The impact of diabetes mellitus on cognitive decline in the oldest of the old: a prospective population-based study

Berg, Esther van den; Craen, Anton J. M. de; Biessels, Geert Jan; Gussekloo, Jacobijn; Westendorp, Rudi G.J.

doi:10.1007/s00125-006-0333-1

Cited by 118 publications

(95 citation statements)

References 42 publications

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“…In a recent longitudinal study, with 4 years follow-up, we observed no accelerated decline in a well controlled T2DM group relative to controls [35]. Other longitudinal studies, that generally used relatively brief cognitive assessment batteries, also reported no or limited (up to 50% on top of the rate of normal aging) accelerated cognitive decline in individuals with T2DM [36][37][38].…”

Section: Cognition In Non-demented Individuals With T2dmmentioning

confidence: 64%

Caffeine, Diabetes, Cognition, and Dementia

Biessels

2010

JAD

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Abstract. People with diabetes mellitus are at increased risk of cognitive dysfunction. This review explores the relation between caffeine intake, diabetes, cognition and dementia, focusing on type 2 diabetes (T2DM). Epidemiological studies on caffeine/coffee intake and T2DM risk are reviewed. Next, the impact of T2DM on cognition is addressed. Finally, the potential for caffeine to modulate the risk of cognitive decline in the context of diabetes is explored. The conclusion is that, although epidemiological studies indicate that coffee/caffeine consumption is associated with a decreased risk of T2DM and possibly also with a decreased dementia risk, we can at present not be certain that these associations are causal. For now, recommendations for coffee consumption in individuals with T2DM or pre-diabetic stages are therefore difficult to establish, but it should be acknowledged that caffeine does appear to have several properties that warrant further investigations in this field.

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Section: Cognition In Non-demented Individuals With T2dmmentioning

confidence: 64%

Caffeine, Diabetes, Cognition, and Dementia

Biessels

2010

JAD

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“…Participants were classified as having diabetes according to previously described criteria. 21 Information on smoking was obtained from questionnaires. Body mass index was calculated by dividing the weight in kilograms by the square of length in meters (kg/m 2 ).…”

Section: Discussionmentioning

confidence: 99%

NT-proBNP, blood pressure, and cognitive decline in the oldest old

et al. 2014

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Objective: To study the relation between N-terminal pro-brain natriuretic peptide (NT-proBNP) levels, used as a marker of heart failure in clinical practice, blood pressure (BP), and cognitive decline in the oldest old.Methods: In 560 participants of the Leiden 85-plus Study, we measured NT-proBNP levels and BP at age 85 years, at baseline, and global cognitive function (Mini-Mental State Examination [MMSE]) annually during the follow-up of 5 years.Results: Subjects in the highest tertile of NT-proBNP levels scored 1.7 points lower on the MMSE at age 85 years than subjects in the lowest tertile (p 5 0.004), and had a 0.24-point-steeper decline in MMSE score per year (p 5 0.021). The longitudinal association disappeared after full adjustment for possible confounders (0.14-point-steeper decline, p 5 0.187). Subjects in the category "highest tertile of NT-proBNP and the lowest tertile of systolic BP" had a 3.7-point-lower MMSE score at baseline (p , 0.001) and a 0.49-point-steeper decline in MMSE score per year (p , 0.001) compared with subjects in the other categories. Conclusions:In the oldest old, high NT-proBNP levels are associated with lower MMSE scores. The combination of high NT-proBNP levels and low systolic BP is associated with worst global cognitive function and the steepest cognitive decline. Possibly, a failing pump function of the heart results in lower BP and lower brain perfusion with resultant brain dysfunction. Cardiovascular diseases, such as myocardial infarction, generalized atherosclerosis, and stroke have been associated with increased dementia risk and cognitive decline.1-4 Hypertension, however, is only a risk factor for dementia when present in middle age, whereas most studies show that dementia and cognitive decline in the oldest old associate with lower blood pressures. 5In the oldest old, blood pressures decrease over time, 6,7 and stronger declines are related to the presence of dementia and cognitive decline. 8,9 One possible explanation for the blood pressure decline in the oldest old might be the increasing prevalence of (subclinical) congestive heart failure.10 Despite this dynamic correlation between blood pressure and cardiac function in relation to cognitive function in old age, previous studies have mainly focused on either the association of blood pressure or cardiac function with cognitive impairment.Congestive heart failure has been associated with an increased risk of cognitive impairment. 11-13A frequently used serum marker of heart failure is the N-terminal pro-brain natriuretic peptide (NT-proBNP), the inactive fragment of the proBNP hormone. 14 NT-proBNP has proven to be a quantitative marker of acute heart failure in clinical practice, with high sensitivity and reasonable specificity, 15 although elevated NT-proBNP levels are not specific for heart failure in the general population. Several studies have shown that higher NT-proBNP levels associate with lower cognitive function. 16,17 However, the relation among NT-proBNP levels, blood pressure, and cognitive f...

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“…Following older adults with and without type 2 diabetes over a 5-year period, van den Berg and associates (present issue of Diabetologia) [39] failed to find a faster rate of cognitive deterioration in diabetic patients over time, although at baseline (age: 85 years), diabetic patients performed more slowly on several speed tests, but this was largely attributable to their history of macrovascular disease (stroke). A greater degree of learning and memory dysfunction, generally considered to be a predictor of progression to dementia [40], was also not evident within the diabetic group.…”

Section: Absence Of Progressive Neurocognitive Deterioration In Oldermentioning

confidence: 93%

Diabetes and brain damage: more (or less) than meets the eye?

Ryan

2006

Diabetologia

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Brain damage is now a well-established complication of diabetes, but its pathophysiological basis remains controversial. Until very recently, most research on this topic was devoted to demonstrating that hypoglycaemic events are the primary cause of neurocognitive dysfunction. This was a plausible hypothesis because the central nervous system (CNS) has very limited stores of glucose and other substrates, but neurons have a very high rate of glucose utilisation; any reduction in glucose availability would probably induce neuroglycopenia, ultimately leading to significant neuronal damage. Support for this view came from research demonstrating that profound hypoglycaemia could produce neuronal necrosis [1] and induce distinctive patterns of neuropathological [2] and neurocognitive [3] impairment in humans who had experienced very low blood glucose levels over an extended period of time. Fortunately, most diabetic patients never experience profound hypoglycaemia. Although some writers have speculated that recurrent episodes of moderately severe hypoglycaemia could induce a less severe degree of neurocognitive dysfunction [4,5], most recent studies of children [6] and adults [7,8] have failed to find compelling evidence for that possibility. Taken together, these findings suggest that there is not a linear relationship between falling blood glucose levels and permanent brain dysfunction. Rather, necrotising neuronal damage occurs only after the threshold for cerebral energy failure is reached-most typically when blood glucose values fall below 1.5 mmol, and the electroencephalogram has reached an isoelectric (flat) state [9]. Retinopathy predicts neurocognitive dysfunctionIf moderately low blood glucose levels are not sufficient to induce detectable brain damage, and if profound hypoglycaemia is a rare event, to what can we attribute the modest, but consistently reported, brain dysfunction found in many diabetic patients? A growing literature now suggests that functional and structural CNS changes may have a vascular basis, and reflect the occurrence of cerebral microangiopathy that is secondary to chronic hyperglycaemia and indicated by the presence of retinopathy. For example, when adults with type 1 diabetes were followed for 7 years, a significant decline in mental efficiency was found over time, but this was limited to those who either had clinically significant diabetic proliferative retinopathy when they entered the study or who subsequently developed diabetic proliferative retinopathy during the follow-up period; those without retinopathy showed no cognitive changes. The magnitude of cognitive decline was further, and independently, influenced by elevated systolic blood pressure and by duration of diabetes [10]. The presence of retinopathy-even relatively early retinopathy-has also been associated with cerebral white matter lesions [11] in otherwise healthy diabetic adults, and a recent exploratory analysis has suggested that increasing severity of retinopathy is related to reductions in cortical grey matter ...

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The impact of diabetes mellitus on cognitive decline in the oldest of the old: a prospective population-based study

Cited by 118 publications

References 42 publications

Caffeine, Diabetes, Cognition, and Dementia

Caffeine, Diabetes, Cognition, and Dementia

NT-proBNP, blood pressure, and cognitive decline in the oldest old

Diabetes and brain damage: more (or less) than meets the eye?

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