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Intensive Glucose-Lowering Does Not Benefit Cognition

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Stage Set for Further Cognition Studies in Type 2 Diabetes

Diabetes is now known to be associated with mild to moderate alterations in cognitive functioning in all age groups. Large epidemiologic studies have established that type 2 diabetes is associated with cognitive dysfunction and an enhanced risk of dementia. Overall, the incidence of dementia is raised by 50%-100% relative to people without diabetes. Hence, currently 1 in 10-15 cases of dementia is attributable to diabetes, making it an obvious target for dementia prevention.

As the data presented by the ACCORD MIND investigators show, intensive glucose-lowering treatment did not benefit cognition. Despite the problems that were encountered in this study and the largely negative results, ACCORD MIND is important. It is the first large, randomized trial to target cognition and abnormalities on brain MRI in persons older than 55 years with type 2 diabetes.

Data from recent cross-sectional studies suggest that trajectories of functional and structural brain changes in most individuals older than 55 years with type 2 diabetes are not clearly different from those of normal aging. However, above the age of 65-70 years, patients with type 2 diabetes are over-represented in the group of individuals that develop more severe and progressive cognitive deficits such as dementia. These mild and severe cognitive deficits might not form a continuum and might relate to separate processes with different risk factors and underlying causes, which might need different treatment strategies.

It remains unclear whether dysglycemia is a key factor in accelerated cognitive decline and dementia in type 2 diabetes. Although cross-sectional studies report associations between raised HbA1c concentrations and cognition, longitudinal studies show no consistent relation with cognitive decline. Therefore, preventive treatment might also need to target factors other than dysglycemia. To identify other potential treatment targets, we need large, prospective, observational cohort studies that have sufficient statistical power to identify determinants of accelerated cognitive decline and dementia in type 2 diabetes. Fortunately, such studies are becoming available.

Dr. Geert Jan Biessels is with the department of neurology at the Rudolf Magnus Institute of Neuroscience, University Medical Center, Utrecht, Netherlands.Dr. Biessels consults for and receives research

support from Boehringer Ingelheim. These remarks were taken from his editorial accompanying the ACCORD MIND article (Lancet Neurol. 2011 [doi:10.1016/S1474-4422[11]70199-5]).


 

FROM LANCET NEUROLOGY

Intensive glycemic lowering did not significantly affect cognition at 40 months in older adults with type 2 diabetes participating in the Action to Control Cardiovascular Risk in Diabetes study.

There were differences in brain structure, however, suggesting that structural changes occur prior to cognitive changes, said Lenore J. Launer, Ph.D., of the National Institute on Aging, Bethesda, Md., and her associates (Lancet Neurol. 2011 [doi:10.1016/S1474-4422[11]70188-0]).

The MIND (Memory in Diabetes) study was a substudy of 2,977 ACCORD participants who had been randomly assigned to receive either intensive glycemic treatment targeting hemoglobin A1c to less than 6.0% or standard treatment targeting HbA1c to 7.0%-7.9%. They were also assigned to either intensive or standard lipid- and blood pressure–lowering treatment arms. The intensive glucose-lowering intervention was stopped early, in February 2008, because it was associated with a significant 22% increased cardiovascular mortality. Participants in that group were switched to standard glycemic treatment, and the lipid and blood pressure arms of the study were continued. No significant cardiovascular benefit was seen with intensive glucose lowering during the period it was studied (N. Engl. J. Med. 2008;358:2545-59).

The MIND study – believed to be the first-ever randomized study to examine the effect of intensive glucose lowering on cognition and brain structure in older people with type 2 diabetes – began in August 2003, 34 months into ACCORD, and continued until December 2005. Of the total 2,794 MIND patients who had at least 20-month and 40-month follow-up, 614 underwent successful brain magnetic resonance imaging (MRI).

The patients had a mean age of 62.5 years at study start, and the separation in median HbA1c achieved between the intensive and standard treatment groups – 6.6% vs. 7.5% – was similar to that of the overall ACCORD study population. At the time the intensive treatment intervention was stopped, the MIND study patients in that group had received treatment for a median of 39 months, and those in the MRI substudy had received 35 months of intensive treatment.

Scores on the primary end point DSST (Digit Symbol Substitution Test), a measure of psychomotor speed that requires reasoning and working memory, declined in both the intensive and standard treatment groups. At 20 months, the difference between the two groups approached statistical significance (P = .076), but by 40 months the difference was attenuated and not significant (P = .23).

Other measures of cognition, the RAVLT (Rey Auditory Verbal Learning Test) and the Stroop test of executive function, also changed similarly in the intensive and standard treatment groups. There were small increases in mean RAVLT scores between groups, but no significant difference between them. Performance on the Stroop test improved slightly in the intensive treatment group and declined slightly in the standard treatment group, but there was no difference between treatments.

"Overall, there is no evidence in this patient group, which had long-standing type 2 diabetes, a high risk of cardiovascular disease, and a mean of 62 years, that an intensive glycemic treatment strategy provides benefit to cognitive function," Dr. Launer and her associates commented.

Differences were seen in brain structure, however. At 40 months, the intensive treatment group had significantly greater total brain volume (TBV), compared with the standard treatment group. Although TBV declined in both groups, the TBV of the intensive treatment group declined less, by 0.41%/year, compared with 0.57%/year. Abnormal white matter (AWM) tissue volume was significantly greater in the intensive treatment group at 40 months (geometric mean 1.89 vs. 1.71 cm3), but this effect seems to be restricted to patients younger than 60 years, they noted.

There was no evidence that measures of peripheral edema or weight gain could explain the differences in TBV or AWM between groups.

"There was a significant but small difference in TBV favoring the intensive strategy. However, this difference does not support the use of intensive treatment to reduce brain atrophy in view of the effects of this intervention in the main ACCORD trial: Raised mortality, no overall benefit on cardiovascular disease events, an increase in hypoglycemic events, and weight gain," the investigators commented.

"Taking the cognitive and MRI findings together, it is reasonable to postulate that, in this age group, structural changes in the brain happen before cognitive changes and that over time cognitive differences between treatment groups would emerge," Dr. Launer and her associates said, noting that ongoing follow-up should be able to establish whether that is the case.

Dr. Launer and all but one of her 21 coauthors declared that they had no conflicts of interest. Dr. Hertzel C. Gerstein, the principal investigator for the overall ACCORD trial, declared that that he has received consulting fees, institutional grant support, and/or lecture fees from numerous pharmaceutical companies including Sanofi-Aventis, GlaxoSmithKline, Eli Lilly, Novo Nordisk, AstraZeneca, and Bristol-Myers Squibb.

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