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PubMedDate not supplied

Why is learning and memory dysfunction in Type 2 diabetes limited to older adults?

Review of the literature on the cognitive correlates and consequences of Type 2 diabetes reveals two very intriguing findings. Not only are verbal learning and memory skills most likely to be disrupted as compared to other cognitive skills (e.g. attention, executive function; psychomotor efficiency), but these mnestic deficits appear to be restricted to individuals with diabetes who are older than 60-65 years of age. Middle-aged adults with either Type 2 or Type 1 diabetes are apparently protected insofar as researchers have only infrequently reported learning and memory impairments in that age group. Why do older adults have such an increased risk of diabetes-associated memory dysfunction? In our view, this phenomenon is a consequence of a synergistic interaction between diabetes-related metabolic derangements and the structural and functional changes occurring in the central nervous system (CNS) that are part of the normal ageing process. To critically evaluate that possibility, we summarise what is known about learning and memory dysfunction in the adult with diabetes, examine the extent to which chronic hyperglycaemia may adversely affect the integrity of the CNS, and selectively review the literature on age-associated changes in brain morphology and cognitive function, paying special attention to the threshold theory of cognitive impairment.

Adult↗
PubMed1993

Verbal learning and/or memory improves with glycemic control in older subjects with non-insulin-dependent diabetes mellitus.

OBJECTIVE: To determine whether cognitive function improves with improved glycemic control in older subjects with non-insulin-dependent diabetes (NIDDM). We hypothesized that with improved glycemic control: 1) learning and memory, 2) attention, and 3) complex perceptual-motor function would improve, but that 4) simple perceptual-motor function would not. DESIGN: Non-randomized control trial. SETTING: Aging Study Unit, Department of Veterans Affairs Medical Center. SUBJECTS: Thirty subjects with NIDDM; 17 on oral hypoglycemic agents; 13 untreated at study entry. Thirteen normal controls. INTERVENTION: Subjects on oral hypoglycemic agents were taken off medications. After 1 month, they and previously untreated subjects began treatment with glipizide. Dose was titrated up weekly until fasting plasma glucose was less than 7.8 mmol/L or maximal dose (40 mg/day). Controls received no medication. MEASUREMENTS: Fasting plasma glucose (FPG), glycated hemoglobin, and measures of cognitive function in four general categories: 1) learning and memory, 2) ability to sustain attention, 3) complex perceptual-motor function, and 4) simple perceptual-motor function. All were evaluated in subjects with NIDDM at baseline (T1), after 1-month washout (T2), and after 2 (T3) and 4 months (T4) of optimal glycemic control or maximal dose. Controls were evaluated at the same intervals. RESULTS: FPG and glycated hemoglobin rose in previously treated subjects from T1 to T2 (9.4 +/- SEM 0.4 to 14.7 +/- 0.7 mmol/L and 10.9 +/- 0.7% to 12.2 +/- 0.6%, respectively) but were unchanged in previously untreated subjects (11.3 +/- 0.6 to 11.8 +/- 0.9 mmol/L and 10.9 +/- 0.7% to 11.7 +/- 0.7%). With glipizide treatment, there was a decrease in FPG level at T3 (9.4 +/- 0.5 mmol/L in previously treated, 6.9 +/- 0.4 mmol/L in previously untreated), which persisted at T4. Glycated hemoglobin fell similarly. FPG and glycated hemoglobin were unchanged in controls. As hypothesized, learning and memory improved over time with treatment in both groups of subjects but was unchanged in controls (P < 0.05). Detailed analysis indicated that the improvement occurred primarily in the learning of verbal material. Contrary to hypothesis, attention and complex perceptual-motor function did not show improvement. As expected, simple perceptual-motor function did not show any improvement with treatment. CONCLUSIONS: The results are consistent with previous findings that poor glycemic control in older subjects with NIDDM is associated with decreased cognitive functioning, and suggest that verbal learning and memory may improve with improved glycemic control.

Aged↗
PubMed1998

Intracerebroventricular administration of streptozotocin causes long-term diminutions in learning and memory abilities and in cerebral energy metabolism in adult rats.

Drastic abnormalities have been demonstrated to occur in cerebral glucose and energy metabolism in sporadic Alzheimer's disease, pointing to a primary disturbance in neuronal insulin and insulin receptor signal transduction and contributing to the causation of dementia. The compound streptozotocin (STZ) is known to inhibit insulin receptor function. The study was designed to investigate whether intracerebroventricularly (icv) applied STZ would inhibit neuronal insulin receptor function and would induce changes in both behavior and neuronal energy metabolism. Adult rats with icv-injected STZ developed long-term and progressive deficits in learning, memory, and cognitive behavior, indicated by decreases in working and reference memory in the holeboard task and the passive avoidance paradigm, along with a permanent and ongoing cerebral energy deficit. This animal model may be appropriate for investigations related to sporadic Alzheimer's dementia.

Adenosine Diphosphate↗
PubMed2001

[Heterochronic effects of neurotrophic factors in neurochemical organization of learning and memory in the adult organism].

Following elaboration of long-term habituation to a startle-response, antibodies to neurotrophic factor protein S100b exerted selective and dose-dependent influence on different learning processes and memory of learned behavioural patterns in adult rats. S100b increased at all stages of behavioural skill development in hippocampus, hypothalamus, frontal cortex, cerebellar hemispheres and vermis, basal ganglia.

Acoustic Stimulation↗
PubMed2004

A novel version of the 8-arm radial maze: effects of cerebral ischemia on learning and memory.

A novel version of the 8-arm radial maze task was developed to quantify spatial learning and memory in rats subjected to transient cerebral ischemia (TCI) using the 4-VO model. This maze uses the rat's natural behavior of avoiding open, illuminated areas, and preference for a darkened, enclosed shelter. Ischemic rats were required to escape from the central area into the darkened goal box. Ischemia was induced before or after training to examine its influence on acquisition and retention of cognition, respectively. During the acquisition test, latency of ischemic rats to find the goal box, and working memory performance were significantly impaired (P < 0.005-0.001). The performance for retention of cognition was also disrupted by ischemia (P < 0.05-0.01). There was no correlation between the degree of CA1 pyramidal cell loss and behavioral deficits. The present data reveal that the aversive version of the 8-arm radial maze is sensitive to the cognitive effects of ischemia. Since it excludes the need for food deprivation or immersion of the animal in water, the method should provide a sensitive and more practical behavioral test with which to evaluate the effects of ischemic brain damage on cognition.

Animals↗
PubMed1997

A concussive-like brain injury model in mice (I): impairment in learning and memory.

The modeling of human concussive brain injury (CBI) in the laboratory has been challenging. In the present study, we developed an experimental CBI model in mice using a novel weight-drop device. Various injury levels were examined by adjusting the height of the falling weight (diameter 10 mm, length 20 cm, weight 21 g). At a height of 50 cm, the impact resulted in a mortality rate of 46.7% with a skull fracture rate of 28.6%. At a height of 25 cm, however, the impact produced a concussive-like brain injury (CLBI) to the mice without skull fracture. A series of pathophysiological and neurobehavioral responses was evaluated at this injury level. The CLBI mice lost muscle tone and righting reflex response immediately following the trauma and recovered from the latter within a short duration of 1.6 +/- 0.32 min (mean +/- SE). Brain edema formation started at 12 h, reached a maximum at 24 h and recovered 48 h. Typically edema was found in the neocortex, hippocampus, and cerebellum, but not in the brain stem. Deficits in the feeding behaviors lasted for 2 days, accompanied by lower body weight persisting for 5 days. The body weight growth rate for 24 h returned to the control levels by the third day postinjury. Learning and memory were evaluated at the end of 1-3 weeks after the trauma using a water-finding task. At 1 week, exploratory behaviors were slightly inhibited while learning and memory were profoundly impaired. Interestingly, the learning and memory deficits lasted for 2 weeks while recovering to the control levels by 3 weeks. No motor disability was found in the CLBI mice during the 3-week evaluations. These results indicate that the weight-drop impact produced graded injury to the brain, and at the injury level of 25 cm it produced a CLBI in the mice in which the characteristics of transient loss of neurobehavioral responses, short duration of brain edema, and long-lasting learning and memory deficits are similar to those of human CBI.

Animals↗
PubMed1992

K(+)-channel blockers restore synaptic plasticity in the neuromuscular junction of dunce, a Drosophila learning and memory mutant.

The effects of K(+)-channel blockers on synaptic transmission in dunce (dnc), a Drosophila learning and memory mutant, were investigated. Larvae dnc mutants lack facilitation and post-tetanic potentiation (PTP) at their motor end-plates; dnc mutants are also deficient in a form of phosphodiesterase, and exhibit abnormally high levels of cyclic adenosine 3',5'-monophosphate (cAMP). A two-microelectrode voltage-clamp was used to record end-plate currents and spontaneous end-plate currents from longitudinal ventrolateral third-instar larval muscle. The K(+)-channel blockers 3,4-diaminopyridine (3,4-DAP) and tetraethylammonium (TEA), at micromolar concentrations, caused a reversible decrease in end-plate current amplitudes both in wild-type and mutant end-plates. In the presence of blockers, a period of high-frequency stimulation (tetanus) of the nerve gave way to a transient increase in the end-plate currents of dnc mutants resembling facilitation and PTP in normal end-plates; 3,4-DAP and TEA also restored facilitation and PTP in normal end-plates after incubation with a non-hydrolysable analogue of cAMP (8Br-cAMP). It is suggested that a specific K+ conductance might be relevant to the lack of synaptic plasticity at the dnc neuromuscular synapses.

4-Aminopyridine↗
PubMed1996

Discovery of genes involved with learning and memory: an experimental synthesis of Hirschian and Benzerian perspectives.

The biological bases of learning and memory are being revealed today with a wide array of molecular approaches, most of which entail the analysis of dysfunction produced by gene disruptions. This perspective derives both from early "genetic dissections" of learning in mutant Drosophila by Seymour Benzer and colleagues and from earlier behavior-genetic analyses of learning and in Diptera by Jerry Hirsh and coworkers. Three quantitative-genetic insights derived from these latter studies serve as guiding principles for the former. First, interacting polygenes underlie complex traits. Consequently, learning/memory defects associated with single-gene mutants can be quantified accurately only in equilibrated, heterogeneous genetic backgrounds. Second, complex behavioral responses will be composed of genetically distinct functional components. Thus, genetic dissection of complex traits into specific biobehavioral properties is likely. Finally, disruptions of genes involved with learning/memory are likely to have pleiotropic effects. As a result, task-relevant sensorimotor responses required for normal learning must be assessed carefully to interpret performance in learning/memory experiments. In addition, more specific conclusions will be obtained from reverse-genetic experiments, in which gene disruptions are restricted in time and/or space.

Animals↗
PubMed2000

Effects of the anticholinesterase drug tacrine on the development of PTZ kindling and on learning and memory processes in mice.

INTRODUCTION: The anticholinesterase drug tacrine (Tac) is known to have a beneficial effect on memory deficit in mice involving in the process the cholinergic system in the brain. Chemically induced kindling is a well-known model of petit mal epilepsy. Kindling develops after repeated administration of subconvulsant doses of pentylenetetrazole (PTZ). This model is suitable for studying the two CNS disturbances associated with epilepsy, i.e. seizure attacks and memory impairment. OBJECTIVE. The aim of the present study was to examine the effect of the anticholinesterase drug Tac on the model of PTZ kindling and on active avoidance in mice. METHODS. Kindling was induced by repeated administration of PTZ (40 mg/kg) s.c. at 48-hour intervals. Tac (at doses of 0.1, 0.5 and 1 mg/kg) was injected 40 minutes before PTZ over an 8 - week period in 4 experimental groups of mice. Seizure intensity was scored using a 5-grade scale. Kindling was defined as 3, 4 or 5 grade seizures evoked by 3 consecutive doses of PTZ and treatment was discontinued. The active avoidance method (training session consisting of 50 trials) was used to test learning and memory functions. On day 7 following the learning session a memory retention test was performed. The challenge dose of PTZ was given after a 15-day discontinuation of treatment. RESULTS: In control mice, kindling was developed over a 7-week period of treatment. Mice injected with Tac (in 3 consecutive doses) showed increased seizure intensity from week 1 through week 7 of the study. On learning and memory retention tests kindled mice showed a reduced learning capabilities whereas a statistically significant upward tendency in the number of conditioned responses (avoidances) was recorded in mice treated with Tac (1 mg/kg), when compared with the controls. Mice treated with Tac (in doses of 0.1 and 0.5 mg/kg) also exhibited an increased number of avoidances on learning and memory retention tests. CONCLUSIONS: 1. The anticholinesterase drug Tac increased the seizure intensity and facilitated the development of PTZ kindling in mice. 2. On the basis of well-developed kindling Tac did not impair the memory of the experimental animals, which is possibly due to its CNS stimulating effect.

Analysis of Variance↗
PubMed2004

Effects of pre-germinated brown rice on beta-amyloid protein-induced learning and memory deficits in mice.

We evaluated the effects of pre-germinated brown rice (hatsuga genmai, PGR) on learning and memory and compared them with those of polished rice or cornstarch. In mice that were fed pellets of polished rice or PGR for two weeks, the learning ability in the Morris water maze test was significantly enhanced compared with mice that were fed cornstarch pellets. In the Y-maze test, the intake of food pellets for two weeks failed to affect spontaneous alternation behavior. Beta-amyloid(25-35) (Abeta(25-35): 3 nmol/mouse, i.c.v.) protein impaired spontaneous alternation behavior in mice that were fed pellets of cornstarch or polished rice. In contrast, PGR pellets prevented the Abeta(25-35)-induced impairment of spontaneous alternation behavior. These results suggest that polished rice and PGR have facilitating effects on spatial learning. In particular, it is surmised that PGR may prevent Alzheimer's disease associated with Abeta.

Amyloid beta-Peptides↗
PubMed2002

Long term administration of Hypericum perforatum improves spatial learning and memory in the water maze.

The aim of the present study is to investigate the effects of long-term Hypericum perforatum treatment on spatial learning and memory in rats. Hypericum preparation (HP) standardized to 0.3% hypericin content was administered orally for 9 weeks in doses of 4.3 and 13 microg/kg corresponding to therapeutic dosages in humans of 0.3 and 0.9 mg of total hypericins daily. A Morris water maze paradigm was used. The mean escape latency over 4 d for the Control group (21.9 s) and HP 4.3 group (21.7 s) was significantly greater than the latency of the HP 13 group (15.8s). In the probe trial on day 5, the HP 13 group crossed the correct annulus in the SE quadrant more often (4.5) than the other groups: Con (2.4) and HP 4.3 (3.1). After completion of the behavioral experiment, the regional brain concentrations of monoamines and metabolites were estimated in selected brain regions, i.e. prefrontal cortex, hippocampus and hypothalamus. Analysis of variance (ANOVA) demonstrated significant differences in the content of monoamines and metabolites between the treatment groups compared to the Control. The increased 5-hydroxytryptamine (5-HT) levels in the prefrontal cortex correlated positively with the retention of spatial memory. These findings show that the long-term administration of Hypericum perforatum can improve learning and spatial memory with significant changes in the content of monoamines in several brain regions.

Animals↗
PubMed1996

Effects of discrete kainic acid-induced hippocampal lesions on spatial and contextual learning and memory in rats.

Substantial information is available concerning the influence of global hippocampal lesions on spatial learning and memory, however the contributions of discrete subregions within the hippocampus to these functions is less well understood. The present investigation utilized kainic acid to bilaterally lesion specific areas of the rat hippocampus. These animals were subsequently tested on a spatial orientation task using a circular water maze, and on an associative/contextual task using passive avoidance conditioning. The results indicate that both the dorsal CA1 and the ventral CA3 subregions play important roles in learning. Specifically, CA1 lesions produced a deficit in the acquisition of the water maze task and a significant memory impairment on the passive avoidance task. CA3 lesions also caused learning deficits in the acquisition of the water maze task, and produced even greater impairments in performance on the passive avoidance task. We conclude that CA1 and CA3 hippocampal subregions each play significant roles in the overall integration of information concerning spatial and associative learning.

Animals↗
PubMed1984

The effects of retroactive and proactive interference on learning and memory in old and young rats.

The effects of interference on learning and memory in old and young rats were compared using a visual discrimination task. In Experiment I, discrimination training was followed by one of three interference treatments and finally by retesting on the discrimination task. There were no age differences in original learning but old rats were significantly impaired in remembering the visual discrimination when a high-interference treatment involving similar stimuli was introduced between original learning and retesting. In Experiment II, old rats were impaired on discrimination learning when the high-interference treatment was administered before discrimination training. Analysis of response patterns showed that the exaggerated susceptibility of old rats to interference effects resulted in a general behavioral inflexibility similar to that observed in young adult rats with damage to the hippocampal region.

Aging↗
PubMed2003

Glutamate receptor function in learning and memory.

The contribution of glutamate to synaptic transmission, plasticity and development is well established; current evidence is based on diverse approaches to decipher function and malfunction of this principal transmitter. With respect to learning and memory, we are now able to identify more specifically the role played by the three main glutamate receptor classes in learning and memory: centre stage is clearly the NMDA receptor, with overwhelming evidence proving its involvement in the actual learning process (encoding), throughout the animal kingdom. This is discussed with respect to many different types of learning. Evidence for the contribution of the AMPA receptors (AMPARs) is less clear-cut due to the general problem of specificity: block of AMPARs will shutdown neuronal communication, and this will affect various components essential for learning. Therefore, the role of AMPARs cannot be established in isolation. Problems of interpretation are outlined and a specific involvement of AMPARs in the regulation of neuronal excitation related to learning is proposed. Metabotropic glutamate receptors (mGluRs) may contribute very little to the actual acquisition of new information. However, memory formation appears to require mGluRs, through the modulation of consolidation and/or recall. Overall, mGluR functions seem variable and dependent on brain structure and learning task.

Animals↗
PubMed2002

[Effect of melatonin on learning and memory impairment induced by aluminum chloride and its mechanism].

AIM: To investigate the effect of melatonin on learning and memory impairment in mice induced by aluminum chloride and its possible mechanism. METHODS: Mice were treated with intracerebroventricular (icv) injection of 2 microL 5% aluminum chloride solution, once a day for 5 d. At the same time, the mice were given intraperitoneally melatonin 0.6, 3 and 15 mg.kg-1, once a day for 14 d. The passive avoidance of the mice was assessed by step-through test on day 15 after the last icv injection, and then the place navigation and spatial probe ability by Morris water maze were tested. After the spatial probe test, the activities of total superoxide dismutase (T-SOD), CuZn superoxide dismutase (CuZn-SOD), glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) in the cerebral cortex and hippocampus of mice brain were determined. RESULTS: Melatonin ameliorated significantly the impairment of passive avoidance memory, the place navigation and spatial probe ability of mice induced by aluminum chloride. Melatonin was found to prevent significantly the decline of T-SOD, CuZn-SOD and GSH-Px activities, the increase of MDA content in the cortex and hippocampus of mouse brain induced by aluminum chloride. CONCLUSION: The results suggest that melatonin improves significantly the learning and memory impairment in mice induced by aluminum chloride, and this effect may be attributed to its antioxidation.

Aluminum Chloride↗
PubMed2001

The role of the entorhinal cortex in two forms of spatial learning and memory.

It is generally acknowledged that the rodent hippocampus plays an important role in spatial learning and memory. The importance of the entorhinal cortex (ERC), an area that is closely interconnected anatomically with the hippocampus, in these forms of learning is less clear cut. Recent studies using selective, fibre-sparing cytotoxic lesions have generated conflicting results, with some studies showing that spatial learning can proceed normally without the ERC, suggesting that this area is not required for normal hippocampal function. The present study compared cytotoxic and aspiration ERC lesions with both fimbria fornix (FFX) lesions and sham-operated controls on two spatial learning tasks which have repeatedly been shown to depend on the hippocampus. Both groups of ERC lesions were impaired during non-matching-to-place testing (rewarded alternation) on the elevated T-maze. However, neither of these lesions subsequently had any effect on the acquisition of a standard spatial reference memory task in the water maze. FFX lesions produced a robust and reliable impairment on both of these tasks. A second experiment confirmed that cytotoxic ERC lesions spared water maze learning but disrupted rewarded alternation on the T-maze, when the order of behavioural testing was reversed. These results confirm previous reports that ERC-lesioned animals are capable of spatial navigation in the water maze, suggesting that the ERC is not a prerequisite for normal hippocampal function in this task. The present demonstration that ERC lesions disrupt non-matching-to-place performance may, however, be consistent with the possibility that ERC lesions affect attentional mechanisms, for example, by increasing the sensitivity to recent reward history.

Animals↗
PubMed1999

Huperzine-A capsules enhance memory and learning performance in 34 pairs of matched adolescent students.

AIM: To study the efficacy of huperzine-A capsules (Hup) on memory and learning performance of adolescent students. METHODS: Using double-blind and matched pair method, 34 pairs of junior middle school students complaining of memory inadequacy were divided into two groups by normal psychological health inventory (PHI), similar memory quotient (MQ), same sex and class. The Hup group was administrated orally 2 capsules of Hup (each contains Hup 50 micrograms) b.i.d., and the placebo group was given 2 capsules of placebo (starch and lactose inside) b.i.d. for 4 wk. RESULTS: At the end of trial, the Hup group's MQ (115 +/- 6) was more than that of the placebo group (104 +/- 9, P < 0.01), and the scores of Chinese language lesson in the Hup group were elevated markedly too. CONCLUSION: The Hup capsules enhance the memory and learning performance of adolescent students.

Adolescent↗