Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 11678970

Cognitive function and information processing in type 2 diabetes.

R Cosway·M W Strachan·A Dougall·B M Frier·I J Deary
View original source ↗Export metadata ↓

Abstract

AIMS: To determine whether uncomplicated Type 2 diabetes is associated with impairment of cognitive function and information processing ability. METHODS: Thirty-eight participants with uncomplicated Type 2 diabetes and 38 non-diabetic controls were studied. The two groups were comparable for age and premorbid intellectual ability, and did not have other medical disorders likely to affect cognitive function. An extensive battery of tests was administered which assessed different levels and domains of cognitive functions including verbal and visual memory, executive function, general mental ability and efficiency of information processing. RESULTS: No significant differences were found between the diabetic and control groups on any measure of cognitive function or information processing. The performance on these tests was not associated with recent glycaemic control (assessed by HbA1c). Duration of diabetes, however, correlated significantly with poorer performance on several measures of verbal memory. CONCLUSIONS: The results of the present study suggest that some aspect of Type 2 diabetes (as indexed by the estimated duration of the disorder) does relate significantly to cognitive function within the group with diabetes. However, other diabetes-related factors, such as macrovascular disease, hypertension and depression, may contribute more to previously observed cognitive decrements in Type 2 diabetes.

Explore related subjects

Age of OnsetAlcohol DrinkingChoice BehaviorCognitionDiabetes Mellitus, Type 2Educational StatusEvoked PotentialsFemaleGlycated HemoglobinHumansHypoglycemic AgentsMaleMemoryMental ProcessesMiddle AgedMotor ActivityReaction TimeReadingReference ValuesTime FactorsVision, OcularWechsler ScalesClinical TrialComparative StudyControlled Clinical TrialJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R Cosway, M W Strachan, A Dougall, B M Frier, I J Deary. 2001. Cognitive function and information processing in type 2 diabetes.. https://doi.org/10.1046/j.1464-5491.2001.00577.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2012

Role of genes linked to sporadic Alzheimer's disease risk in the production of β-amyloid peptides.

Alzheimer's disease (AD) is characterized by the presence of toxic protein aggregates or plaques composed of the amyloid β (Aβ) peptide. Various lengths of Aβ peptide are generated by proteolytic cleavages of the amyloid precursor protein (APP). Mutations in many familial AD-associated genes affect the production of the longer Aβ42 variant that preferentially accumulates in plaques. In the case of sporadic or late-onset AD, which accounts for greater than 95% of cases, several genes are implicated in increasing the risk, but whether they also cause the disease by altering amyloid levels is currently unknown. Through loss of function studies in a model cell line, here RNAi-mediated silencing of several late onset AD genes affected Aβ levels is shown. However, unlike the genes underlying familial AD, late onset AD-susceptibility genes do not specifically alter the Aβ42/40 ratios and suggest that these genes probably contribute to AD through distinct mechanisms.

Age of Onset↗
PubMed2012

Clinical and biomarker changes in dominantly inherited Alzheimer's disease.

BACKGROUND: The order and magnitude of pathologic processes in Alzheimer's disease are not well understood, partly because the disease develops over many years. Autosomal dominant Alzheimer's disease has a predictable age at onset and provides an opportunity to determine the sequence and magnitude of pathologic changes that culminate in symptomatic disease. METHODS: In this prospective, longitudinal study, we analyzed data from 128 participants who underwent baseline clinical and cognitive assessments, brain imaging, and cerebrospinal fluid (CSF) and blood tests. We used the participant's age at baseline assessment and the parent's age at the onset of symptoms of Alzheimer's disease to calculate the estimated years from expected symptom onset (age of the participant minus parent's age at symptom onset). We conducted cross-sectional analyses of baseline data in relation to estimated years from expected symptom onset in order to determine the relative order and magnitude of pathophysiological changes. RESULTS: Concentrations of amyloid-beta (Aβ)(42) in the CSF appeared to decline 25 years before expected symptom onset. Aβ deposition, as measured by positron-emission tomography with the use of Pittsburgh compound B, was detected 15 years before expected symptom onset. Increased concentrations of tau protein in the CSF and an increase in brain atrophy were detected 15 years before expected symptom onset. Cerebral hypometabolism and impaired episodic memory were observed 10 years before expected symptom onset. Global cognitive impairment, as measured by the Mini-Mental State Examination and the Clinical Dementia Rating scale, was detected 5 years before expected symptom onset, and patients met diagnostic criteria for dementia at an average of 3 years after expected symptom onset. CONCLUSIONS: We found that autosomal dominant Alzheimer's disease was associated with a series of pathophysiological changes over decades in CSF biochemical markers of Alzheimer's disease, brain amyloid deposition, and brain metabolism as well as progressive cognitive impairment. Our results require confirmation with the use of longitudinal data and may not apply to patients with sporadic Alzheimer's disease. (Funded by the National Institute on Aging and others; DIAN ClinicalTrials.gov number, NCT00869817.).

Age of Onset↗
PubMed2002

Identification of a presymptomatic molecular phenotype in Hdh CAG knock-in mice.

The hallmark striatal neurodegeneration of Huntington's disease (HD) is first triggered by a dominant property of the expanded glutamine tract in mutant huntingtin that increases in severity with glutamine size. Indeed 111-glutamine murine huntingtin leads to a dominant cascade of phenotypes in Hdh(Q111) mice, although these abnormalities are not manifest in Hdh(Q50) mice, with 50-glutamine mutant protein. Therefore, to identify phenotypes that might reflect events closer to the fundamental trigger mechanism, and that can be measured as a consequence of adult-onset HD mutant huntingtin, we have screened for altered expression of genes conserved in evolution, which are likely to encode essential proteins. Probes generated from Hdh(Q111) homozygote and wild-type striatal RNAs were hybridized to human gene segments on filter arrays, disclosing a mutant-specific increase in hybridization to Rrs1, encoding a ribosomal protein. Subsequent, quantitative RT-PCR assays demonstrated increased Rrs1 mRNA from 3 weeks of age in homozygous and heterozygous Hdh(Q111) striatum and increased Rrs1 mRNA expression with a single copy's worth of 50-glutamine mutant huntingtin in Hdh(Q50) striatum. Moreover, quantitative RT-PCR assays for the human homologue demonstrated elevated Rrs1 mRNA in HD compared with control postmortem brain. These findings, therefore, support a chronic impact of mutant huntingtin on an essential ribosomal regulatory gene to be investigated for its role very early in HD pathogenesis.

Age of Onset↗