Biomedical subjects

Claude Messier

Publications and source records attributed to Claude Messier.

16 recordsLinked to original sources

PubMed2006

The effects of a high-fat, high-fructose, and combination diet on learning, weight, and glucose regulation in C57BL/6 mice.

The objective of the study was to determine the effects of a high-fructose diet, a high-fat diet and a combination high-fructose/high-fat diet on weight gain, blood glucose regulation, and cognitive function in C57BL/6 mice. Thirty-eight male mice aged 7 weeks were placed on one of four different diets for 3 months: standard chow and water (n=8), standard diet and access to a fructose solution as the only intake of water (n=8), high-fat diet and water (n=11), and high-fat diet and fructose solution (n=11). Weights were measured 10 times over a 3-month period. Blood glucose regulation was measured using a glucose tolerance test. Cognitive testing consisted of learning an operant bar-pressing task and was performed in the absence of fructose intake. At the end of the experiment, the density of the fructose-specific glucose transporter GLUT5 was measured in the hippocampus, frontal cortex, sensori-motor cortex and cerebellum. The high-fat and the combined high-fat/high-fructose groups gained significantly more weight than the control group. The high-fat group and combined group had significantly higher levels of blood glucose than the control group. The high-fructose group learned the operant task faster than the control group, but the high-fat/high-fructose group was not different from control indicating that the facilitative effect of prior fructose intake was abolished when a high-fat diet was added. Addition of fructose to the diet did not result in an increase of brain GLUT5 density suggesting that the learning improvement were not dependent on plastic upregulation of GLUT5 fructose transporter. The results show that, contrary to high-fat diets, access to fructose in mice did not lead to increased weight and impaired glucose tolerance. The present experiment confirm the deleterious impact of high-fat diets on glucose regulation and weight but suggest that high-fructose diets, contrary to what has been observed in hamsters, do not have the same effect.

Animals↗

PubMed2006

Longitudinal study of the effects of a high-fat diet on glucose regulation, hippocampal function, and cerebral insulin sensitivity in C57BL/6 mice.

Although the increasing rate of obesity has stimulated interest in the effects of diet composition on peripheral systems, comparatively little work has been done to examine effects upon the brain. A diet high in fat is one of many factors that can promote obesity, and previous research has shown that such a diet can produce learning and memory impairment in rodents. In the present study, C57BL/6 mice were placed on either a high-fat (45% kcal fat) or regular (5% kcal fat) diet, and examined at different points during the subsequent year. The high-fat diet led to increased weight gain, significant impairment in glucoregulation, and altered insulin-mediated signaling within the hippocampus, an area of the brain believed to be important for the acquisition of memory. Following ten months on either diet, synaptic function in ex vivo hippocampal slices was examined, and neither stimulus-response curves nor electrically induced long-term potentiation were found to be different. As well, performance in the Morris water maze, a hippocampal-dependent test of spatial memory, was not influenced by diet. However, mice consuming a high-fat diet failed to perform an operant bar-pressing task, indicating a significant impairment to procedural learning and consolidation processes. Despite causing broad peripheral changes in C57BL/6 mice, consuming a large proportion of calories from saturated fat had only a limited effect upon learning and memory, which suggests that certain aspects of brain function are selectively vulnerable to the influences of diet.

Analysis of Variance↗

PubMed2006

Exploratory factor analysis of neuropsychological tests and their relationship to the Brown-Peterson task.

The interference condition of the Brown-Peterson task and the auditory consonant trigrams test was designed to evaluate working memory in that it required a division of attentional processes to complete two cognitive tasks. However, the specific cognitive functions contributing to the performance of this interference task have yet to be determined. The objective of this study was to determine what other tasks are comparable to the Brown-Peterson task and conduct an exploratory factor analysis that included the measures from the Brown-Peterson task and other neuropsychological measures. A neuropsychological battery was administered to younger participants (n=107, mean age=20.83) and older participants (n=93, mean age=70.14). Factor analysis yielded a two-factor solution. Performance after the intervening serial subtraction task loaded on an auditory/visual working memory and complex attention factor and had common loadings with working memory subtests of the WAIS-III and the spatial span subtest of the WMS-III. Results suggest that the performance after the intervening serial subtraction task evaluates dual information processing, complex attention, and working memory.

Adolescent↗

PubMed2005

Impact of impaired glucose tolerance and type 2 diabetes on cognitive aging.

Type 2 diabetes is becoming increasingly common in most Westernized countries and it now occurs at a younger age. There are pathologies associated with diabetes, mostly systemic ones. However, a growing number of studies is also showing that diabetes is associated with impaired cognitive processes in older adults and hasten the progression to dementia. The most common cognitive deficits are decreases in processing speed and verbal memory; these may extend to other aspects of cognition with increasing age. The link between diabetes and cognitive decline is obscured by depression, hypertension, as well as cardio- and cerebrovascular diseases, all of which occur to varying degrees in diabetic patients. A few studies indicate that controlling blood glucose with anti-diabetic treatments may help prevent the cognitive decline in diabetic patients before they are 70 years old. After that age, diabetes appears to produce faster cognitive decline and may increase the occurrence of pathological changes associated with vascular dementia or Alzheimer's disease.

Aging↗

PubMed2005

Longitudinal evaluation of memory performance and peripheral neuropathy in the Ins2C96Y Akita mice.

Ins2C96Y Akita mice represent a model of spontaneous early-onset diabetes mellitus, expressing a mutant non-functional isoform of insulin. These mice are characterized by a reduced number of pancreatic beta cells resulting in hypoinsulinemia and hyperglycemia. We obtained longitudinal measures of morning fasting blood glucose levels and gait performance. Sciatic nerve electrophysiology was also performed and the performance of these mice on spatial memory tasks was measured longitudinally. We observed a progressive increase in fasting blood glucose levels that was proportionally associated with increased gait disturbances. Diabetes induced a decrease in the sensory nerve conduction velocity up to the age of 40 weeks. Glucose transporter (GLUT) 3 levels were reduced in the hippocampus of the aged Ins2C96Y Akita mice. However, we failed to detect any significant deficits during reference, reversal or probe tests in the Morris water maze or in a spontaneous alternation task up to the age of 34 weeks old. We found that, up to the age of 34 weeks old, uncontrolled hyperglycemia produced peripheral neuropathy and reduced hippocampal GLUT3 levels in the absence of any effect on spatial memory processing.

Age Factors↗

PubMed2005

The role of insulin, insulin growth factor, and insulin-degrading enzyme in brain aging and Alzheimer's disease.

Most brain insulin comes from the pancreas and is taken up by the brain by what appears to be a receptor-based carrier. Type 2 diabetes animal models associated with insulin resistance show reduced insulin brain uptake and content. Recent data point to changes in the insulin receptor cascade in obesity-related insulin resistance, suggesting that brain insulin receptors also become less sensitive to insulin, which could reduce synaptic plasticity. Insulin transport to the brain is reduced in aging and in some animal models of type 2 diabetes; brain insulin resistance may be present as well. Studies examining the effect of the hyperinsulinic clamp or intranasal insulin on cognitive function have found a small but consistent improvement in memory and changes in brain neuroelectric parameters in evoked brain potentials consistent with improved attention or memory processing. These effects appear to be due to raised brain insulin levels. Peripheral levels of Insulin Growth Factor-1 (IGF-I) are associated with glucose regulation and influence glucose disposal. There is some indication that reduced sensitivity to insulin or IGF-I in the brain, as observed in aging, obesity, and diabetes, decreases the clearance of Abeta amyloid. Such a decrease involves the insulin receptor cascade and can also increase amyloid toxicity. Insulin and IGF-I may modulate brain levels of insulin degrading enzyme, which would also lead to an accumulation of Abeta amyloid.

Aging↗

PubMed2004

Glucose improvement of memory: a review.

The memory-improving action of glucose has now been studied for almost 20 years and the study of this phenomenon has led to a number of important developments in the understanding of memory, brain physiology and pathological consequences of impaired glucose tolerance. Glucose improvement of memory appears to involve two optimal doses in animals (100 mg/kg and 2 g/kg) that may correspond to two physiological mechanisms underlying glucose effects on memory. In humans, there have been few dose-response studies so the existence of more than one effective dose in humans is uncertain. Many tasks are facilitated by glucose in humans but tasks that are difficult to master or involve divided attention are improved more readily that easier tasks. There are a number of hypotheses about the physiological bases of the memory-improving action of glucose. Peripheral glucose injections could alleviate localized deficits in extracellular glucose in the hippocampus. These localized deficits may be due to changes in glucose transporters in that structure. Because certain neurotransmitters such as acetylcholine are directly dependent on the glucose supply for their synthesis, glucose is thought to facilitate neurotransmitter synthesis under certain circumstances. However, these hypotheses cannot account for the specificity of the dose-response effect of glucose. A number of peripheral mechanisms have been proposed, including the possibility that glucose-sensitive neurons in the brain or in the periphery may serve as glucose sensors and eventually produce neural changes that would facilitate memory processing. These latter results could be of importance because the mechanisms they suggest appear to be dose-dependent, a crucial characteristic to explain the dose-dependent effects of glucose. There may be an advantage to develop hypotheses that include both peripheral and central actions of glucose. There is evidence that impaired glucose regulation is associated with impaired cognition, particularly episodic memory. This impairment is minimal in young people but increases in older people (65 years and over) where it may compound other aging processes leading to reduced brain function. A small number of studies showed that glucose improvement of memory is associated with poor glucose regulation although this may not be the case for diabetic patients. Results of a few studies also suggest that drug treatments that improve glucose regulation also produce cognitive improvement in diabetic patients.

Animals↗

PubMed2004

Explicit and objective scoring criteria for the taylor complex figure test.

The Rey and Taylor figures are two constructional and visual memory tests used interchangeably. The purpose of this study was to develop a scoring system for the Taylor figure based on the explicit guidelines established by Meyers and Meyers (1995) for the Rey figure. Younger (n = 97; mean age = 21 years) and older (n = 61; mean age = 72 years) participants' performance on the Taylor figure was scored according to the proposed scoring system and the original scoring system devised by Taylor (1989). Both scoring systems yielded comparable scores on the Taylor figure as well as comparable patterns of validity and good interrater reliabilities (0.85-0.98). Although the present system does not further improve scoring reliability, it renders both tests similar in methodology and simplifies training to evaluate the two figures. The present study also reveals the limitations of the use of the Taylor and the Rey in test-retest situations but suggests that administering the Taylor first would improve the comparability of the two figures in a test-retest situation.

Adult↗

PubMed2004

The relationship between impaired glucose tolerance, type 2 diabetes, and cognitive function.

The present review integrates findings of published studies that have evaluated the cognitive function of treated and untreated type 2 diabetic patients and provides a detailed overview of the neuropsychological assessments conducted. Cognitive deficits are observed in older people with glucose intolerance or untreated diabetes but these deficits appear to be attenuated by treatments that improve glycemic control. Cognitive decrements in treated type 2 diabetic patients are most consistently observed on measures of verbal memory (35% of the measures) and processing speed (45% of the measures) while preserved function is observed on measures of visuospatial, attention, semantic and language function. Some studies suggest that deficits in cognitive functions are associated with poorer glycemic control. A number of other factors, such as depression, cardiovascular and cerebrovascular disease, increase these deficits. We conclude that, in diabetic patients who achieve and maintain good glycemic control, type 2 diabetes only has a small impact on cognitive functions before the age of 70 years. However, early onset of type 2 diabetes, poor glycemic control and the presence of micro- and macrovascular disease may interact to produce early cognitive deficits. In older adults (70 years and over), diabetes likely interacts with other dementing processes such as vascular disease and Alzheimer's disease to hasten cognitive decline.

Cognition↗

PubMed2004

The relationships between atherosclerosis, heart disease, type 2 diabetes and dementia.

Type 2 diabetes in the elderly is associated with increased incidence of vascular disease, particularly, atherosclerosis of large blood vessels. Together with other risk factors such as dyslipidemia, atherosclerosis increases the risk for coronary heart disease and stroke. Most studies that have examined the impact of type 2 diabetes and other heart disease risk factors on cognitive functions do not provide evidence that heart disease risk factors (with the possible exception of triglycerides) further increase the likelihood of observing cognitive deficits in diabetic patients. However, none of these studies used imaging techniques to evaluate atherosclerosis or evidence of cerebrovascular disease, such as infarctions. The few studies that have included brain imaging suggest that evidence of cerebrovascular disease further increases the risk for dementia in diabetic patients. The results of longitudinal studies suggest that diabetes is an independent risk factor for cognitive decline and dementia. The pattern of neuropsychological performance observed in type 2 diabetic patients appears to be the result of multiple interacting processes developing over time. In addition to the detrimental effects of protracted impaired glucose regulation on the central nervous system, type 2 diabetes pathology also encompasses the detrimental effects of associated complications such as cerebrovascular disease, which is likely the main cause of the observed processing speed/reaction time decrements.

Causality↗

PubMed2004

Addressing the differences in speed of processing of the intervening calculation task on the modified Brown-Peterson task.

The Modified Brown-Peterson task (MBPT) is a task of divided attention and working memory that requires central executive functioning. It is a variant of the Brown-Peterson technique and is useful for studying short-term retention of information. It involves the recall of auditory information under conditions of interference (i.e., counting backwards). Previous research has not addressed the effect of individual differences in processing speed for the intervening calculations. In a sample of 81 young participants, we determined whether the number of correct calculations performed is related to recall performance on the MBPT. Results indicated that the number of calculations performed was not significantly related to the recall performance on the MBPT. Rather, the number of correct calculations performed during the interference task of the MBPT was associated with arithmetic ability as measured by the arithmetic subtest of the Adult Intelligence Scale-III (Wechsler, 1997). These results suggest that the subtractions in the MBPT create interference regardless of mathematical ability or speed at which the subtractions are performed during the interference condition of the MBPT task. This observation suggests that the results on this test are independent of mathematical ability and represent a useful measure of working memory.

Adult↗

PubMed2003

Effect of age and glucoregulation on cognitive performance.

Non-insulin dependent diabetes mellitus (NIDDM) has been associated with a number of physiological consequences including neuropathy, retinopathy and incidence of vascular disease. Recently, several authors reviewed studies that suggested that NIDDM is associated with cognitive impairments leading to a higher incidence of dementia. In the present experiment, we measured cognitive function in 57 healthy male and female non-diabetic older participants who ranged in age from 55 to 84. Various biological measures were obtained including a glucose tolerance test during which glucose and insulin were measured. Participants were separated into better and poorer glucoregulatory groups on the basis of their blood glucose levels during the tolerance test. Participants were evaluated twice, once after drinking a saccharin solution and on another occasion after drinking a glucose solution (50 g). Older participants (72 years and over) with poorer glucoregulation had the worse performance in tests evaluating working memory, verbal declarative memory and executive functions. Glucose administration appeared to only attenuate the decrements observed in the saccharin condition in the older participants for some of the tests. These results suggest that cognitive functions may be impaired before glucoregulatory impairment reaches levels consistent with a type II diabetes diagnosis.

Age Factors↗

PubMed2003

Diabetes, Alzheimer's disease and apolipoprotein genotype.

Non-insulin dependent diabetes mellitus (NIDDM) has been associated with a number of physiological consequences including neuropathy, retinopathy and incidence of vascular disease. Recently, several authors reviewed studies that suggested that NIDDM is associated with cognitive impairments leading to a higher incidence of dementia and Alzheimer's disease. The current diagnostic practices that typically exclude from an AD diagnostic any patients with suspected vascular dementia, makes it very hard to resolve this issue and likely result in an underestimation of the number of people with Alzheimer's disease and diabetes. When people with cerebrovascular disease are included, diabetes is associated with an increased risk for Alzheimer's disease. Studies that have examined peripheral glucoregulation in Alzheimer's disease are not consistent but some show small to moderate impairments in insulin sensitivity. One recent study suggest that in people that have both diabetes and an ApoE4 allele, the risk of developing Alzheimer's disease is more than double the risk of people with an ApoE4 allele without diabetes. Although diabetes does not produce any of the usual brain pathology associated with Alzheimer's disease, one study has shown that diabetes dramatically increases the amyloid deposition and neurofibrillary tangles in people with the ApoE4 genotype. Taken together, the data available suggest that diabetes is probably a risk factor for Alzheimer's disease mainly through the cerebrovascular disease diabetes causes. In people with other risk factors such as ApoE4 allele, diabetes appears to lead to a more dramatic increase in Alzheimer's disease pathology.

Alzheimer Disease↗

PubMed2003

Comparing the Rey and Taylor complex figures: a test-retest study in young and older adults.

The Rey and Taylor figures, two visual perception and memory tests, are not equivalent in terms of their difficulty. The purpose of this study was to examine factors such as age, gender, order of administration, copy time, and copy score that could account for the variability in recall performance. Copy score was shown to be the best overall predictor of recall. Younger participants recalled more units than older participants on both complex figures. Furthermore, older participants appeared to benefit more from the presentation of the Taylor figure first compared to when they were presented with the Rey figure first. The present findings reveal the importance of test order and provide equations that can be used to facilitate the comparison of scores derived from the two figures in test-retest situations.

Adult↗

PubMed2002

Infralimbic kappa opioid and muscarinic M1 receptor interactions in the concurrent modulation of anxiety and memory.

RATIONALE: Spontaneous working memory and anxiety-like behaviour can be concurrently influenced following kappa opioid or muscarinic M1 antagonist infusions in the infralimbic (IL) area of the ventromedial prefrontal cortex (vmPFC) in CD-1 mice. Further dose-response analyses of our previous norBNI and pirenzepine data revealed significant dose x drug interactions on trial-1 and -2 anxiety-related elevated plus-maze indices. These data prompted us to evaluate the effects of simultaneous IL norBNI/pirenzepine infusions on anxiety and spontaneous working memory. OBJECTIVE: The present study sought to evaluate whether (a) our previously reported anxiogenic and working memory disruptive effects of norBNI, and anxiolytic and working memory disruptive effects of pirenzepine data could be replicated using the most effective dose (10 nmol) of each drug and (b) IL infusions of mixed kappa/M1 receptor inhibitor drugs might interactively influence these cognitive, behavioural processes. METHODS: Anxiety was evaluated in the elevated plus maze, and spontaneous alternation memory was evaluated in the Y-maze following pirenzepine, norBNI or two levels of norBNI/pirenzepine drug mix infusions in the IL vmPFC. RESULTS: Pretreatment with the M1 antagonist pirenzepine was anxiolytic in trial 1 (10 nmol) and trial 2 (no-injection) in the elevated plus maze 24 h later, and disrupted alternation performance and some aspects of attention in the Y-maze. Pretreatment with the kappa antagonist norBNI was anxiogenic in trial 1 (10 nmol) and trial 2 (no-injection) in the elevated plus maze 24 h later, and also disrupted alternation performance and some aspects of attention in the Y-maze. The norBNI-10 nmol/pirenzepine-10 nmol mixed drug infusion was somewhat anxiogenic in trial 1, exerted no carry-over effects in trial 2 in the elevated plus maze, and disrupted alternation memory and some aspects of attention in the Y-maze. The norBNI-5 nmol/pirenzepine-10 nmol drug mix had no effect on trial-1 or -2 anxiety measures in the elevated plus maze, yet also disrupted Y-maze spontaneous memory performance. CONCLUSIONS: (1) The effects of IL infusions of norBNI or pirenzepine (10 nmol/0.5 microl) alone on anxiety-like behaviour and aversive learning and memory in the elevated plus-maze replicated previously reported data. (2) Mixed M1/kappa receptor inhibition in the IL cortex exerted counteractive effects on anxiety-like behaviour and aversive learning in the elevated plus maze. (3) Mixed M1/kappa receptor inhibition appeared to exert additive disruptive effects on alternation performance and aspects of attention related to active working memory in the Y-maze.

Animals↗

PubMed2002

Impact of peripheral glucoregulation on memory.

Impaired glucoregulation is associated with neuropsychological deficits, particularly for tests that measure verbal declarative memory performance in older diabetic patients. The performances of 74 undergraduate students (mean age = 21 years) on several verbal declarative measures, including immediate and delayed paragraph recall, verbal free recall, and order reconstruction tasks, were correlated with glucoregulatory indices. The indices were obtained from glucose and insulin levels after a 75-g glucose load. In general, higher blood glucose levels were associated with poorer performance on all memory tests. Glucose ingestion did not interact with performance except on the most difficult task. Subjects with poorer glucoregulation showed higher evoked glucose and insulin, suggestive of a mild glucose intolerance accompanied by mild insulin insensitivity. Results suggest that poor peripheral glucoregulation has an impact on central nervous system functions.

Adult↗