Neuropsychological Profiles of Children With Type 1 Diabetes 6 Years After Disease Onset

Department of Psychology, Royal Children's Hospital, Melbourne, Parkville, Victoria 3052, Australia.
Diabetes Care (Impact Factor: 8.42). 10/2001; 24(9):1541-6. DOI: 10.2337/diacare.24.9.1541
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To describe neuropsychological profiles and their relationship to metabolic control in children with type 1 diabetes 6 years after the onset of disease.
Children with type 1 diabetes (n = 90), aged 6-17 years, who had previously been assessed soon after diagnosis and 2 years later, were reevaluated 6 years after the onset of disease. Their neuropsychological profiles were compared with those of individuals in a community control group (n = 84), who had been assessed at similar intervals. Relationships between illness variables, such as age at the onset of disease and metabolic control history, and neuropsychological status were also examined.
Six years after onset of disease, children with type 1 diabetes performed more poorly than control subjects on measures of intelligence, attention, processing speed, long-term memory, and executive skills. Attention, processing speed, and executive skills were particularly affected in children with onset of disease before 4 years of age, whereas severe hypoglycemia was associated with lower verbal and full-scale intelligence quotient scores.
Neuropsychological profiles of children with type 1 diabetes 6 years after the onset of disease are consistent with subtle compromise of anterior and medial temporal brain regions. Severe hypoglycemia, particularly in very young children, is the most plausible explanation for neuropsychological deficits, but the contributory role of chronic hyperglycemia warrants further exploration.

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    • "In this sense, tight regulation of insulin levels seems to be mandatory to regulate central function. Central nervous system insulin receptors are highly expressed in regions associated to learning and memory, such as the cortex and the hippocampus and previous studies have reported that cognition impairment detected in type 1 diabetic children, might be related to hypoinsulinemia (Northam et al., 2001; Schoenle et al., 2002). Also, AD brains present lower insulin levels and higher insulin receptors density when compared to control patients (for review see (El Khoury et al., 2014)). "
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    ABSTRACT: Aging remains the main risk factor to suffer Alzheimer's disease (AD), though epidemiological studies also support that type 2 diabetes (T2D) is a major contributor. In order to explore the close relationship between both pathologies we have developed an animal model presenting both AD and T2D, by crossing APP/PS1 mice (AD model) with db/db mice (T2D model). We traced metabolic and cognitive evolution before T2D or AD pathology is present (4 weeks of age), when T2D has debuted but no senile plaques are present (14 weeks of age) and when both pathologies are well established (26 weeks of age). APP/PS1xdb/db mice showed an age-dependent synergistic effect between T2D and AD. Significant brain atrophy and tau pathology were detected in the cortex by 14 weeks, that spread to the hippocampus by 26 weeks of age. Severe cognitive impairment was also detected as soon as at 14 weeks of age. Interestingly, in APP/PS1xdb/db mice we observed a shift in Aβ soluble/insoluble levels, and whereas more toxic soluble species were favoured, senile plaques (SP) were reduced. An overall increase of microglia activation was observed in APP/PS1xdb/db mice. We also found exacerbated hemorrhagic burden in APP/PS1xdbd/db mice, suggesting that blood brain barrier alterations may be responsible for the early pathological features observed. Moreover, metabolic parameters can predict many of these alterations, supporting a role for T2D in AD pathology. This new model provides a relevant tool to further explore the relationship between T2D, AD and vascular implications, offering the possibility to assess therapeutic approaches, that by improving T2D metabolic control could delay or prevent AD pathology. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Psychoneuroendocrinology 07/2015; 62:69-79. DOI:10.1016/j.psyneuen.2015.07.606 · 4.94 Impact Factor
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    • "Lastly, although it is not the focus of this review, another variable to be considered is the possibility of hypoglycemic episodes occurring within a context of hyperglycemia resulting from inappropriate insulin treatment, since it must be considered that acute [119, 120] and chronic [121–124] hyperglycemia, gestational hyperglycemia [125], and glycemic variability [126, 127] can also contribute towards the reduction of cognitive performance, since the excess of glucose can lead to brain damage regardless of the occurrence of IIH [128]. Moreover, studies in laboratory animals suggest that hyperglycemia after hypoglycemia, a condition frequent in poorly controlled diabetes, would lead to more neuronal death than isolated hypoglycemia [129]. "
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    ABSTRACT: This paper provides an overview of insulin-induced hypoglycemia as a triggering factor of cognitive deficit in children with type 1 diabetes mellitus. For this purpose, databases from 1961 to 2013 were used with the objective of detecting the primary publications that address the impact of hypoglycemia on cognitive performance of diabetic children. The results obtained from experimental animals were excluded. The majority of studies demonstrated that the cognitive deficit in diabetic children involves multiple factors including duration, intensity, severity, and frequency of hypoglycemia episodes. Additionally, age at the onset of type 1 diabetes also influences the cognitive performance, considering that early inception of the disease is a predisposing factor for severe hypoglycemia. Furthermore, the results suggest that there is a strong correlation between brain damage caused by hypoglycemia and cognitive deterioration. Therefore, a more cautious follow-up and education are needed to impede and treat hypoglycemia in children with diabetes mellitus.
    The Scientific World Journal 03/2014; 2014:616534. DOI:10.1155/2014/616534 · 1.73 Impact Factor
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    • "E-mail: White, 1997; Hershey, Lillie, Sadler, & White, 2003, 2004; Hershey et al., 2005; Lin et al., 2010; Naguib, Kulinskaya, Lomax, & Garralda, 2009; Northam et al., 2001; Perantie et al., 2008; Rovet & Ehrlich, 1999) or brain changes (Ferguson et al., 2003; Haumont, Dorchy, & Pelc, 1979; Hyllienmark, Maltez, Dandenell, Luvigsson, & Brismar, 2005; Musen et al., 2006; Northam et al., 2009; Perantie et al., 2011, 2007; Perros, Deary, Sellar, Best, & Frier, 1997). There is preliminary evidence to suggest that this association can be detected quite early in young children and youth with recent onset diabetes (Aye et al., 2011). "
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    ABSTRACT: The aim of this study was to assess cognitive functioning in children with type 1 diabetes (T1D) and examine whether glycemic history influences cognitive function. Neuropsychological evaluation of 216 children (healthy controls, n = 72; T1D, n = 144) ages 4-10 years across five DirecNet sites. Cognitive domains included IQ, Executive Functions, Learning and Memory, and Processing Speed. Behavioral, mood, parental IQ data, and T1D glycemic history since diagnosis were collected. The cohorts did not differ in age, gender or parent IQ. Median T1D duration was 2.5 years and average onset age was 4 years. After covarying age, gender, and parental IQ, the IQ and the Executive Functions domain scores trended lower (both p = .02, not statistically significant adjusting for multiple comparisons) with T1D relative to controls. Children with T1D were rated by parents as having more depressive and somatic symptoms (p < .001). Learning and memory (p = .46) and processing speed (p = .25) were similar. Trends in the data supported that the degree of hyperglycemia was associated with Executive Functions, and to a lesser extent, Child IQ and Learning and Memory. Differences in cognition are subtle in young children with T1D within 2 years of onset. Longitudinal evaluations will help determine whether these findings change or become more pronounced with time. (JINS, 2014, 20, 238-247).
    Journal of the International Neuropsychological Society 02/2014; 20(2):238-47. DOI:10.1017/S1355617713001434 · 2.96 Impact Factor
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