Age-related Changes In Learning Research Articles

Age-related decline in cognitive flexibility is associated with the levels of hippocampal neurogenesis.

Aging is associated with impairments in learning, memory, and cognitive flexibility, as well as a gradual decline in hippocampal neurogenesis. We investigated the performance of 6-and 14-month-old mice (considered mature adult and late middle age, respectively) in learning and memory tasks based on the Morris water maze (MWM) and determined their levels of preceding and current neurogenesis. While both age groups successfully performed in the spatial version of MWM (sMWM), the older mice were less efficient compared to the younger mice when presented with modified versions of the MWM that required a reassessment of the previously acquired experience. This was detected in the reversal version of MWM (rMWM) and was particularly evident in the context discrimination MWM (cdMWM), a novel task that required integrating various distal cues, local cues, and altered contexts and adjusting previously used search strategies. Older mice were impaired in several metrics that characterize rMWM and cdMWM, however, they showed improvement and narrowed the performance gap with the younger mice after additional training. Furthermore, we analyzed the adult-born mature and immature neurons in the hippocampal dentate gyrus and found a significant correlation between neurogenesis levels in individual mice and their performance in the tasks demanding cognitive flexibility. These results provide a detailed description of the age-related changes in learning and memory and underscore the importance of hippocampal neurogenesis in supporting cognitive flexibility.

Lifespan developmental invariance in memory consolidation: evidence from procedural memory.

Characterizing ontogenetic changes across the lifespan is a crucial tool in understanding neurocognitive functions. While age-related changes in learning and memory functions have been extensively characterized in the past decades, the lifespan trajectory of memory consolidation, a critical function that supports the stabilization and long-term retention of memories, is still poorly understood. Here we focus on this fundamental cognitive function and probe the consolidation of procedural memories that underlie cognitive, motor, and social skills and automatic behaviors. We used a lifespan approach: 255 participants aged between 7 and 76 years performed a well-established procedural memory task in the same experimental design across the whole sample. This task enabled us to disentangle two critical processes in the procedural domain: statistical learning and general skill learning. The former is the ability to extract and learn predictable patterns of the environment, while the latter captures a general speed-up as learning progresses due to improved visuomotor coordination and other cognitive processes, independent of acquisition of the predictable patterns. To measure the consolidation of statistical and general skill knowledge, the task was administered in two sessions with a 24-h delay between them. Here, we report successful retention of statistical knowledge with no differences across age groups. For general skill knowledge, offline improvement was observed over the delay period, and the degree of this improvement was also comparable across the age groups. Overall, our findings reveal age invariance in these two key aspects of procedural memory consolidation across the human lifespan.

Aging is not equal across memory systems.

The present experiments compared the effects of aging on learning several hippocampus- and striatum-sensitive tasks in young (3-4month) and old (24-28month) male Fischer-344 rats. Across three sets of tasks, aging was accompanied not only by deficits on hippocampal tasks but also by maintained or even enhanced abilities on striatal tasks. On two novel object recognition tasks, rats showed impaired performance on a hippocampal object location task but enhanced performance on a striatal object replacement task. On a dual solution task, young rats predominately used hippocampal solutions and old rats used striatal solutions. In addition, on two maze tasks optimally solved using either hippocampus-sensitive place or striatum-sensitive response strategies, relative to young rats, old rats had impaired learning on the place version but equivalent learning on the response version. Because glucose treatments can reverse deficits in learning and memory across many tasks and contexts, levels of available glucose in the brain may have particular importance in cognitive aging observed across tasks and memory systems. During place learning, training-related rises in extracellular glucose levels were attenuated in the hippocampus of old rats compared to young rats. In contrast, glucose levels in the striatum increased comparably in young and old rats trained on either the place or response task. These extracellular brain glucose responses to training paralleled the impairment in hippocampus-sensitive learning and the sparing of striatum-sensitive learning seen as rats age, suggesting a link between age-related changes in learning and metabolic substrate availability in these brain regions.

Inactivation of the striatum in aged rats rescues their ability to learn a hippocampus-sensitive spatial navigation task.

Studies of age-related changes in learning and memory often focus on hippocampus-sensitive tasks and reveal age-associated impairments across numerous species and contexts. However, cognitive decline with advanced age is not all-encompassing; for example, forms of striatum-sensitive learning are conserved or enhanced with age. Under certain conditions, hippocampal and striatal memory systems function in opposition. In young adult rodents, disruption of one structure can enhance learning on tasks dependent on the other, suggesting that competitive interactions across memory systems contribute to learning and memory abilities. This report examines whether imbalances across memory systems might contribute to cognitive aging. We inactivated the striatum using central infusions of lidocaine (sodium channel blocker) prior to hippocampus-sensitive spatial (place) training in young (3-4-month-old) and old (24-25-month-old) F344 male rats. Consistent with prior work, vehicle-infused old rats exhibited place learning impairments relative to young rats. Additionally, striatal inactivation enhanced learning in old rats, but not young rats, abolishing the age-related impairment. These findings suggest that age-related declines in learning tasks thought to engage the hippocampus may stem from exaggerated interference from other memory systems and that interventions to target the striatum may reverse some age-related learning decrements.

Vitamin transporters in mice brain with aging.

Its high metabolic rate and high polyunsaturated fatty acid content make the brain very sensitive to oxidative damage. In the brain, neuronal metabolism occurs at a very high rate and generates considerable amounts of reactive oxygen species and free radicals, which accumulate inside neurons, leading to altered cellular homeostasis and integrity and eventually irreversible damage and cell death. A misbalance in redox metabolism and the subsequent neurodegeneration increase throughout the course of normal aging, leading to several age-related changes in learning and memory as well as motor functions. The neuroprotective function of antioxidants is crucial to maintain good brain homeostasis and adequate neuronal functions. Vitamins E and C are two important antioxidants that are taken up by brain cells via the specific carriers αTTP and SVCT2, respectively. The aim of this study was to use immunohistochemistry to determine the distribution pattern of these vitamin transporters in the brain in a mouse model that shows fewer signs of brain aging and a higher resistance to oxidative damage. Both carriers were distributed widely throughout the entire brain in a pattern that remained similar in 4-, 12-, 18- and 24-month-old mice. In general, αTTP and SVCT2 were located in the same regions, but they seemed to have complementary distribution patterns. Double-labeled cell bodies were detected only in the inferior colliculus, entorhinal cortex, dorsal subiculum, and several cortical areas. In addition, the presence of αTTP and SVCT2 in neurons was analyzed using double immunohistochemistry for NeuN and the results showed that αTTP but not SVCT2 was present in Bergmann's glia. The presence of these transporters in brain regions implicated in learning, memory andmotor control provides an anatomical basis that may explain the higher resistance of this animal modelto brain oxidative stress, which is associated with better motor performance and learning abilities in old age.

Activation of NO-cGMP Signaling Rescues Age-Related Memory Impairment in Crickets.

Age-related memory impairment (AMI) is a common feature and a debilitating phenotype of brain aging in many animals. However, the molecular mechanisms underlying AMI are still largely unknown. The cricket Gryllus bimaculatus is a useful experimental animal for studying age-related changes in learning and memory capability; because the cricket has relatively short life-cycle and a high capability of olfactory learning and memory. Moreover, the molecular mechanisms underlying memory formation in crickets have been examined in detail. In the present study, we trained male crickets of different ages by multiple-trial olfactory conditioning to determine whether AMI occurs in crickets. Crickets 3 weeks after the final molt (3-week-old crickets) exhibited levels of retention similar to those of 1-week-old crickets at 30 min or 2 h after training; however they showed significantly decreased levels of 1-day retention, indicating AMI in long-term memory (LTM) but not in anesthesia-resistant memory (ARM) in olfactory learning of crickets. Furthermore, 3-week-old crickets injected with a nitric oxide (NO) donor, a cyclic GMP (cGMP) analog or a cyclic AMP (cAMP) analog into the hemolymph before conditioning exhibited a normal level of LTM, the same level as that in 1-week-old crickets. The rescue effect by NO donor or cGMP analog injection was absent when the crickets were injected after the conditioning. For the first time, an NO donor and a cGMP analog were found to antagonize the age-related impairment of LTM formation, suggesting that deterioration of NO synthase (NOS) or molecules upstream of NOS activation is involved in brain-aging processes.

Aging in the cerebellum and hippocampus and associated behaviors over the adult life span of CB6F1 mice

In the present study we examined the effects of normal aging in the hippocampus and cerebellum, as well as behaviors associated with these substrates. A total of 67 CB6F1 hybrid mice were tested at one of five ages (4, 8, 12, 18 or 25months) on the context pre-exposure facilitation effect (CPFE) modification of fear conditioning, rotorod, Barnes maze, acoustic startle, Morris water maze (MWM) and 500-ms trace eyeblink classical conditioning (EBCC). Behavioral tasks were chosen to increase the ability to detect age-related changes in learning, as trace EBCC is considered a more difficult paradigm (compared to delay EBCC) and the CPFE has been found to be more sensitive to hippocampus insults than standard contextual fear conditioning. To assess the effects of age on the brain, hippocampus volume was calculated and unbiased stereology was used to estimate the number of Purkinje neurons in the cerebellar cortex. A significant, age-related loss of Purkinje neurons was found—beginning at 12months of age—and hippocampus volume remained stable over the adult life span. Age-related impairment was found, beginning at 12–18months in the rotorod, and mice with fewer Purkinje neurons showed greater impairment in this task. CB6F1 mice retained auditory acuity across the life span and mice aged 25months showed significant age-related impairment in the EBCC task; however, deficits were not associated with the loss of Purkinje neurons. Although the CPFE task is considered more sensitive to hippocampus insult, no age-related impairment was found. Spatial memory retention was impaired in the Barnes maze at 25months, but no significant deficits were seen in the MWM. These results support the finding of differential aging in the hippocampus and cerebellum.

Age-associated learning and memory deficits in two mouse versions of the stone T-maze

We have previously reported that a modified Stone T-maze (STM), using escape from water as motivation, was effective in evaluating learning and memory ability in young C57/BL6 mice. Here we report on the effectiveness and sensitivity of the STM in the assessment of age-related learning and memory deficits in mice using either escape from foot shock or water as the motivational manipulations. C57BL/6Nia mice 7-, 12-, 20- and 24-months old received 15 massed trials in the escape from foot shock motivated STM while C57BL/6Nia mice 5-, 12-, and 25-months old were tested in the escape from water STM. Analysis of errors, the main performance variable, revealed similar results in both versions of the task with younger mice making fewer errors. Notably, mice of all ages in the water-motivated version moved quickly through the maze, while all ages of mice in the shock-motivated version tended to wait for shock to be initiated to move forward. Overall, both versions of the STM appear to be sensitive to age-related changes in learning and memory and provide an alternative to other testing paradigms such as the Morris water maze which are susceptible to performance confounds which can lead to uninterpretable results.

Age sensitivity of behavioral tests and brain substrates of normal aging in mice.

Knowledge of age sensitivity, the capacity of a behavioral test to reliably detect age-related changes, has utility in the design of experiments to elucidate processes of normal aging. We review the application of these tests in studies of normal aging and compare and contrast the age sensitivity of the Barnes maze, eyeblink classical conditioning, fear conditioning, Morris water maze, and rotorod. These tests have all been implemented to assess normal age-related changes in learning and memory in rodents, which generalize in many cases to age-related changes in learning and memory in all mammals, including humans. Behavioral assessments are a valuable means to measure functional outcomes of neuroscientific studies of aging. Highlighted in this review are the attributes and limitations of these measures in mice in the context of age sensitivity and processes of brain aging. Attributes of these tests include reliability and validity as assessments of learning and memory, well-defined neural substrates, and sensitivity to neural and pharmacological manipulations and disruptions. These tests engage the hippocampus and/or the cerebellum, two structures centrally involved in learning and memory that undergo functional and anatomical changes in normal aging. A test that is less well represented in studies of normal aging, the context pre-exposure facilitation effect (CPFE) in fear conditioning, is described as a method to increase sensitivity of contextual fear conditioning to changes in the hippocampus. Recommendations for increasing the age sensitivity of all measures of normal aging in mice are included, as well as a discussion of the potential of the under-studied CPFE to advance understanding of subtle hippocampus-mediated phenomena.

Age differences in reward sensitivity during decision-making and learning

Event Abstract Back to Event Age differences in reward sensitivity during decision-making and learning Benjamin Eppinger1, 2*, Leigh Nystrom1 and Jonathan D. Cohen1 1 Princeton University, Princeton Neuroscience Institute, United States 2 Max Planck Institute for Human Development, Neurocognition of Decision Making, Germany Older adults are often assumed to be more conservative and risk-avoidant in their decision-making than younger adults. These age-related changes in choice behavior might be associated with age differences in the sensitivity to reward. In this project we examined the relation between age differences in inter-temporal decision-making and age-related changes in reward-based learning. To identify the neural systems involved in learning and decision making in the two age groups we combined experimental approaches and functional magnetic resonance imaging (fMRI). Results from the decision-making study show less impulsive choice behavior and reduced time discounting (devaluation) of rewards for older than younger adults. These age-related changes in decision-making are associated with reduced hemodynamic activations in the dorsal and ventral striatum in the elderly. Thus, our findings indicate that less impulsive choice behavior in older adults may be due to age-related reductions in the sensitivity of limbic areas to reward. The behavioral data from the learning study show learning impairments as well as a greater bias toward learning from negative outcomes in older than younger adults. Similar to the findings of the decision-making study, age-related changes in learning are associated with age differences in the dynamics of fMRI activations in the dorsal striatum. Taken together, our results suggest that less impulsive decision-making in older adults, as well as age-related changes in learning are due to a reduced sensitivity of limbic areas to reward. These age-related changes in reward sensitivity most likely result from transformations in dopaminergic neuromodulation with age and may have an important societal impact by affecting economic decision-making in older adults. Keywords: age differences, Decision Making, Reward sensitivity Conference: Decision Neuroscience From Neurons to Societies, Berlin, Germany, 23 Sep - 25 Sep, 2010. Presentation Type: Poster Topic: Abstracts Citation: Eppinger B, Nystrom L and Cohen JD (2010). Age differences in reward sensitivity during decision-making and learning. Front. Neurosci. Conference Abstract: Decision Neuroscience From Neurons to Societies. doi: 10.3389/conf.fnins.2010.82.00035 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 19 Aug 2010; Published Online: 07 Sep 2010. * Correspondence: Dr. Benjamin Eppinger, Princeton University, Princeton Neuroscience Institute, Princeton, NJ, United States, Benjamin.Eppinger@tu-dresden.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Benjamin Eppinger Leigh Nystrom Jonathan D Cohen Google Benjamin Eppinger Leigh Nystrom Jonathan D Cohen Google Scholar Benjamin Eppinger Leigh Nystrom Jonathan D Cohen PubMed Benjamin Eppinger Leigh Nystrom Jonathan D Cohen Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

The effects of TNF deficiency on age-related cognitive performance

Growing evidence suggests that 'pro-inflammatory' cytokines such as TNF play a role in cognitive processes and in aging. To test the effects of TNF on cognitive function throughout aging, we used transgenic mice which were TNF deficient. We then tested these mice along with wild-type mice, at 3, 6 and 12 months of age, using the Barnes maze. Wild-type controls showed better memory than TNF knock-out mice at 3 months of age, but not at 6 and 12 months of age. Results of our experiment show that endogenous TNF plays an important role in cognitive processes throughout aging processes. The implications of these findings are far-reaching and include a possible role for cytokines in the molecular and cellular mechanisms subserving age-related changes in learning, memory and cognition.

Age-related deficit in behavioural extinction is counteracted by long-term ethanol consumption: Correlation between 5-HIAA/5HT ratio in dorsal raphe nucleus and cognitive parameters

We investigated age-related changes in learning and memory performance and behavioural extinction in the water maze; and in endogenous levels of serotonin (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) in the neocortex, hippocampus, thalamus and dorsal raphe nucleus of Wistar rats. Another aim was to assess the correlation between behavioural and biochemical parameters, which were measured in rodents of two different ages: 5 months (adults) and 16 months (middle-aged). The middle-aged subjects succeeded in learning the behavioural task, albeit with significantly worse performance when compared to adult animals. Aging also had significant main effects on memory and extinction. An age-dependent decrease in 5-HIAA levels was observed in both hippocampus and dorsal raphe nucleus (DRN). The decrease in DRN 5-HIAA was paralleled by a decrease in 5-HIAA/5-HT ratio in this brain area, which was significantly correlated to the animals’ spatial memory performance and behavioural extinction. In addition, using middle-aged rats, a 2 × 2 factorial study was carried out to examine the effects of food restriction and chronic ethanol consumption on rat's performance in a spatial behavioural task and on central serotonergic parameters. None of these two treatments had a significant effect on the behavioural and biochemical parameters assessed, with the exception of extinction index, which was significantly affected by ethanol consumption. Long-term ethanol ameliorated the impairment in behavioural flexibility caused by aging. In conclusion, long-term ethanol consumption may have a role in protecting against age-related deficit in behavioural extinction. Moreover, the present results also indicate that DRN serotonergic system is involved in spatial memory and behavioural extinction.

Reference memory, anxiety and estrous cyclicity in C57BL/6NIA mice are affected by age and sex

Age-related changes in learning and memory are common in rodents. However, direct comparisons of the effects of aging on learning and memory in both males and females are lacking. The present study examined whether memory deteriorates with increasing age in C57BL/6NIA mice, and whether age-related changes in learning and memory are similar in both sexes. Male and female mice (five, 17 and 25 months of age) were tested in a battery of behavioral tasks including the Morris water maze (spatial and non-spatial reference memory), simple odor discrimination (olfactory reference memory), plus maze (anxiety/exploration), locomotor activity, and basic reflexes. Five-month-old mice learned the water maze and odor discrimination tasks rapidly. Relative to five-month-old mice, 25-month-old mice exhibited impaired spatial and olfactory reference memory, but intact non-spatial reference memory. The spatial reference memory of 17-month-old mice was also impaired, but less so than 25-month mice. Seventeen-month-old mice exhibited intact non-spatial (visual and olfactory) reference memory. Five and 25-month-old mice had similar levels of plus maze exploration and locomotor activity, whereas 17-month-old mice were more active than both groups and were slightly less exploratory than five-month-old mice. Although sex differences were not observed in the five- and 25-month groups, 17-month-old females exhibited more impaired spatial reference memory and increased anxiety relative to 17-month-old males. Estrous cycling in females deteriorated significantly with increased age; all 25-month-old females had ceased cycling and 80% of 17-month-old females displayed either irregular or absent estrous cycling. This study is the first to directly compare age-related mnemonic decline in male and female mice. The results suggest that: (i) aged mice exhibit significant deficits in spatial and olfactory reference memory relative to young mice, whereas middle-aged mice exhibit only a moderate spatial memory deficit and; (ii) spatial reference memory decline begins at an earlier age in females than in males, a finding that may be related to the cessation of estrous cycling.

1401 Decrease in the learning and memorial ability induced by reduction of masticatory movement in the senescence-accelerated mouse

A novel inbred strain of mouse ‘SAM-P/10’ (Senescence Accelerated Mouse) is a model of age-related brain atrophy characterized by age-related loss and shrinkage of neurons in the cerebral neocortex. Age-related changes in learning and memory skills of SAM-P/10 mice were investigated usinng a newly developed conditional avoidance task in a T-maze. Comparisons were made with findings in the SAM-R/1 strain which shows a little loss and no shrinkage of neocortical neurons. Four-month-old SAM-R/1 and SAM-P/10 performed well during a 10-day training schedule of the conditional avoidance task. SAM-R/1 mice over 17 months of age were slower learners than younger SAM-R/1 mice but reached nearly the same high percentage avoidance as seen in the 4-month-old mice during the last 4 days of the schedule. Performance of the SAM-P/10 mice gradually worsened with aging and 10- to 12-month-old SAM-P/10 mice could not reach the percentage avoidance seen with the 4-month-old mice, even after the 10-day training. When the mean percentage of succesful avoidance or escape behavior on every training day was plotted, the curves were much the same for both SAM-R/1 and SAM-P/10 mice, of any age. These results show that aged SAM-P/10 mice retained the left-right turning discrimination in the T-maze and lost the ability to predict the forthcoming aversive shock by associating conditioned stimulus and unconditioned stimulus.

Age-related changes in learning and memory and cholinergic neuronal function in senescence accelerated mice (SAM)

The senescence-accelerated mouse (SAM) has been established as a murine model of accelerated aging. We investigated learning ability and memory in various tasks in a SAM strain, SAMPITA, and in a control strain of SAMR1TA at the ages of 20, 30 and 40 weeks. We also measured choline acetyltransferase (ChAT) and cholinesterase (ChE) activity in the brains of these mice at the same ages. In a Y-maze task, in which short-term memory can be examined, there was no difference in learning ability between SAMP1TA and SAMR1TA at any age. Ability in latent learning and passive-avoidance tasks was less in SAMP1TA at 30 weeks of age than in age-matched SAMR1TA. The level of ChAT activity in the striatum of SAMP1TA was lower, than that of SAMR1TA at the ages of 20 and 30 weeks. At the ages of 40 and 50 weeks, ChE activity in the striatum of SAMP1TA was lower than that of SAMR1TA. These results suggest that SAMP1TA has a deficit, with cholinergic neuronal dysfunction, in learning ability and memory, as shown by impairment of performance in latent learning and long-term memory, but not in short-term memory.

Age-related changes in learning, memory, and lipofuscin as a function of the percentage of SAMP8 genes

SAMP8 (P8) mice are characterized by impaired learning and memory relatively early in their life, while CD-1 mice show impairment later in life. A series of paternal backcross strains were developed from a CD-1 dame and P8 sire. Siblings from each backcross were bred to establish strains with 50% to 97% P8 genes. F4 mice, 4 or 12 mo of age, were trained to avoid foot shock in a T-maze with retention tested 1 wk later. After testing, brain sections were examined for lipofuscin autofluorescence. At 4 mo of age, all strains, including the CD-1 and P8 strains, showed no significant differences in learning, retention or lipofuscin deposits. At 12 mo of age, groups with 94%, 97% P8 genes or P8 mice (100%) required significantly more trials to learn the task or relearn the task 1 wk later than groups with 88% or fewer P8 genes. Lipofuscin deposits increased in the hippocampus as the percentage of P8 genes increased suggesting that many genes control aging of the brain. However, the sudden appearance of impaired learning in the 94% strain suggests that the mechanism(s) responsible for the impairment involves a few recessive genes and are independent of the mechanisms controlling the general aging of the brain.

Age-related deterioration in conditional avoidance task in the SAM-P/10 mouse, an animal model of spontaneous brain atrophy

A novel inbred strain of mouse ‘SAM-P/10’ (Senescence Accelerated Mouse) is a model of age-related brain atrophy characterized by age-related loss and shrinkage of neurons in the cerebral neocortex. Age-related changes in learning and memory skills of SAM-P/10 mice were investigated usinng a newly developed conditional avoidance task in a T-maze. Comparisons were made with findings in the SAM-R/1 strain which shows a little loss and no shrinkage of neocortical neurons. Four-month-old SAM-R/1 and SAM-P/10 performed well during a 10-day training schedule of the conditional avoidance task. SAM-R/1 mice over 17 months of age were slower learners than younger SAM-R/1 mice but reached nearly the same high percentage avoidance as seen in the 4-month-old mice during the last 4 days of the schedule. Performance of the SAM-P/10 mice gradually worsened with aging and 10- to 12-month-old SAM-P/10 mice could not reach the percentage avoidance seen with the 4-month-old mice, even after the 10-day training. When the mean percentage of succesful avoidance or escape behavior on every training day was plotted, the curves were much the same for both SAM-R/1 and SAM-P/10 mice, of any age. These results show that aged SAM-P/10 mice retained the left-right turning discrimination in the T-maze and lost the ability to predict the forthcoming aversive shock by associating conditioned stimulus and unconditioned stimulus.

Age-related changes in radial-arm maze learning and basal forebrain cholinergic systems in senescence accelerated mice (SAM)

Age-related changes in learning performance and the brain cholinergic system were studied in a senescence accelerated mice-prone series (SAM-P/8) and a senescence accelerated mice-resistant series (SAM-R/1, control) bred under specific pathogen-free conditions. In a radial-arm maze task, SAM-P/8 mice at 4 and 12 months of age showed virtually no significant impairment in working memory or reference memory compared with SAM-R/1 mice at the same age, although they needed more time to complete a trial than SAM-R/1. In contrast, in a passive avoidance task, SAM-P/8 showed a marked age-accelerated deficit in acquisition performance relative to SAM-R/1. Also, SAM-P/8 showed an age-accelerated decrease in locomotion and rearing in an open-field box. At the end of these behavioral tasks, neurochemical analyses showed that there were no differences in the concentrations of acetylcholine (ACh) in the cortex, hippocampus, striatum, midbrain, or cerebellum between SAM-P/8 and SAM-R/1. Although SAM-P/8 mice did not demonstrate any age-accelerated decline in radial-arm maze performance, they showed a normal age-related decline particularly in working memory, equal to that observed in SAM-R/1. Also, ACh levels in the aged groups of SAM-P/8 showed a significant decrease related to normal aging in the hippocampus and striatum, and a slight decrease in the cortex compared to the young group of the same strain. Thus, we found that SAM-P/8 show dissociative effects of aging in spatial learning and passive avoidance performance.

Adult Day Care Center: A Unique Clinical Experience for Dietetic Students

Senior dietetic students worked closely with an elderly population and respective caregivers in an adult day-care program. Experiences included preparation of nutritional assessments, design of appropriate case management, and counseling clients and families. Nutrition education programs consonant with age-related changes in learning were planned and implemented. The food service system was monitored to assure that the needs of an aging group with diverse dietary needs were met. Students enjoyed a valuable experience working with a growing population and gained an appreciation of how heterogeneous today's elders are.

Age-related changes in associative learning: Studies in rabbits and rats

Two experimental models for studying age-related changes in associative learning are described. One involves classical (Pavlovian) conditioning of eyeblink and heart rate in the rabbit. The second involves Pavlovian leg flexion and heart rate conditioning in the rat. Advantages and disadvantages of each model are discussed. Results with both models suggest differential effects of aging on acquisition of autonomic and somatomotor responses, thus underlining the utility of assessing multiple response systems to adequately characterize age-related changes in learning and memory.