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Memory Impairment (memory + impairment)
Kinds of Memory Impairment Selected AbstractsA Novel Cyclic Squamosamide Analogue Compound FLZ Improves Memory Impairment in Artificial Senescence Mice Induced by Chronic Injection of D-Galactose and NaNO2BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 6 2007Fang Fang Artificially senescent mouse model was induced by consecutive injection of D-galactose (120 mg/kg) and NaNO2 (90 mg/kg) once daily for 60 days. Compound FLZ (75 and 150 mg/kg) was orally administered once daily for 30 days after D-galactose and NaNO2 injection for 30 days. The water maze test was used to evaluate the learning and memory function of mice. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in serum were determined using different biochemical kits. The alterations in hippocampus morphology were assessed by light and electronic microscope. Immunoreactive cells of Bcl-2 in the hippocampus were counted by immunohistochemical staining, and Bcl-2 protein expression was analysed by Western blot method. The results indicate that injection of D-galactose and NaNO2 induces memory impairment and neuronal damage in hippocampus of mice. In addition, serum SOD and GSH-Px activities decreased, while MDA level increased. Bcl-2-positive neurons and Bcl-2 protein expression in the hippocampus decreased remarkably. Oral administration of FLZ for 30 days significantly improved the cognitive deficits and the biochemical markers mentioned above, and also reduced the pathological alterations in mouse hippocampus. The results suggest that FLZ ameliorates memory deficits and pathological injury in artificially senescent mice induced by chronic injection of D-galactose and NaNO2, indicating that FLZ is worth further studies for fighting antisenescence and dementia. [source] Effect of Episodic and Working Memory Impairments on Semantic and Cognitive Procedural Learning at Alcohol Treatment EntryALCOHOLISM, Issue 2 2007Anne Lise Pitel Background: Chronic alcoholism is known to impair the functioning of episodic and working memory, which may consequently reduce the ability to learn complex novel information. Nevertheless, semantic and cognitive procedural learning have not been properly explored at alcohol treatment entry, despite its potential clinical relevance. The goal of the present study was therefore to determine whether alcoholic patients, immediately after the weaning phase, are cognitively able to acquire complex new knowledge, given their episodic and working memory deficits. Methods: Twenty alcoholic inpatients with episodic memory and working memory deficits at alcohol treatment entry and a control group of 20 healthy subjects underwent a protocol of semantic acquisition and cognitive procedural learning. The semantic learning task consisted of the acquisition of 10 novel concepts, while subjects were administered the Tower of Toronto task to measure cognitive procedural learning. Results: Analyses showed that although alcoholic subjects were able to acquire the category and features of the semantic concepts, albeit slowly, they presented impaired label learning. In the control group, executive functions and episodic memory predicted semantic learning in the first and second halves of the protocol, respectively. In addition to the cognitive processes involved in the learning strategies invoked by controls, alcoholic subjects seem to attempt to compensate for their impaired cognitive functions, invoking capacities of short-term passive storage. Regarding cognitive procedural learning, although the patients eventually achieved the same results as the controls, they failed to automate the procedure. Contrary to the control group, the alcoholic groups' learning performance was predicted by controlled cognitive functions throughout the protocol. Conclusion: At alcohol treatment entry, alcoholic patients with neuropsychological deficits have difficulty acquiring novel semantic and cognitive procedural knowledge. Compared with controls, they seem to use more costly learning strategies, which are nonetheless less efficient. These learning disabilities need to be considered when treatment requiring the acquisition of complex novel information is envisaged. [source] Cognitive Screening Using a Tape Recorder: A Pilot StudyJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 3 2003Peter W. Schofield MD OBJECTIVES: To determine whether a tape recorder can be used to administer cognitive tests efficiently and yield valid results. DESIGN: Convenience sample. Administration of cognitive test materials by tape recorder and conventional technique. SETTING: Outpatient clinic. PARTICIPANTS: Subjects from memory disorder clinic, hostel accommodation, and community. MEASUREMENTS: Responses to Hopkins Verbal Learning Test,revised, verbal fluency items from the controlled oral word association test, 10-item naming task, a construction task, and speed writing task. RESULTS: Performances on the tape- and clinician-administered battery of tests were highly correlated. Memory impairment was accurately detected using the tape battery. Data from 30 minutes of testing via tape were obtained at the cost to the clinician of 2 to 3 minutes of scoring time. CONCLUSION: Tape-administration of cognitive test material warrants further study as an efficient means of cognitive screening. [source] Selective death of newborn neurons in hippocampal dentate gyrus following moderate experimental traumatic brain injuryJOURNAL OF NEUROSCIENCE RESEARCH, Issue 10 2008Xiang Gao Abstract Memory impairment is one of the most significant residual deficits following traumatic brain injury (TBI) and is among the most frequent complaints heard from patients and their relatives. It has been reported that the hippocampus is particularly vulnerable to TBI, which results in hippocampus-dependent cognitive impairment. There are different regions in the hippocampus, and each region is composed of different cell types, which might respond differently to TBI. However, regional and cell type-specific neuronal death following TBI is not well described. Here, we examined the distribution of degenerating neurons in the hippocampus of the mouse brain following controlled cortical impact (CCI) and found that the majority of degenerating neurons observed were in the dentate gyrus after moderate (0.5 mm cortical deformation) CCI-TBI. In contrast, there were only a few degenerating neurons observed in the hilus, and we did not observe any degenerating neurons in the CA3 or CA1 regions. Among those degenerating cells in the dentate gyrus, about 80% of them were found in the inner granular neuron layer. Analysis with cell type-specific markers showed that most of the degenerating neurons in the inner granular neuron layer are newborn immature neurons. Further quantitative analysis shows that the number of newborn immature neurons in the dentate gyrus is dramatically decreased in the ipsilateral hemisphere compared with the contralateral side. Collectively, our data demonstrate the selective death of newborn immature neurons in the hippocampal dentate gyrus following moderate injury with CCI in mice. This selective vulnerability of newborn immature dentate neurons may contribute to the persistent impairment of learning and memory post-TBI and provide an innovative target for neuroprotective treatment strategies. © 2008 Wiley-Liss, Inc. [source] Effects of desmopressin (DDAVP) on memory impairment following electroconvulsive therapy (ECT)ACTA NEUROPSYCHIATRICA, Issue 3 2004Ebrahim Abdollahian Background:, Memory impairment is a common adverse effect of electroconvulsive therapy (ECT). Studies on animals and humans suggest that vasopressin improves the cognitive function, and positive effects of desmopressin on memory and learning have been reported. This research was performed for evaluation of the effects of desmopressin in the prevention of memory impairment following ECT. Methods:, This randomized, double-blind controlled clinical trial with placebo administration was performed on 50 patients with psychiatric disorders who were candidates for ECT. Subjects in the case group received 60 µm of intranasal desmopressin daily (in three doses of 20 µm). For the control group 0.9% saline solution was administered in the same way. Memory function was evaluated using Wechsler's Memory Scale three times a week (the first time before the start of ECT and the second and third times after the third and sixth sessions, respectively). Results were analyzed by t -test and Paired t -test. Results:, The mean age of patients was 29 years (range 20,40). During the course of ECT, patients in the control group demonstrated a meaningful decrease in memory scores (from a base score of 80.15,75.45 in the second test and 72.60 in the third test). Despite this, a meaningful increase in memory scores was observed during the treatment with desmopressin in the case group (from a base score of 73.27,75.70 and 79.13 in the second and the third tests, respectively). There was a meaningful difference between the two groups (P < 0.0001). Conclusion:, This study confirms the protective effect of desmopressin against memory impairment. The results confirm that memory impairment is a common side-effect of ECT and suggest that desmopressin may prevent ECT-induced memory impairment by its effects on memory and the learning process. [source] Selective memory and memory deficits in depressed inpatientsDEPRESSION AND ANXIETY, Issue 4 2003Thomas Ellwart Dipl. Abstract We investigated memory impairment and mood-congruent memory bias in depression, using an explicit memory test and an implicit one. Thirty-six severely depressed inpatients that fulfilled DSM-IV criteria for major depressive disorder and 36 healthy controls matched for sex, age, and educational level participated in the study. Explicit memory was assessed with a free recall task and implicit memory with an anagram solution task. Results showed that depressed and controls differed in explicit memory performance, depending on the amount of cognitive distraction between incidental learning and testing. Implicit memory was not affected. In addition, severely depressed patients showed a mood-congruent memory bias in implicit memory but not in explicit memory. The complex pattern of results is discussed with regard to relevant theories of depression. Depression and Anxiety 17:197,206, 2003. © 2003 Wiley-Liss, Inc. [source] Biofeedback for foot offloading in diabetic patients with peripheral neuropathyDIABETIC MEDICINE, Issue 1 2010Z. Pataky Diabet. Med. 27, 61,64 (2010) Abstract Aims, The reduction of high plantar pressure in diabetic patients with peripheral neuropathy is mandatory for prevention of foot ulcers and amputations. We used a new biofeedback-based method to reduce the plantar pressure at an at-risk area of foot in diabetic patients with peripheral neuropathy. Methods, Thirteen diabetic patients (age 60.8 ± 12.3 years, body mass index 29.0 ± 5.0 kg/m2) with peripheral neuropathy of the lower limbs were studied. Patients with memory impairment were excluded. The portable in-shoe foot pressure measurement system (PEDAR®) was used for foot offloading training by biofeedback. The learning procedure consisted in sequences of walking (10 steps), each followed by a subjective estimation of performance and objective feedback. The goal was to achieve three consecutive walking cycles of 10 steps, with a minimum of seven steps inside the range of 40,80% of the baseline peak plantar pressure. The peak plantar pressure was assessed during the learning period and at retention tests. Results, A significant difference in peak plantar pressure was recorded between the beginning and the end of the learning period (when the target for plantar pressure was achieved) (262 ± 70 vs. 191 ± 53 kPa; P = 0.002). The statistically significant difference between the beginning of learning and all retention tests persisted, even at the 10-day follow-up. Conclusions, Terminal augmented feedback training may positively affect motor learning in diabetic patients with peripheral neuropathy and could possibly lead to suitable foot offloading. Additional research is needed to confirm the maintenance of offloading in the long term. [source] The novel nootropic compound DM232 (UNIFIRAM) ameliorates memory impairment in mice and ratsDRUG DEVELOPMENT RESEARCH, Issue 1 2002Carla Ghelardini Abstract The favorable pharmacological profile exhibited by piracetam stimulated the synthesis of related compounds potentially endowed with a higher nootropic potency. The antiamnesic and procognitive activity of DM232 (unifiram), a new compound structurally related to piracetam, was investigated. Mouse passive avoidance and rat Morris water maze and Social learning tests were employed. DM232 (0.001,1 mg kg,1 i.p. , 0.01,0.1 1 mg kg,1 p.o.) prevented amnesia induced by scopolamine (1.5 mg kg,1 i.p.), mecamylamine (20 mg kg,1 i.p.), baclofen (2 mg kg,1 i.p.), and clonidine (0.125 mg kg,1 i.p.). Furthermore, The antiamnesic effect of the investigated compound was comparable to that exerted by well-known nootropic drugs such as piracetam (30,100 mg kg,1 i.p.), aniracetam (100 mg kg,1 p.o.), rolipram (30 mg kg,1 p.o.), and nicotine (5 mg kg,1 i.p). DM232 (0.1 mg kg,1 i.p.) was also able to prevent amnesia induced by scopolamine (0.8 mg kg,1 i.p.) in the rat Morris watermaze test. In the rat social learning test, DM232 (0.1 mg kg,1 i.p.) injected in adults rats reduced the duration of active exploration of the familiar partner in the second session of the test. DM232, similarly to piracetam, reduced the duration of hypnosis induced by pentobarbital. At the highest effective doses, the investigated compound did not impair motor coordination (rota rod test), nor modified spontaneous (Animex). These results indicate DM232 (unifiram) as a novel cognition enhancer, strictly related to piracetam-like compounds, able to ameliorate memory impairment at doses about 1,000 times lower than the most active available nootropic compounds. Drug Dev. Res. 56:23,32, 2002. © 2002 Wiley-Liss, Inc. [source] The Localization and Lateralization of Memory Deficits in Children with Temporal Lobe EpilepsyEPILEPSIA, Issue 1 2007Linda M. Gonzalez Summary:,Purpose: It is often reported that children with temporal lobe epilepsy (TLE) experience nonlateralized memory impairments. However, many of these studies have been exploratory and not based on memory theory. Further, differences between mesial and lateral subgroups have not been adequately examined. This study aimed to discern more specific patterns of memory impairment in children with TLE. Methods: Forty-three children (5,16 years) with lesional TLE participated. Subjects were categorized in terms of lesion laterality (left, n = 21; right, n = 22) and intratemporal location (mesial, n = 31; lateral, n = 12). Verbal and nonverbal memory tasks were administered that reflected associative, allocentric and recognition paradigms. Results: Facial recognition was poorer in right TLE (p = 0.03). There were no differences between left and right groups on any other memory task, even when comparisons were restricted to cases with mesial involvement. Irrespective of laterality, clear differences were observed between mesial and lateral lesion subgroups (arbitrary associative learning, p = 0.01; complex figure recall, p = 0.03). The lateral lesion subgroup displayed intact memory function relative to normative standards. Conclusions: Memory is more frequently impaired in children with mesial as opposed to lateral TLE. Tasks with an associative component discriminated between these subgroups, supporting an associative model of hippocampal function. With the exception of facial recognition, memory deficits were not lateralized. Therefore, the nature of memory impairment experienced by children with TLE cannot be extrapolated from adult models. [source] Memory, Emotional and Vocational Impairments before and after Anterior Temporal Lobectomy for Complex Partial SeizuresEPILEPSIA, Issue 11 2006Mario F. Dulay Summary:,Purpose: To assess the pre- and postsurgical frequency of memory, emotional, and vocational impairments in patients who underwent anterior temporal lobectomy (ATL), and to assess the relationship between emotional disturbance and memory abilities after ATL. Methods: Retrospective analysis of data was performed on 90 patients with medically intractable complex partial seizures who underwent ATL between 1981 and 2003. Patients were evaluated an average of 5 months before surgery and 11.3 months after surgery. Results: A moderate to high frequency of memory impairment (44.4%; verbal or nonverbal), emotional disturbance (38.9%) and unemployment (27.8%) existed in the same individuals both before and after surgery. There were small to moderate rates of new onset memory (18.9%), emotional (11.1%), and vocational (7.8%) difficulties after surgery often regardless of seizure control outcome. Patients who underwent left-ATL and had emotional disturbance after surgery had the lowest verbal memory test scores. Conclusions: Results highlight the importance of taking into account emotional status when assessing memory abilities after ATL. Results replicate the finding of moderate to high frequencies of memory impairment, emotional disturbance, and unemployment both before and after ATL. Results provide support for the rationale that cognitive, psychiatric and vocational interventions are indicated to mitigate the problems that exist before and persist after ATL. [source] Anomia for people's names, a restricted form of transient epileptic amnesiaEUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2003F. Ghika-Schmid A 37-year-old man consulted after two episodes of transient anomia for people's names over a period of 6 months. The first episode lasted about 10 min and was restricted to an inability to remember his 2-year-old son's first name. The second, was limited to an inability to recall his daughter's first name for 5 min with clear abnormal experiential quality. Witnessed descriptions of the attacks confirmed the absence of any other cognitive impairment or motor automatisms. The neurological examination was normal except for hyposmia. Inter-ictal cognitive evaluation was normal apart from the anomia for people's names or retrieval of names of familiar people in his childhood on definition and on famous faces naming test. A wake electroencephalograph showed left temporal epileptiform abnormalities, following hyperpnea. On magnetic resonance imaging, quantitative analysis revealed a mildly decreased volume of the left hippocampus. The diagnosis of transient epileptic amnesia (TEA) was considered and the patient did not recur for 6 months under lamotriginum. Thus anomia for people's names may be the sole clinical manifestation of TEA. Such a clinical presentation may easily be overlooked. Treatment may prevent further recurrence and the installation of more important and permanent autobiographical memory impairment. Our observation may suggest an isolated system not only for people's knowledge, but for people's naming. It is consistent with the notion of proper name as pure referring expression. [source] Similar subcortical pattern of cognitive impairment in AIDS patients with and without dementiaEUROPEAN JOURNAL OF NEUROLOGY, Issue 2 2000S. V. Suarez The aim of this study was to develop a series of neuropsychological tests that define the cortical and subcortical features of cognitive impairment and the characteristics of memory in demented and mildly cognitively impaired AIDS patients. We attempted to establish a usable method to assess and determine the type and degree of cognitive impairment in individual AIDS patients. We examined 53 patients without central nervous system opportunistic infections. A short battery included two scales of global efficiency (the Mattis dementia rating scale and the Mini Mental State Examination), a psychomotor speed test, an executive control assessment and explicit memory evaluation. Patients were categorized into four groups based on their score on both the Mattis dementia rating scale and the DSM-IV criteria: (1) asymptomatic; (2) having AIDS without cognitive impairment; (3) having AIDS with mild cognitive impairment; and (4) having AIDS dementia. Patients with mildly impaired cognition demonstrated slowed thinking, abnormal initiation and conceptualization, and memory impairment. AIDS dementia patients had slower motor activity and memory recall was more severely affected. The short neuropsychological battery was able to characterize modified cognitive performances in both severely and mildly cognitively impaired AIDS patients. The subcortical pattern of the memory disorder was obvious, regardless of the degree of cognitive impairment. [source] Effect of tooth loss on spatial memory and trkB-mRNA levels in ratsHIPPOCAMPUS, Issue 6 2008Kaoruko Yamazaki Abstract The mechanism by which tooth loss accelerates spatial memory impairment is unknown. The purpose of this study was to test the hypothesis that tooth loss affects trkB-mRNA levels and leads to an accelerated decrease in the hippocampal cell density in rats. A radial maze was used to evaluate the spatial memory of male Wistar rats that were categorized based on the number of extracted molar teeth. Number of hippocampal pyramidal cells and the trkB-mRNA expressions in the amygdala, perirhinal cortex, thalamus, and the hippocampal CA1, CA3, and CA4 areas, were evaluated using molecular biological techniques. Seven weeks after tooth extraction, maze performance was significantly lower in each tooth loss group than in the control group, and the number of extracted teeth was inversely proportional to the induction of the trkB-mRNA and the hippocampal cell density. The average weight of rats increased by controlled feeding throughout the experiment without showing a significant difference between the control and experimental groups. The results indicated that, in rats, the spatial memory-linked trkB-mRNA was reduced in association with the tooth loss; this supports the hypothesis and suggests that teeth have a role in the prevention of spatial memory impairment. © 2008 Wiley-Liss, Inc. [source] Hippocampal neuron and glial cell numbers in Parkinson's disease,A stereological study,HIPPOCAMPUS, Issue 10 2006F.C. Joelving Abstract Hippocampal atrophy and neuron loss are early and reproducible findings in Alzheimer's disease, and recent magnetic resonance imaging studies indicate that hippocampal atrophy may also be present in Parkinson's disease (PD). To determine whether or not cell loss occurs in PD, we estimated the total neuron and glial cell numbers as well as the total volume unilaterally in the hippocampi of eight demented PD patients and eight control subjects. Cell numbers were estimated in the neuron-containing layers of CA1, CA2-(3), CA4, the dentate gyrus, and subiculum using the optical-fractionator technique. The Cavalieri method was used to estimate the volume of the total hippocampus and its subregions. We did not find significant differences in cell numbers or volumes in PD brains when compared with control subjects. Our results thus indicate that hippocampal atrophy and cell loss are not necessarily involved in the memory impairment and dementia observed in PD. © 2006 Wiley-Liss, Inc. [source] Individual differences in spatial memory among aged rats are related to hippocampal PKC, immunoreactivityHIPPOCAMPUS, Issue 2 2002Paul J. Colombo Abstract We reported previously that the extent of spatial memory impairment among aged rats was correlated positively with levels of protein kinase C, in hippocampal homogenates measured by quantitative Western blotting (Colombo et al., 1997). In the current study, immunocytochemistry was used to test whether the relationship between elevated PKC, and memory impairment among aged rats could be localized further within regions of the hippocampus. Six- and 24-month-old male Long-Evans rats were first trained in the water maze on a standard place-learning task and then trained 2 weeks later on a transfer task designed for rapid acquisition. In comparison with young rats, aged rats with impaired spatial memory had increased PKC,-immunoreactivity (PKC,-ir) in CA1 of the hippocampus, but not the dentate gyrus. In addition, PKC,-ir in CA1 was correlated positively with spatial memory impairment among aged rats on the standard place-learning and the transfer training tasks. The current results are consistent with our previous report of PKC, in hippocampal homogenates, and show further that the relationships between PKC,-ir and memory impairments among aged rats are most evident in area CA1. Thus age-related impairments of spatial memory, as well as deficits in the flexible use of previously acquired information, may result from dysregulation of PKC,. Hippocampus 2002;12:285,289. © 2002 Wiley-Liss, Inc. [source] Lie detection by functional magnetic resonance imagingHUMAN BRAIN MAPPING, Issue 3 2002Tatia M.C. Lee Abstract The accurate detection of deception or lying is a challenge to experts in many scientific disciplines. To investigate if specific cerebral activation characterized feigned memory impairment, six healthy male volunteers underwent functional magnetic resonance imaging with a block-design paradigm while they performed forced-choice memory tasks involving both simulated malingering and under normal control conditions. Malingering that demonstrated the existence and involvement of a prefrontal-parietal-sub-cortical circuit with feigned memory impairment produced distinct patterns of neural activation. Because astute liars feign memory impairment successfully in testing once they understand the design of the measure being employed, our study represents an extremely significant preliminary step towards the development of valid and sensitive methods for the detection of deception. Hum. Brain Mapping 15:157,164, 2002. © 2002 Wiley-Liss, Inc. [source] Diazepam-induced prospective memory impairment and its relation to retrospective memory, attention, and arousalHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 2 2006Jill B. Rich Abstract The amnestic effects of benzodiazepines are well documented on a variety of memory tasks. However, prospective memory (PM), or remembering to execute an action at a future time, has not been studied previously. This study examined the effect of diazepam on word list recall, PM, sustained attention, and subjective ratings of arousal. Forty-eight healthy participants, aged 19,35, received an average of 0.19,mg/kg oral diazepam or placebo in a double-blind manner. Retrospective memory and PM were assessed by free recall of unrelated word lists and by instructing participants to request a hidden belonging at the end of the session, respectively. Sustained attention was measured by multiple trials of a digit cancellation task, and subjective arousal was assessed by self-ratings of drowsiness. Diazepam impaired performance on all measures, including PM. Reduced PM performance was associated with decreased subjective arousal in the diazepam group but was unrelated to sustained attention. This is the first report of the effects of benzodiazepines on prospective remembering, and further supports the view that the arousal/attentional system is composed of partially independent subsystems that have differential relationships to memory. Copyright © 2005 John Wiley & Sons, Ltd. [source] SSRIs and cognitive performance in a working sampleHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 8 2005Emma J. K. Wadsworth Abstract Background Studies of the impact of antidepressant use on cognitive performance have frequently been carried out among the elderly or on healthy volunteers. Comparatively little research has considered their impact on a relatively young, working population, particularly within the context of everyday life. Aims To examine any association between SSRI use and cognitive performance, mood and human error at work. Methods SSRI users and controls completed a battery of laboratory based computer tasks measuring mood and cognitive function pre- and post-work at the start and end of a working week. They also completed daily diaries reporting their work performance. Results SSRI use was associated with memory impairment: specifically poorer episodic, though not working or semantic memory. Effects of SSRI use on recognition memory seemed to vary according to the underlying psychopathology, while effects on delayed recall were most pronounced among those whose symptoms had not (yet) resolved. There were no detrimental effects on psychomotor speed, attention, mood or perceived human error at work. Conclusions The findings lend support to the SSRIs comparative safety, even among workers, particularly as the symptoms of the underlying psychopathology are successfully addressed. Possible memory impairments may, however, be found in those taking SSRIs. Copyright © 2005 John Wiley & Sons, Ltd. [source] Use of the Brief Smell Identification Test for olfactory deficit in a Norwegian population with Alzheimer's diseaseINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 10 2007Grete Kjelvik Abstract Aims Several studies have shown that Alzheimer's disease (AD) is associated with hyposmia. Olfactory identification may be a cheap and simple additional test in the assessment of early cognitive changes. The sense of smell is influenced by factors such as experience and culture and the aim of the present study was to assess the validity of the Brief Smell Identification Test (B-SIT) in distinguishing patients with AD from healthy gender and age-matched controls in a Norwegian population. Methods The study included 39 patients with a diagnosis of probable AD, and 52 gender and age-matched controls. Olfactory function was assessed with B-SIT, and a non-standardized olfactory identification task (freshly ground coffee). Results The difference in olfactory performance between patients and controls was highly significant, both for the whole AD patient group and the subgroup of patients with MMSE,,,24. Receiver operating curve (ROC) analyses indicated that B-SIT distinguished patients from controls with high sensitivity and specificity. All the odours in B-SIT with the exception of turpentine showed highly significant differences between patients and controls. AD-associated memory impairment did not seem to affect the answers given for B-SIT in this population. Conclusions For patients with AD, the Brief Smell Identification Test (B-SIT) appears to be well-suited for detecting a deficit in olfactory identification in a Norwegian population. Copyright © 2007 John Wiley & Sons, Ltd. [source] Patient versus informant reported quality of life in the earliest phases of Alzheimer's diseaseINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 12 2006Asmus Vogel Abstract Objectives The study investigated if patient and informant reported Quality of Life (QoL) differed in early Alzheimer's disease (AD). In addition, we examined whether anosognosia had an impact on the agreement between patient and informant ratings of QoL and whether anosognosia, dementia severity, depression and behavioural symptoms were significantly correlated to QoL in early AD. Methods From a prospective research program including newly referred patients (age >60 years and MMSE,,,20), 48 patients with very early AD were included. QoL was assessed using the QoL-AD and EQ-5D scales. Anosognosia was rated on a categorical scale by an examiner. MMSE, Geriatric Depression Scale, Danish Adult Reading Test and Frontal Behavioural Inventory were also administered. Results On most QoL measures patients rated their QoL higher than their informants. Anosognosia was not associated with QoL but significantly with an inverse impact on the agreement between patient and informant ratings of QoL. Self-reported QoL was significantly correlated to depression but not to age, dementia severity, behavioural symptoms or memory impairment. Informant ratings of QoL were significantly correlated to behavioural symptoms and informant ratings on the EQ-5D Visual Analogue Scale were significantly correlated to patient reported depression. Conclusion Patients with early AD generally reported higher QoL than their informants. This disagreement was associated with the presence of anosognosia. Self-reported QoL did not correlate with the MMSE score. Behavioural changes and depressive symptoms may be associated with low QoL. Copyright © 2006 John Wiley & Sons, Ltd. [source] Validation of a memory inventory for the assessment of awareness of memory deficits in Alzheimer's disease in Chinese elderlyINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 10 2006Victor Wing Cheong Lui Abstract Background This paper describes the development and validation of the Memory Inventory for Chinese (MIC), for measuring the awareness of memory deficits in the Chinese population with Alzheimer's disease (AD). Methods A combination of qualitative and quantitative approaches was adopted. The MIC was developed with focus group discussion and pilot testing. It has a patient and a caregiver version. A consecutive series of 79 new out-patients with the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorder Association (NINCDS-ADRDA) criteria of probable and possible AD and 20 non-demented elderly subjects were recruited. Results A high internal consistency was found, with Cronbach alpha of 0.89 for the patient version and 0.90 for the caregiver version of MIC. The inter-rater reliability was satisfactory. For validity assessment, the caregiver score of the MIC correlated significantly with cognitive score of the subject as assessed by the Mini-Mental State Examination (rp,=,,0.37; p,<,0.01). The Memory Deficit Awareness Score, calculated by subtracting the patient score from the caregiver score, correlated significantly with clinician ratings of awareness of memory impairment (rs,=,,0.67; p,<,0.01). Conclusions The MIC appears to be a culturally appropriate and valid instrument for the measurement of awareness of memory deficits in Chinese patients with AD. Potential applications of the MIC should be further explored in other subtypes of dementia and in prospective studies. Copyright © 2006 John Wiley & Sons, Ltd. [source] The association between depressive symptoms and cognitive decline in community-dwelling elderly personsINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 4 2001Hannie C. Comijs Abstract Objective To investigate whether depressive symptoms predict specific types of cognitive decline in order to elucidate the association between late life depression and cognitive decline. Background Mechanisms underlying the association between late life depression and cognitive decline are still unclear. Method Six hundred and forty-one elderly persons of the Longitudinal Aging Study Amsterdam (LASA) aged 70,85 were examined by means of two measurement occasions over a period of 3 years. Depressive symptoms were assessed by means of the CES-D. Various cognitive functions were examined using neuropsychological tests. Results Depressive symptoms were associated with decline in speed of information processing over a 3-year period, whereas there was no association between depression and increasing memory impairment or global mental deterioration. Conclusion These findings suggest that depressive symptoms are associated with subcortical pathology, most probable white matter lesions. Copyright © 2001 John Wiley & Sons, Ltd. [source] Burnout and physical and mental health among Swedish healthcare workersJOURNAL OF ADVANCED NURSING, Issue 1 2008Ulla Peterson Abstract Title.,Burnout and physical and mental health among Swedish healthcare workers Aim., This paper is a report of a study to investigate how burnout relates to self-reported physical and mental health, sleep disturbance, memory and lifestyle factors. Background., Previous research on the possible relationship between lifestyle factors and burnout has yielded somewhat inconsistent results. Most of the previous research on possible health implications of burnout has focused on its negative impact on mental health. Exhaustion appears to be the most obvious manifestation of burnout, which also correlates positively with workload and with other stress-related outcomes. Method., A cross-sectional study was conducted, using questionnaires sent to all employees in a Swedish County Council (N = 6118) in 2002. The overall response rate was 65% (n = 3719). A linear discriminant analysis was used to look for different patterns of health indicators and lifestyle factors in four burnout groups (non-burnout, disengaged, exhausted and burnout). Results., Self-reported depression, anxiety, sleep disturbance, memory impairment and neck- and back pain most clearly discriminated burnout and exhausted groups from disengaged and non-burnout groups. Self-reported physical exercise and alcohol consumption played a minor role in discriminating between burnout and non-burnout groups, while physical exercise discriminated the exhausted from the disengaged group. Conclusion., Employees with burnout had most symptoms, compared with those who experienced only exhaustion, disengagement from work or no burnout, and the result underlines the importance of actions taken to prevent and combat burnout. [source] Vasodilators and Nootropics as Predictors of Dementia and Mortality in the PAQUID CohortJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 3 2007Jean-François Dartigues MD OBJECTIVES: To assess the effects of treatment for memory impairment and the Ginkgo biloba extract (EGb 761) on dementia, mortality, and survival without dementia. DESIGN: Prospective community-based cohort study. SETTING: France. PARTICIPANTS: Three thousand five hundred thirty-four subjects aged 65 and older. MEASUREMENTS: Information on drug consumption was obtained by interview and visual assessment of patients' medicine chests. Active screening of dementia was performed every 2 years over a 13-year period. The independent effects of treatment for memory impairment and the Ginkgo biloba extract on the risks of dementia and death were estimated using Cox proportional hazards models, adjusted for potentially confounding factors (including comorbidities). RESULTS: The initial consumption of Ginkgo biloba did not modify the risk of dementia (relative risk (RR)=1.16, 95% confidence interval (CI)=0.84,1.60), whereas the consumption of other treatments for memory impairment was associated with a higher risk of dementia (RR=1.35, 95% CI=1.11,1.63). Subjects who took Ginkgo biloba had a significantly lower risk of mortality in the long term (RR=0.76, 95% CI=0.62,0.93), even after adjustment for potentially confounding factors. The initial consumption of treatment for memory impairment other than Ginkgo biloba did not modify the risk of mortality. CONCLUSION: These results suggest that treatment with EGb 761 may increase the probability of survival in the elderly population. These findings need to be corroborated and further assessed using randomized, controlled trials. [source] Mild Cognitive Impairment Subtypes and Vascular Dementia in Community-Dwelling Elderly People: A 3-Year Follow-Up StudyJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 4 2006Mariella Zanetti MD OBJECTIVES: To investigate whether mild cognitive impairment (MCI) with multiple impaired cognitive domains (mcd-MCI) is a prodromal manifestation of vascular dementia (VaD). DESIGN: Prospective cohort study. SETTING: Geriatric unit of the Ospedale Maggiore Istituto di Ricovero e Cura a Carattere Scientifico, Milan, Italy. PARTICIPANTS: Four hundred community-dwelling subjects aged 65 and older who came freely to the geriatric unit as part of a comprehensive geriatric assessment program were evaluated for memory impairment or other cognitive disorders. Subjects with MCI were kept under observation for 3 years. MEASUREMENTS: Subjects with MCI were studied by applying a standardized clinical evaluation and a conducting a computed tomography brain scan. Cognitive performance was assessed using the Mini-Mental State Examination, the Clock Drawing Test, and a comprehensive battery of neuropsychological tests. Cardiovascular comorbidity was assessed on the basis of medical history and using electrocardiography, echocardiography, and carotid color Doppler ultrasound. RESULTS: MCI was found in 65 of the 400 community-dwelling subjects; 31 were classified with amnestic MCI (a-MCI) and 34 with mcd-MCI. A dysexecutive syndrome characterized people with mcd-MCI, who had significantly more vascular comorbidity and signs of vascular disease on brain imaging as well as a higher prevalence of extra pyramidal features, mood disorders, and behavioral symptoms than people with a-MCI. Twenty of the 65 subjects with MCI (31%) progressed to dementia within 3 years of follow-up: 11 subjects with Alzheimer's disease (AD) and nine with VaD. All patients who evolved to AD had been classified with a-MCI at baseline, whereas all patients who evolved to subcortical VaD had been classified with mcd-MCI at baseline. CONCLUSION: All subjects who converted to subcortical VaD had been classified with mcd-MCI, suggesting that mcd-MCI might be an early stage of subcortical VaD. [source] Vascular Dementia: Distinguishing Characteristics, Treatment, and PreventionJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 5s2 2003Gustavo C. Román MD Vascular dementia (VaD) is the second-most-common cause of dementia in the elderly, after Alzheimer's disease (AD). VaD is defined as loss of cognitive function resulting from ischemic, hypoperfusive, or hemorrhagic brain lesions due to cerebrovascular disease or cardiovascular pathology. Diagnosis requires the following criteria: cognitive loss, often predominantly subcortical; vascular brain lesions demonstrated by imaging; a temporal link between stroke and dementia; and exclusion of other causes of dementia. Poststroke VaD may be caused by large-vessel disease with multiple strokes (multiinfarct dementia) or by a single stroke (strategic stroke VaD). A common form is subcortical ischemic VaD caused by small-vessel occlusions with multiple lacunas and by hypoperfusive lesions resulting from stenosis of medullary arterioles, as in Binswanger's disease. Unlike with AD, in VaD, executive dysfunction is commonly seen, but memory impairment is mild or may not even be present. The cholinesterase inhibitors used for AD are also useful in VaD. Prevention strategies should focus on reduction of stroke and cardiovascular disease, with attention to control of risk factors such as hypertension, diabetes mellitus, hypercholesterolemia, and hyperhomocysteinemia. [source] Calcium/calmodulin-dependent protein kinase type IV is a target gene of the Wnt/,-catenin signaling pathway,JOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2009Macarena S. Arrázola Calcium/calmodulin-dependent protein kinase IV (CaMKIV) plays a key role in the regulation of calcium-dependent gene expression. The expression of CaMKIV and the activation of CREB regulated genes are involved in memory and neuronal survival. We report here that: (a) a bioinformatic analysis of 15,476 promoters of the human genome predicted several Wnt target genes, being CaMKIV a very interesting candidate; (b) CaMKIV promoter contains TCF/LEF transcription motifs similar to those present in Wnt target genes; (c) biochemical studies indicate that lithium and the canonical ligand Wnt-3a induce CaMKIV mRNA and protein expression levels in rat hippocampal neurons as well as CaMKIV promoter activity; (d) treatment of hippocampal neurons with Wnt-3a increases the binding of ,-catenin to the CaMKIV promoter: (e) In vivo activation of the Wnt signaling improve spatial memory impairment and restores the expression of CaMKIV in a mice double transgenic model for Alzheimer's disease which shows decreased levels of the kinase. We conclude that CaMKIV is regulated by the Wnt signaling pathway and that its expression could play a role in the neuroprotective function of the Wnt signaling against the Alzheimer's amyloid peptide. J. Cell. Physiol. 221: 658,667, 2009. © 2009 Wiley-Liss, Inc. [source] Lack of neprilysin suffices to generate murine amyloid-like deposits in the brain and behavioral deficit in vivoJOURNAL OF NEUROSCIENCE RESEARCH, Issue 8 2006Rime Madani Abstract Accumulation of the ,-amyloid peptide (A,) in the brain is a major pathological hallmark of Alzheimer's disease (AD), leading to synaptic dysfunction, neuronal death, and memory impairment. The levels of neprilysin, a major A,-degrading enzyme, are decreased in AD brains and during aging. Because neprilysin cleaves A, in vivo, its down-regulation may contribute to the pathophysiology of AD. The aim of this study was to assess the consequences of neprilysin deficiency on accumulation of murine A, in brains and associated pathologies in vivo by investigating neprilysin-deficient mice on biochemical, morphological, and behavioral levels. Aged neprilysin-deficient mice expressed physiological amyloid precursor protein (APP) levels and exhibited elevated brain A, concentrations and amyloid-like deposits in addition to signs of neuronal degeneration in their brains. Behaviorally, neprilysin-deficient mice acquired a significantly weaker conditioned taste aversion that extinguished faster than the aversion of age-matched controls. Our data establish that, under physiological APP expression levels, neprilysin deficiency is associated with increased A, accumulation in the brain and leads to deposition of amyloid-like structures in vivo as well as with signs of AD-like pathology and with behavioral deficits. © 2006 Wiley-Liss, Inc. [source] Nicotine reverses adult-onset hypothyroidism-induced impairment of learning and memory: Behavioral and electrophysiological studiesJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2006K.H. Alzoubi Abstract Nicotine alleviates cognitive impairment associated with a variety of health conditions. We examined the effect of chronic nicotine treatment on adult-onset hypothyroidism-induced impairment of learning and memory in rats. Hypothyroidism was induced by surgical removal of thyroid glands (thyroidectomy). One month later, chronic nicotine treatment (1 mg/kg sc, twice/day) was instituted for 4,6 weeks. Test of hippocampus-dependent spatial learning and memory in the radial arm water maze showed that hypothyroidism impaired learning as well as short-term and long-term memory retention. Chronic nicotine treatment reversed the hypothyroidism-induced learning and memory impairment. In normal rats, chronic nicotine treatment had no effect on learning and memory. Extracellular recordings from the CA1 region of anesthetized hypothyroid rats showed severe reduction of both early-phase and late-phase long-term potentiation (LTP) magnitude, which was reversed in nicotine-treated hypothyroid rats. These results show that chronic nicotine treatment prevents hypothyroidism-induced impairment of spatial cognition and LTP. © 2006 Wiley-Liss, Inc. [source] Apathy may herald cognitive decline and dementia in Parkinson's disease,MOVEMENT DISORDERS, Issue 16 2009Kathy Dujardin PhD Abstract Apathy is usually defined as a lack of motivation. It may occur as part of another disorder (notably depression and dementia) or as an isolated syndrome. In Parkinson's disease (PD), apathy is common and several studies have reported an association between this condition and more severe cognitive symptoms, such as executive dysfunction. However, this association has not been thoroughly investigated. The aim of this study (in nondepressed, nondemented PD patients) was to examine whether or not cognitive decline and/or dementia occurred more frequently in apathetic subjects than in nonapathetic subjects. Forty consecutive PD patients participated in the study (20 with apathy and 20 without). None of the subjects were either demented or depressed at the time of study entry. The patients' cognitive functions were extensively assessed twice: at study entry and after an 18-month follow-up period. At study entry, the apathetic PD patients had significantly lower global cognitive status and executive function scores than the nonapathetic subjects. After a median period of 18 months, the rate of conversion to dementia was found to be significantly higher in the apathetic group than in the nonapathetic group (8 of 20 and 1 of 20, respectively). Even in nondemented patients, the decrease over time in cognitive performance (mainly executive function but also memory impairment) was significantly greater in apathetic subjects than in nonapathetic subjects. These findings suggest that in nondemented, nondepressed PD patients, apathy may be a predictive factor for dementia and cognitive decline over time. © 2009 Movement Disorder Society [source] | |||||||||||||||||||||||||||||||