28) and microvascular complications (OR 9.68, 95% CI 1.67-56.06). Further, elderly patients with HbA1c <7% had increased odds of psychomotor slowness (OR 7.75, 95% CI 1.55-38.73) and abstract reasoning impairment (OR 4.49, 95% CI: 1.15-17.46). However, such significant associations were not shown in adult patients aged <65. CONCLUSION Amputation, microvascular diseases and glycemic control were associated with impaired global cognitive function and its domains among patients aged ≥65.

Diabetes in midlife and risk of cancer in late life: A nationwide Swedish twin study: Midlife diabetes and later life cancer risk in twins

The association between diabetes and cancer risk remains controversial. Hence, we examined whether midlife diabetes is related to the risk of cancer in late‐life, and whether genetic and early‐life environmental factors play a role in this association. This study included 25,154 twin individuals born in 1958 or earlier from the Swedish Twin Registry. Information on cancer diagnosis in late life (aged ≥ 65) during 1998–2014, was derived from the National Patient and Cancer Registries. Diabetes was ascertained based on self‐ or informant‐reported history, patient registry and antidiabetic medication use. Midlife diabetes was defined when diabetes was diagnosed before 65 years. Data were analyzed following two strategies: (i) unmatched case‐control analysis for all participants using generalized estimating equation (GEE) models, and (ii) co‐twin control analysis for cancer‐discordant twin pairs using conditional logistic regression. Overall, 1,766 (7.0%) had midlife diabetes and 5,293 (21.0%) had cancer in late‐life. In multiadjusted GEE models, the odds ratios (95% CIs) of diabetes were 10.55 (2.95–37.67) for pharynx cancer, 5.78 (1.72–19.40) for small intestine cancer, 2.37 (1.14–4.91) for liver cancer and 0.48 (0.35–0.67) for prostate cancer. In people with diabetes, diabetes duration was dose‐dependently associated with cancer risk. In conditional logistic regression analysis of 176 prostate cancer‐discordant twin pairs, the association between midlife diabetes and prostate cancer in later life became stronger. Midlife diabetes increases the risk of pharynx, small intestine and liver cancers, but reduces prostate cancer risk in late life. Genetic and early‐life environmental factors may partially contribute to the diabetes–prostate cancer association.

PREDIABETES AND DIABETES ACCELERATE COGNITIVE DECLINE AND PREDICT MICROVASCULAR LESIONS

cohort is the chilean core clinical project of the new Gerocenter on Brain Health and Metabolism (GERO). Methods: The Gero cohort aims at recruiting 300 elderly subjects (>70 years) from three areas of Santiago(Chile) following them up for at least 3 years. Eligible people are non-demented adults with a subjective cognitive complaint, which is reported by the participant and/or a knowledgeable informant. Participants are identified through a household census . The protocol of evaluation is based on a multidimensional approach: socio-demographic, general medical/ nursing, psychosocial, neuropsychological, neuropsychiatric, motor, neuroimaging, blood biomarkers and a genetic sample. Gero’s biobank stores blood samples which keep for long-term storage at -80 C in liquid nitrogen. The multidimensional protocol of evaluation is administered in months 0 (baseline), 18, and 36. In addition, in months 6, 24, and 30 a telephone interview will be done to collect data for a follow up protocol. Results: To our date the Gero cohort now includes over 50 subjects, and the majority of these have had a multilevel assessment and blood intake. Conclusions: Our work will allow us to determine the risks factors (biomedical, clinical and psychosocial) associated with the prognosis of elderly with cognitive complaint on the evolution to a significant functional decline. The Gero cohort will help to design public health policies tailored to prevent aging disease, and contribute to a better understanding of cognitive impairment and dementia in Latin America and the world. Gero’s aim is to establish a center for studying Brain Ageing in Chile including basic and clinical research.

Prediabetes and diabetes accelerate cognitive decline and predict microvascular lesions: A population-based cohort study

The impact of prediabetes and diabetes on cognitive decline and the potential underlying mechanisms remain unclear. We investigated whether prediabetes and diabetes accelerate cognitive decline and brain aging, and the initial pathological changes linked to microvascular processes.

LONG-TERM EFFECTS OF PREDIABETES AND DIABETES ON COGNITIVE TRAJECTORIES IN A POPULATION-BASED COHORT

participants with lower SDNN scored 1.76 points worse on DSST (p1⁄40.01) and 1.14 points worse on Stroop (p1⁄40.02). After adjusting for behavioral and cardiovascular risk factors, lower SDNN remained significantly associated with worse stroop (p1⁄40.01) but not with DSST. There was no association between RMSSD and cognitive function. Conclusions: Our findings suggest that lower SDDN is associated with worse executive function among middle-aged adults, above and beyond cardiovascular risk factors.

CARDIOMETABOLIC DISORDERS ACCELERATE COGNITIVE DECLINE AND TOTAL BRAIN VOLUME LOSS: A POPULATION-BASED LONGITUDINAL STUDY

of benzodiazepineswas associatedwith an increased risk of dementia (OR1⁄41.36, 95%CI 1.09-1.70), as was former (OR1⁄41.63, 95%CI 1.51-1.76) but not current use (OR1⁄41.64, 95%CI 0.83-3.27). Studies with no lag time had an increased risk estimate (OR1⁄41.53, 95%CI 1.14-2.04) compared to thosewhich introduced a lag time to eliminate protopathic bias (OR1⁄41.16, 95%CI 1.03-1.31), but importantly the latter resultwas still statistically significant. The association persisted in studies with a 5-year lag time. Conclusions:Benzodiazepine use increases the risk of dementia by about 16%, after corrections to eliminate protopathic bias. Given the high prevalence of benzodiazepine use, this increase in risk would translate into a large number of real cases and hence benzodiazepine prescribing practices should be reviewed.

EFFECT OF PREDIABETES AND DIABETES ON COGNITIVE TRAJECTORIES: A LONG-TERM FOLLOW-UP STUDY

P3-370 EFFECT OF PREDIABETES AND DIABETES ON COGNITIVE TRAJECTORIES: A LONG-TERM FOLLOW-UP STUDY Anna Marseglia, Anna K. Dahl Aslan, Laura Fratiglioni, Nancy L. Pedersen, Weili Xu, Aging Research Center, Karolinska Institutet & Stockholm University, Stockholm, Sweden; 2 Karolinska Institutet, Stockholm, Sweden; 3 Jonkoping University, Jonkoping, Sweden; Stockholm Gerontology Research Center, Stockholm, Sweden; University of Southern California, Los Angeles, CA, USA; Tianjin Medical University, Tianjin, China. Contact e-mail: weili.xu@ki.se