Moderate hypoglycemia impairs multiple memory functions in healthy adults.

Sommerfield, Andrew J.; Deary, Ian J.; McAulay, Vincent; Frier, Brian M.

doi:10.1037/0894-4105.17.1.125

Cited by 55 publications

(48 citation statements)

References 45 publications

(77 reference statements)

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“…Immediate recall performance for the two verbal memory tasks (AVLT and logical memory) was impaired significantly during hypoglycaemia, which is consistent with previous studies [15,16]. Delayed recall was always tested during euglycaemia, and it can be inferred that the significant impairment in delayed recall following hypoglycaemia resulted from a hypoglycaemic effect on learning and/or consolidation.…”

Section: Discussionsupporting

confidence: 89%

“…We have studied previously the effects of hypoglycaemia on various components of memory using consistent experimental techniques and validated memory tasks. Hypoglycaemia impairs the auditory and visual processing subsystems of sensory memory, short-term memory, working memory and delayed memory in both diabetic and nondiabetic subjects [11][12][13][14][15][16]. Working memory and delayed memory are particularly susceptible to hypoglycaemia [17].…”

Section: Introductionmentioning

confidence: 99%

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The effects of acute hypoglycaemia on memory acquisition and recall and prospective memory in type 1 diabetes

et al. 2006

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Aims/hypothesis Global memory performance is impaired during acute hypoglycaemia. This study assessed whether moderate hypoglycaemia disrupts learning and recall in isolation, and utilised a novel test of prospective memory which may better reflect the role of memory in daily life than conventional tests. Subjects and methods Thirty-six subjects with type 1 diabetes participated, 20 with normal hypoglycaemia awareness (NHA) and 16 with impaired hypoglycaemia awareness (IHA). Each underwent a hypoglycaemic clamp with target blood glucose 2.5 mmol/l. Prior to hypoglycaemia, subjects attempted to memorise instructions for a prospective memory task, and recall was assessed during hypoglycaemia. Subjects then completed the learning and immediate recall stages of three conventional memory tasks (word recall, story recall, visual recall) during hypoglycaemia. Euglycaemia was restored and delayed memory for the conventional tasks was tested. The same procedures were completed in euglycaemic control studies (blood glucose 4.5 mmol/l). Results Hypoglycaemia impaired performance significantly on the prospective memory task (p=0.004). Hypoglycaemia also significantly impaired both immediate and delayed recall for the word and story recall tasks (p<0.01 in each case). There was no significant deterioration of performance on the visual memory task. The effect of hypoglycaemia did not differ significantly between subjects with NHA and IHA. Conclusions/interpretation Impaired performance on the prospective memory task during hypoglycaemia demonstrates that recall is disrupted by hypoglycaemia. Impaired performance on the conventional memory tasks demonstrates that learning is also disrupted by hypoglycaemia. Results of the prospective memory task support the relevance of these findings to the everyday lives of people with diabetes.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

The effects of acute hypoglycaemia on memory acquisition and recall and prospective memory in type 1 diabetes

et al. 2006

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“…Indeed, hypoglycemia has been demonstrated to impair many neuronal functions, including short-term memory processing Sommerfield et al, 2003). Recent studies have demonstrated that glucose levels fall dramatically in the hippocampus during performance of spatial working memory tasks in rodents (McNay et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

ADrosophilaTemperature-Sensitive Seizure Mutant in Phosphoglycerate Kinase Disrupts ATP Generation and Alters Synaptic Function

Wang

Saraswati²,

Guan³

et al. 2004

J. Neurosci.

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A novel paralytic mutant, nubian, was identified in a behavioral screen for conditional temperature-sensitive seizure mutants in Drosophila melanogaster. nubian mutants display reduced lifespan, abnormal motor behavior, altered synaptic structure, and defective neurotransmitter release. The nubian mutant disrupts phosphoglycerate kinase (PGK), an enzyme required for ATP generation in the terminal stage of the glycolytic pathway. Consistent with altered ATP generation in nubian animals, brain extracts show a threefold reduction in resting ATP levels compared with controls. Microarray analysis of nubian mutants reveals altered transcription of genes implicated in glucose and lipid metabolism. Disruption of ATP generation in nubian animals is accompanied by temperature-dependent defects in neuronal activity, with initial seizure activity, followed by an activity-dependent loss of synaptic transmission. nubian mutants also display structural defects at the synapse, with larger varicosity size but normal varicosity number, indicating that these synaptic parameters are regulated independently. Both exocytotic (NSF) and endocytotic (dynamin) ATPase/GTPase activity are required for normal synaptic transmission. Biochemical and physiological analyses indicate that synaptic defects in nubian animals are secondary to defective endocytosis, suggesting that endocytotic pathways may be generally more sensitive to altered ATP levels than those used for exocytosis. Alterations in ATP metabolism likely disrupt similar pathways in humans, because PGK deficiency is associated with mental retardation, seizures, and exercise intolerance. Given the behavioral similarities between disruptions of PGK function in Drosophila and humans, the analysis of nubian animals may reveal conserved neuronal responses associated with altered ATP generation within the brain.

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“…In healthy adults, induced hypoglycaemia via a hyperinsulinemic glucose clamp has been found to impair working and delayed visual memory [13]. Aung and colleagues [14] reported that DM2 patients who had a selfreported history of severe hypoglycaemia performed significantly worse on age-sensitive neuropsychological tests (Verbal Fluency, the Digit Symbol test and Letter-Number sequencing from the Wechsler Adult Intelligence Scale III and the Trail-Making Test Part B) compared to those who had no history of this condition.…”

Section: Dm2 and Cognitive Impairment: The Mechanismsmentioning

confidence: 99%

Type 2 Diabetes and Memory: Using Neuroimaging to Understand the Mechanisms

Jones¹,

Riby²,

Mitchell³

et al. 2014

CDR

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Abstract:The most robust and frequently reported cognitive deficits in type 2 diabetes (DM2) are those that relate to memory. Behavioural research has identified a number of potential contributory physiological factors, including abnormalities in glucose metabolism, such as hyperglycaemia and hypoglycaemia. The impact of these mechanisms on memory has been further investigated through the use of both structural and functional neuroimaging. Structural brain imaging has indicated that memory impairments in DM2 are associated with global atrophy of the brain. Further data suggest that localised atrophy in the hippocampal area, a brain region critical to memory formation and consolidation, may be primarily responsible for the memory deficits seen in this population. Functional imaging data has corroborates these findings, with functional magnetic resonance imaging (fMRI) suggesting reduced connectivity between the hippocampus and surrounding brain regions, particularly the frontal and temporal gyri. Despite this, little functional neuroimaging research has directly investigated differences in regional brain activity between healthy and DM2 participants whilst memory tasks are being performed. By using neuroimaging techniques to their full potential, we can acquire a fuller, more comprehensive picture of the impact that DM2 has on memory.Keywords: Brain, cognition, EEG, memory, MRI, neuroimaging, type 2 diabetes.Type 2 diabetes (DM2) in older adults is associated with cognitive impairment, reflecting accelerated cognitive decline relative to that expected in normal ageing [1][2][3]. The most frequently reported and most robust deficits are seen in verbal episodic memory [4], although other domains of memory such as face recognition and working memory may also be affected [5,6]. However, it is still unclear whether these deficits reflect impairments in their encoding or retrieval. These memory impairments have been attributed to varied physiological mechanisms, including abnormalities in glucose metabolism, insulin resistance, dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and vascular complications [7,8]. The role of these physiological mechanisms in neurocognitive functioning in individuals withDM2 has been investigated using a variety of neuroimaging techniques. Methods such as magnetic resonance imaging (MRI) and electroencephalography (EEG), have allowed researchers to examine both the structural and functional impact of DM2 on the brain. This review will consider these neuroimaging studies and speculate on how these innovative techniques could be informative in identifying underlying mechanisms of memory deficits in DM2. DM2 AND COGNITIVE IMPAIRMENT: THE MECHANISMSDisturbances in glucose metabolism, including hyperglycaemia and hypoglycaemia, have been associated with cognitive dysfunction [7,9]. Summerfield, Deary and Frier [7] observed that induced acute hyperglycaemia in adults with DM2 impaired cognitive performance, most notably in the working memory domain. Relatively few studies have inve...

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Moderate hypoglycemia impairs multiple memory functions in healthy adults.

Cited by 55 publications

References 45 publications

The effects of acute hypoglycaemia on memory acquisition and recall and prospective memory in type 1 diabetes

The effects of acute hypoglycaemia on memory acquisition and recall and prospective memory in type 1 diabetes

ADrosophilaTemperature-Sensitive Seizure Mutant in Phosphoglycerate Kinase Disrupts ATP Generation and Alters Synaptic Function

Type 2 Diabetes and Memory: Using Neuroimaging to Understand the Mechanisms

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