Greater Memory Deficits Research Articles

Autobiographical memory specificity and restrained eating: examining the influence of priming with images of healthy and unhealthy foods

BackgroundDietary restraint has been linked to deficits in the ability to recall detailed memories of personally experienced events (referred to as autobiographical memory specificity). As priming with healthy foods increases the salience of restraint it would be expected to lead to greater deficits in memory specificity.ObjectiveTo determine if priming word cues with images of healthy or unhealthy foods would influence the specificity of memory retrieval, and if deficits in memory specificity would be more evident in those reporting higher levels of dietary restraint, or currently dieting.MethodsSixty female undergraduates self-reported if they were currently dieting and completed measures of mood, restraint, and disinhibition, and a modified version of the autobiographical memory task. Participants were presented with positive and negative words (unrelated to eating concerns) and asked to retrieve a specific memory in response to each cue. A food image was shown prior to each word cue; half of the participants were primed with images of healthy foods and half with images of unhealthy foods.ResultsAs expected, participants primed with healthy foods retrieved fewer specific memories than did those primed with unhealthy foods. However, neither restraint nor current dieting behaviour was associated with memory specificity.ConclusionsDifferences in memory specificity between the priming conditions cannot be explained in terms of increased salience of restraint. However, it is plausible that unhealthy images led to an increase in positive affect, which in turn improved memory specificity.Level of evidenceLevel I: Evidence obtained from: at least one properly designed experimental study.

Molecular imaging of the association between serotonin degeneration and beta-amyloid deposition in mild cognitive impairment

BackgroundDegeneration of the serotonin system has been observed in Alzheimer’s disease (AD) and in mild cognitive impairment (MCI). In transgenic amyloid mouse models, serotonin degeneration is detected prior to widespread cortical beta-amyloid (Aβ) deposition, also suggesting that serotonin degeneration may be observed in preclinical AD. MethodsThe differences in the distribution of serotonin degeneration (reflected by the loss of the serotonin transporter, 5-HTT) relative to Aβ deposition was measured with positron emission tomography in a group of individuals with MCI and a group of healthy older adults. A multi-modal partial least squares (mmPLS) algorithm was applied to identify the spatial covariance pattern between 5-HTT availability and Aβ deposition. ResultsForty-five individuals with MCI and 35 healthy older adults were studied, 22 and 27 of whom were included in the analyses who were “amyloid positive” and “amyloid negative”, respectively. A pattern of lower cortical, subcortical and limbic 5-HTT availability and higher cortical Aβ deposition distinguished the MCI from the healthy older control participants. Greater expression of this pattern was correlated with greater deficits in memory and executive function in the MCI group, not in the control group. ConclusionA spatial covariance pattern of lower 5-HTT availability and Aβ deposition was observed to a greater extent in an MCI group relative to a control group and was associated with cognitive impairment in the MCI group. The results support the application of mmPLS to understand the neurochemical changes associated with Aβ deposition in the course of preclinical AD.

Sex-dependent consequences of neonatal brain hypoxia-ischemia in the rat.

Neonatal hypoxia-ischemia (HI) is an important cause of neurological deficits in humans, and the Levine-Rice model of experimental HI in the rat mimics the human brain lesion and the following sensory motor deficits and cognitive disabilities. With the growing evidence that sex influences all levels of brain functions, this Mini-Review highlights studies in which sex was a controlled variable and that provided evidence of sexual dimorphism in behavioral outcome, extension of brain damage, mechanisms of lesion, and treatment efficacy in the rat neonatal HI model. It was shown that 1) females have greater memory deficits; 2) cell death is dependent mainly on caspase activation in females; 3) males are more susceptible to oxidative stress; and 4) treatments acting on distinct cell death pathways afford sex-dependent neuroprotection. These tentative conclusions, along with growing evidence from other fields of neurobiology, support the need for scientists to design their experiments considering sex as an important variable; otherwise, important knowledge will continue to be missed. It is conceivable that sex can influence the development of efficacious therapeutic tools to treat neonates suffering from brain HI. © 2016 Wiley Periodicals, Inc.

Older individuals with HIV infection have greater memory deficits than younger individuals

The prevalence of HIV-associated neurocognitive disorder (HAND) remains persistently high in the era of combination antiretroviral therapy. We aimed to characterize the pattern of neurocognitive dysfunction in older subjects with HAND in particular amnestic versus non-amnestic impairment. One hundred six subjects from the Johns Hopkins University NIMH Clinical Outcomes cohort underwent standardized neuropsychological (NP) testing between November 2006 and June 2010. We examined performance in seven cognitive domains (memory, attention, speed of processing,visuospatial, language, motor, and executive). Older subjects were defined as age >50 years at the time of NP testing.Subjects were diagnosed with HAND according to established criteria and dichotomized into amnestic cognitive impairment or non-amnestic cognitive impairment with deficit defined as z scores <−1.5 for the verbal and nonverbal memory domains.There were 32 older subjects with a mean age (SD) of 54.2 (2.8) years and 74 younger subjects, 43.7 (4.3) years. Older age was associated with a 4.8-fold higher odds of memory deficits adjusted for potential confounders (p =0.035) identified a priori. With age modeled as a continuous covariate,every 1 year increase in age was associated with a 1.11-fold higher odds of memory deficit (p =0.05). There was a higher proportion of amnestic cognitive impairment among older subjects than younger subjects with HIV infection. Neurodegenerative processes other than those directly due to HIV maybe increasingly important as individuals with chronic HIV infection and HAND survive into older age.

170. Characterization of the neuroendocrine system in healthy aged rats

Healthy aged individuals are more likely to suffer profound memory impairments following a challenging life event such as a severe bacterial infection, surgery, or an intense psychological stressor, than are younger adults. Importantly, these peripheral challenges are capable of producing a neuroinflammatory response (e.g., increased pro-inflammatory cytokines) and in the healthy aged brain this response is exaggerated and prolonged. Normal aging primes or sensitizes microglia and this appears to be the source of this amplified response. Here, we present data suggesting that a dysregulated neuroendocrine response in the aged (24 mos) F344xBN rat is skewed toward higher brain corticosterone (CORT) levels and greater hippocampal glucocorticoid receptor activation compared to young adult rats (3 mos). In addition, we confirm others’ findings that 11beta-hydroxysteroid dehydrogenase (11beta-HSD1), the enzyme that transforms cortisone (an inactive metabolite of CORT) to the active hormone CORT, is elevated in the aged hippocampus. In concert, these factors may play a critical role in priming microglia in the aged rat brain, resulting in exaggerated and longer lasting cytokine responses in the brain and greater memory deficits following a challenge.

Depression and cognitive deficits in geriatric schizophrenia

ObjectivePast reports have found patients with comorbid depression and schizophrenia spectrum disorders exhibit greater deficits in memory and attention compared to schizophrenia spectrum disorder patients without depressive symptoms. However, in contrast to younger schizophrenia patients, the few past studies using cognitive screens to examine the relationship between depression and cognition in inpatient geriatric schizophrenia have found that depressive symptomatology was associated with relatively enhanced cognitive performance. In the current study we examined the relationship between depressive symptoms and cognitive deficits in geriatric schizophrenia spectrum disorder patients (n=71; mean age=63.7) on an acute psychiatric inpatient service. MethodPatients completed a battery of cognitive tests assessing memory, attention and global cognition. Symptom severity was assessed via the PANSS and Calgary Depression Scale for Schizophrenia. ResultsResults revealed that geriatric patients' depression severity predicted enhancement of their attentional and verbal memory performance. Patients' global cognitive functioning and adaptive functioning were not associated with their depression severity. ConclusionContrary to patterns typically seen in younger patients and non-patient groups, increasing depression severity is associated with enhancement of memory and attention in geriatric schizophrenia spectrum disorder patients. Also, diverging from younger samples, depression severity was unassociated with patients adaptive and global cognitive functioning.

Aberrant Expression of Myeloperoxidase in Astrocytes Promotes Phospholipid Oxidation and Memory Deficits in a Mouse Model of Alzheimer Disease

Myeloperoxidase (MPO) is expressed in Alzheimer disease (AD) but not normal aged brain. A functional -463G/A MPO promoter polymorphism has been associated with AD risk through as yet unidentified mechanisms. Here we report that human MPO-463G allele, but not MPO-463A or mouse MPO, is strongly expressed in astrocytes and deposited in plaques in huMPO transgenic mice crossed to the APP23 model. MPO is similarly expressed in astrocytes in human AD tissue. In cortical homogenates of the MPOG-APP23 model, MPO expression correlated with increased levels of a lipid peroxidation product, 4-hydroxynonenal. Fluorescence high-performance liquid chromatography and electrospray ionization mass spectroscopy identified selective accumulation of phospholipid hydroperoxides in two classes of anionic phospholipids, phosphatidylserine (PS-OOH) and phosphatidylinositol (PI-OOH). The same molecular species of PS-OOH and PI-OOH were elevated in human AD brains as compared with non-demented controls. Augmented lipid peroxidation in MPOG-APP23 mice correlated with greater memory deficits. We suggest that aberrant huMPO expression in astrocytes leads to a specific pattern of phospholipid peroxidation and neuronal dysfunction contributing to AD.

Sex Differences in Ethanol-Induced Hypnosis and Hypothermia in Young Long-Evans Rats

Introduction: Females experience greater liver damage, have reduced brain size, and have greater memory deficits than do males with a similar history of alcoholism. Females have higher peak alcohol levels and faster elimination rates than males. Our goal was to study sex differences in the response of young ethanol-naïve outbred Long-Evans rats to acute ethanol exposure so that we may better understand why females are more sensitive to alcohol toxicity than males. Methods: Females aged 49 days and males aged 43 days, weighing 153.6 and 177.5 g, respectively, were tested for their initial response to ethanol. Fasted (12 hr) females (in diestrous) and males were given an intraperitoneal injection of 3.0 g/kg of ethanol (v/v in 0.9% sterile saline). Body temperature, loss of the righting reflex (LORR), return of the righting reflex, and tail blood alcohol concentration (BAC) were monitored. Results: LORR occurred at the same time in females and males. The return of the righting reflex occurred later in males than in females. BACs were the same in the males and females except at LORR, when BAC was lower in the males. Acute ethanol tolerance developed in more males than females. Females demonstrated a slower recovery from peak ethanol-induced hypothermia than males. The proportions of lean body mass, ethanol elimination, and ethanol metabolism were similar in the females and males. Conclusions: Ethanol-naïve young male and female Long-Evans rats demonstrated sex differences in their initial responses to ethanol. Males were more sensitive than females to the hypnotic effect of ethanol, whereas females were more sensitive than males to ethanol-induced hypothermia. In addition, more males than females developed acute ethanol tolerance. Investigating the mechanisms underlying these differences may help us to understand why females experience more of the adverse effects of alcohol consumption than males.

Sex Differences in Ethanol‐Induced Hypnosis and Hypothermia in Young Long‐Evans Rats

Females experience greater liver damage, have reduced brain size, and have greater memory deficits than do males with a similar history of alcoholism. Females have higher peak alcohol levels and faster elimination rates than males. Our goal was to study sex differences in the response of young ethanol-naïve outbred Long-Evans rats to acute ethanol exposure so that we may better understand why females are more sensitive to alcohol toxicity than males. Females aged 49 days and males aged 43 days, weighing 153.6 and 177.5 g, respectively, were tested for their initial response to ethanol. Fasted (12 hr) females (in diestrous) and males were given an intraperitoneal injection of 3.0 g/kg of ethanol (v/v in 0.9% sterile saline). Body temperature, loss of the righting reflex (LORR), return of the righting reflex, and tail blood alcohol concentration (BAC) were monitored. LORR occurred at the same time in females and males. The return of the righting reflex occurred later in males than in females. BACs were the same in the males and females except at LORR, when BAC was lower in the males. Acute ethanol tolerance developed in more males than females. Females demonstrated a slower recovery from peak ethanol-induced hypothermia than males. The proportions of lean body mass, ethanol elimination, and ethanol metabolism were similar in the females and males. Ethanol-naïve young male and female Long-Evans rats demonstrated sex differences in their initial responses to ethanol. Males were more sensitive than females to the hypnotic effect of ethanol, whereas females were more sensitive than males to ethanol-induced hypothermia. In addition, more males than females developed acute ethanol tolerance. Investigating the mechanisms underlying these differences may help us to understand why females experience more of the adverse effects of alcohol consumption than males.

Attention deficits and reading disabilities: Are immediate memory defects additive?

This study examined the interaction of Attention Deficits and Learning Disabilities on the immediate memory abilities of children. Forty children, between 7 years 0 months and 13 years 11 months old, independently diagnosed with Attention Deficit Hyperactivity Disorder (ADHD; criteria from the Diagnostic and Statistical Manual of Mental Disorders [3rd ed., rev. [DSM‐III‐R]; American Psychiatric Association, 1987]) by a pediatrician and a pediatric psychologist were matched to 40 children who were independently diagnosed with Undifferentiated Attention Deficit Disorder (UADD; criteria from DSM‐III‐R) according to Full Scale IQ, grade, and sex. These children were further subgrouped based on the presence of an identified Learning Disability (LD) in reading. Consequently four groups of children were formed, ADHD+LD, ADHD‐LD, UADD+LD, and UADD‐LD. All children were administered the Color Span Test, a test of immediate visual and verbal memory. The findings revealed that, overall, children with attention deficits and a comorbid LD (ADHD+LD, UADD+LD) had greater memory deficits, suggesting that LD had an “additive effect.” In addition, children with ADHD exhibited significantly more memory deficits than children with UADD.

Treatment of the damaged rat hippocampus with a locally applied electric field.

Previous studies have indicated that axons may be directed to regenerate toward the cathodal source of a locally applied D.C. electric field. In the present studies, similar galvanotropic effects were tested after partial denervation of the rat hippocampus. Following unilateral fimbrial lesions, 1.5 microA of direct current was applied locally to the tissue for 4 weeks. In the experimental group, the distal (temporal) portion of the hippocampus was located near the cathodal electrode, while the proximal (nasal) portion was located near the anode. In two control groups, either the current was reversed, or there was not current delivered to the tissue. Spontaneous alternation behavior 4 weeks post-operatively in the "cathode distal" rats provided results comparable to those in unoperated (normal) animals, whereas the control animals exhibited statistically significantly greater deficits in memory. The ability to learn the location of a submerged platform in a water tank was evident in unoperated and "cathode distal" animals, but not in either of the control groups. Hippocampal acetylcholinesterase activity in "cathode distal" animals was lower than in unoperated animals, but statistically significantly greater than in the other control animals. Results are consistent with the contention that locally applied weak direct current can modulate long term sequellae of hippocampal injury.