Glucose, relational memory, and the hippocampus

Stollery, Brian T; Christian, Leonie M

doi:10.1007/s00213-014-3842-5

Cited by 13 publications

(6 citation statements)

References 81 publications

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“…colour-location) bindings would determine whether glucose operates selectively on tasks with a spatial component or more generally on binding processes. This is important because the hippocampal system supports a wide range of binding processes (Olsen et al 2012 ) and while there is some evidence that glucose does not enhance the short-term maintenance of non-spatial (word-word) bindings (Stollery and Christian 2015 ), it would seem prudent to establish the proposed role of spatial memory in the observed enhancement. Thus, the possibility that spatial processing is an important feature of binding tasks that show short-term enhancement due to glucose remains to be determined.…”

Section: Discussionmentioning

confidence: 97%

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Glucose improves object-location binding in visual-spatial working memory

Stollery

Christian

2015

Psychopharmacology

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RationaleThere is evidence that glucose temporarily enhances cognition and that processes dependent on the hippocampus may be particularly sensitive. As the hippocampus plays a key role in binding processes, we examined the influence of glucose on memory for object-location bindings.ObjectiveThis study aims to study how glucose modifies performance on an object-location memory task, a task that draws heavily on hippocampal function.MethodsThirty-one participants received 30 g glucose or placebo in a single 1-h session. After seeing between 3 and 10 objects (words or shapes) at different locations in a 9 × 9 matrix, participants attempted to immediately reproduce the display on a blank 9 × 9 matrix. Blood glucose was measured before drink ingestion, mid-way through the session, and at the end of the session.ResultsGlucose significantly improves object-location binding (d = 1.08) and location memory (d = 0.83), but not object memory (d = 0.51). Increasing working memory load impairs object memory and object-location binding, and word-location binding is more successful than shape-location binding, but the glucose improvement is robust across all difficulty manipulations. Within the glucose group, higher levels of circulating glucose are correlated with better binding memory and remembering the locations of successfully recalled objects.ConclusionsThe glucose improvements identified are consistent with a facilitative impact on hippocampal function. The findings are discussed in the context of the relationship between cognitive processes, hippocampal function, and the implications for glucose’s mode of action.

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Section: Discussionmentioning

confidence: 97%

“…McNay and Gold 2001 ; Riby and Riby 2006 ; Winocur 1995 ), only a few human studies have undertaken a focussed evaluation of hippocampal-based cognitive tasks to explore this (e.g. Stollery and Christian 2015 ).…”

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confidence: 99%

Glucose improves object-location binding in visual-spatial working memory

Stollery

Christian

2015

Psychopharmacology

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“…3). Logical memory is known to be used for the assessment of verbal declarative memory (Hori et al, 2013; Muller et al, 2007a; Perry and Hodges, 2000), whereas visual paired associates have been used to assess visual declarative memory (Kessels et al, 2011; Papalambros et al, 2017; Stollery and Christian, 2015). Declarative memory is mediated by the circuitry involving bidirectional connections between the neocortex, the parahippocampal region, and the hippocampus (Eichenbaum, 2000).…”

Section: Discussionmentioning

confidence: 99%

High serum high-density lipoprotein-cholesterol is associated with memory function and gyrification of insular and frontal opercular cortex in an elderly memory-clinic population

Kinno

Mori

Kubota

et al. 2019

NeuroImage: Clinical

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The issue of whether serum lipid marker values are cognitively and neurologically significant for elderly individuals attending a memory clinic has been controversial. We investigated the associations of serum lipid markers with the memory function and cortical structure in 52 patients aged ≥75 years who had attended our memory clinic based on their subjective memory complaints. None had a history of medication for hyperlipidemia. The Wechsler Memory Scale-Revised (WMS-R) was administered to all patients for the assessment of their memory function. Serum low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDLC), and triglyceride (TG) were measured for each patient. Surface-based morphometry (SBM) was performed for the calculation of each patient's cortical thickness and gyrification index based on structural MRI data. Our analyses revealed that the serum HDLC level was positively and significantly correlated with the WMS-R subtests of visual paired associates I/II and logical memory I (p < 0.05). The serum TG level was negatively correlated with the logical memory I subtest. The SBM results showed positive correlations between the serum HDLC level and the gyrification indices of the bilateral insular and frontal opercular cortices, and those two gyrification indices were positively correlated with the logical memory I and visual paired associates I/II. These results suggest that in these elderly patients, a high serum HDLC level was associated with not only preserved memory function but also gyrification of the insular and frontal opercular cortex. We conclude that elderly individuals' serum lipid markers should be carefully assessed in memory clinic settings, because serum HDLC may be a biomarker for memory function and cortical structure.

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“…Previous studies have shown that hyperglycemia in T2DM plays an important role in the development of cognitive dysfunction pointing to the conceivable impairment in the hippocampus which is an important anatomical basis and nerve center for learning, memory, and spatial orientation in the human brain. 14 Numerous clinical and fundamental studies have demonstrated discovery of cognition and memory dysfunction in both T1D and T2D, but the pathogenesis remains unclear. 15 In this study, we aimed to validate the hypothesis that GF is a more critical factor that would promote the neuron apoptosis and impaired hippocampus function than continuous hyperglycemia using an idiopathic T2DM animal model for the first time.…”

Section: Introductionmentioning

confidence: 99%

Acute glucose fluctuation induces inflammation and neurons apoptosis in hippocampal tissues of diabetic rats

Wang

Deng

Chen

et al. 2019

J of Cellular Biochemistry

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It is well‐recognized that glycemic disorders are leading causes of diabetic complications and acute fluctuation of blood glucose and reported more likely being related to oxidative stress, vasculopathy, and other diabetic complications than continuous hyperglycemia in patients with diabetic and animal models. To explore the hypothesis that acute glucose fluctuation (GF) aggravates inflammatory lesions and neuron apoptosis in the hippocampus of diabetic rats. Twenty female GK rats were randomly allocated into a glucose fluctuating group (GK‐GF) and a continuous hyperglycemia group (GK‐CHG) and 10 age‐matched female Wistar rats served as controls. GF was induced in the GK‐GF group by injection with glucose and insulin at different periods of time per day for 6 weeks. Body weight was determined weekly. At the end of the study, blood hemoglobin A1c (HbA1c) and serum lipids were measured. Serum and hippocampus interleukin 1β (IL‐1β), IL‐6, IL‐8, and tumor necrosis factor‐α (TNF‐α) were measured by enzyme‐linked immunosorbent assay and real‐time quantitative reverse transcription‐polymerase chain reaction (qRT‐PCR). Hippocampus Bcl‐2, Bax, Pten, fas, and myc were quantified by qRT‐PCR and Western blot analysis and Mirror Water Maze (MWM) test was performed. We successfully established an animal model with daily GF and a control model with CHG using GK diabetic rats. The GF and CHG rats showed lower weight gain during the 6‐week experimental period with no significant difference in the levels of serum lipids such as total triglyceride, total cholesterol, high‐density lipoprotein cholesterol, and low‐density lipoprotein cholesterol compared with the control rats at the end of the study. Meanwhile, the GF and CHG rats showed higher blood HbA1c levels than that of control rats. MWM trainings tests detected that glucose disorders in GF and CHG rats tend to present longer latencies, more cross times and longer path length compared with those of the control rats, indicating impaired the hippocampus‐regulated behavioral function such as spatial orientating and memory. Importantly, it was found that GF promoted the expression of TNF‐α and IL‐1β in the hippocampus of the GF rats while continuous hyperglycemia in CHG rats had little effect on that. Furthermore, both GF and CHG diabetic rats had abnormal expression of apoptosis‐associated genes in the hippocampus compared with control Wistar rats and neurons apoptosis in GF rats appears to be more severe than CHG rats. Overall, this study confirmed that GF is a more critical factor that would promote the neuron apoptosis and induce inflammation in the hippocampus than continuous hyperglycemia in diabetic animals, which shed new light on the importance of monitoring and administration of blood glucose in the prevention and therapy for diabetes.

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Glucose, relational memory, and the hippocampus

Cited by 13 publications

References 81 publications

Glucose improves object-location binding in visual-spatial working memory

Glucose improves object-location binding in visual-spatial working memory

High serum high-density lipoprotein-cholesterol is associated with memory function and gyrification of insular and frontal opercular cortex in an elderly memory-clinic population

Acute glucose fluctuation induces inflammation and neurons apoptosis in hippocampal tissues of diabetic rats

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