scholarly journals The impact of memory impairment on the test of memory malingering (TOMM)

1999 ◽  
Vol 14 (1) ◽  
pp. 99-99
Author(s):  
C. H. Kennedy ◽  
L. M. Ryan ◽  
H. J. Riordan ◽  
M. R. Sperling ◽  
B. L. Malamut
Keyword(s):  
Memory Impairment ◽  
Test Of Memory Malingering ◽  
The Impact

scholarly journals A-221 The Impact of Visuospatial Memory Impairment on Rey 15-Item Test and Test of Memory Malingering Performance: Implications for Performance Validity Assessment

2020 ◽  
Vol 35 (6) ◽  
pp. 1016-1016
Author(s):  
Carter D ◽  
Ovsiew G ◽  
Rhoads T ◽  
Resch Z ◽  
Soble J
Keyword(s):  
Visual Memory ◽  
Memory Impairment ◽  
Visuospatial Memory ◽  
Performance Validity ◽  
Test Of Memory Malingering ◽  
Cross Sectional ◽  
Validity Assessment ◽  
Severe Impairment ◽  
The Impact ◽  
With Memory

Abstract Objective This study examined Rey 15-Item Test (RFIT), RFIT/Recognition Trial, and Test of Memory Malingering-Trial 1 (TOMM-T1) performance as a function of increasing visual memory impairment to assess the effect of bona fide memory deficits on these performance validity tests (PVTs). Method Cross-sectional data from 146 patients who were administered the RFIT, TOMM-T1, and Brief Visuospatial Memory Test-Revised Delayed Recall (BVMT-R DR) trial were examined. In total, 120/146 (82%) were classified as valid and 26/146 (18%) as invalid per 4 independent criterion PVTs. The valid sample was 55% female/45% male, 39% Caucasian, 33% African American, 19% Hispanic, 7% Asian, and 3% other, with mean age of 46.2 (SD = 16.7) and education of 14.0 years (SD = 2.6). BVMT-R DR memory impairment bands were defined as ≥40 T (unimpaired; N = 70), 30-39 T (mild impairment; N = 26), and ≤ 29 T (severe impairment; N = 24). Results Multivariate analysis of variance with memory impairment bands as the fixed factor was significant, (p < .001, np2 = .21). Follow-up ANOVAs for RFIT (p < .001, np2 = .29) and RFIT/Recognition (p < .001, np2 = .34) were significant with large effect sizes, whereas TOMM-T1 (p < .05, np2 = .07) exhibited significant, albeit smaller, differences across memory bands. Post-hoc comparisons showed the unimpaired group outperformed the mild and severe impairment groups on the RFIT and RFIT/Recognition, whereas nonsignificant TOMM-T1 differences emerged between the three memory groups. Finally, significantly more patients with memory impairment failed the RFIT (X2 = 18.01, p < .001), and RFIT/Recognition (X2 = 23.70, p < .001), but not TOMM-T1 (X2 = 3.70, p = .16). Conclusions Results showed the RFIT and RFIT/Recognition were more highly affected by memory impairment and yielded significantly greater false positives with increasing memory impairment compared to TOMM-T1.

scholarly journals Interleukin-1β mediates alterations in mitochondrial fusion/fission proteins and memory impairment induced by amyloid-β oligomers

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Andre F. Batista ◽  
Tayná Rody ◽  
Leticia Forny-Germano ◽  
Suzana Cerdeiro ◽  
Maria Bellio ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mitochondrial Dysfunction ◽  
Memory Impairment ◽  
Mitochondrial Dynamics ◽  
Interleukin 1 ◽  
Amyloid Β ◽  
Mitochondrial Fusion ◽  
Synapse Loss ◽  
Cynomolgus Macaques ◽  
The Impact

Abstract Background The lack of effective treatments for Alzheimer’s disease (AD) reflects an incomplete understanding of disease mechanisms. Alterations in proteins involved in mitochondrial dynamics, an essential process for mitochondrial integrity and function, have been reported in AD brains. Impaired mitochondrial dynamics causes mitochondrial dysfunction and has been associated with cognitive impairment in AD. Here, we investigated a possible link between pro-inflammatory interleukin-1 (IL-1), mitochondrial dysfunction, and cognitive impairment in AD models. Methods We exposed primary hippocampal cell cultures to amyloid-β oligomers (AβOs) and carried out AβO infusions into the lateral cerebral ventricle of cynomolgus macaques to assess the impact of AβOs on proteins that regulate mitochondrial dynamics. Where indicated, primary cultures were pre-treated with mitochondrial division inhibitor 1 (mdivi-1), or with anakinra, a recombinant interleukin-1 receptor (IL-1R) antagonist used in the treatment of rheumatoid arthritis. Cognitive impairment was investigated in C57BL/6 mice that received an intracerebroventricular (i.c.v.) infusion of AβOs in the presence or absence of mdivi-1. To assess the role of interleukin-1 beta (IL-1β) in AβO-induced alterations in mitochondrial proteins and memory impairment, interleukin receptor-1 knockout (Il1r1−/−) mice received an i.c.v. infusion of AβOs. Results We report that anakinra prevented AβO-induced alteration in mitochondrial dynamics proteins in primary hippocampal cultures. Altered levels of proteins involved in mitochondrial fusion and fission were observed in the brains of cynomolgus macaques that received i.c.v. infusions of AβOs. The mitochondrial fission inhibitor, mdivi-1, alleviated synapse loss and cognitive impairment induced by AβOs in mice. In addition, AβOs failed to cause alterations in expression of mitochondrial dynamics proteins or memory impairment in Il1r1−/− mice. Conclusion These findings indicate that IL-1β mediates the impact of AβOs on proteins involved in mitochondrial dynamics and that strategies aimed to prevent pathological alterations in those proteins may counteract synapse loss and cognitive impairment in AD.

Age of major depression onset, depressive symptoms, and risk for subsequent dementia: results of the German Study on Ageing, Cognition, and Dementia in Primary Care Patients (AgeCoDe)

2012 ◽  
Vol 43 (8) ◽  
pp. 1597-1610 ◽  
Author(s):  
K. Heser ◽  
F. Tebarth ◽  
B. Wiese ◽  
M. Eisele ◽  
H. Bickel ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Sex Education ◽  
Memory Impairment ◽  
Late Onset ◽  
Subjective Memory ◽  
Subjective Memory Impairment ◽  
Dementia Risk ◽  
Incident Dementia ◽  
History Of ◽  
The Impact

BackgroundWhether late-onset depression is a risk factor for or a prodrome of dementia remains unclear. We investigated the impact of depressive symptoms and early- v. late-onset depression on subsequent dementia in a cohort of elderly general-practitioner patients (n = 2663, mean age = 81.2 years).MethodRisk for subsequent dementia was estimated over three follow-ups (each 18 months apart) depending on history of depression, particularly age of depression onset, and current depressive symptoms using proportional hazard models. We also examined the additive prediction of incident dementia by depression beyond cognitive impairment.ResultsAn increase of dementia risk for higher age cut-offs of late-onset depression was found. In analyses controlling for age, sex, education, and apolipoprotein E4 genotype, we found that very late-onset depression (aged ⩾70 years) and current depressive symptoms separately predicted all-cause dementia. Combined very late-onset depression with current depressive symptoms was specifically predictive for later Alzheimer's disease (AD; adjusted hazard ratio 5.48, 95% confidence interval 2.41–12.46, p < 0.001). This association was still significant after controlling for cognitive measures, but further analyses suggested that it was mediated by subjective memory impairment with worries.ConclusionsDepression might be a prodrome of AD but not of dementia of other aetiology as very late-onset depression in combination with current depressive symptoms, possibly emerging as a consequence of subjectively perceived worrisome cognitive deterioration, was most predictive. As depression parameters and subjective memory impairment predicted AD independently of objective cognition, clinicians should take this into account.

scholarly journals Aripiprazole ameliorates scopolamine-induced amnesia in mice

2021 ◽  
Vol 18 (1) ◽  
pp. 12-24
Author(s):  
Lawrence Adedayo ◽  
Godgift Offor ◽  
Olalekan Jolayemi ◽  
Gideon Ojo ◽  
Olubayode Bamidele ◽  
...  
Keyword(s):  
Memory Impairment ◽  
First Generation ◽  
Memory Performance ◽  
Anti Psychotic ◽  
Amnesic Effect ◽  
Group 4 ◽  
Y Maze ◽  
Group 5 ◽  
Group 2 ◽  
The Impact

Aripiprazole, a known third generation anti-psychotic drug. The drug has shown to have lesser side effects on extrapyramidal system and enhance memory when compared with the first-generation anti-psychotic drugs. However, studies on the impact of aripiprazole on scopolamine-induced memory impairment in mice have been poorly reported. This study was designed to investigate the impact of aripiprazole on scopolamine-induced amnesia in mice. Thirtysix (36) mice weighing between 20-23g were randomly divided into six groups. Group 1 was given 10 ml/kg distilled water. Group 2 received 3 mg/kg scopolamine alone. Group 3 was given 1 mg/kg  donepezil. Group 4 received 0.5 mg/kg aripiprazole. Group 5 was given 0.3 mg/kg aripiprazole. Group 6 received 0.1mg/kg aripiprazole. Thirty minutes after administration of either aripiprazole or donepezil, scopolamine (3 mg/kg) was administered, intraperitoneally. The administration was for 7days, during which their memory was assessed using Morris water maze and Y-maze models. The results showed that the anti-amnesic effect of aripiprazole appeared to be dosedependent; the animals administered with 0.5 mg/kg aripiprazole showed the greatest improved memory performance against scopolamine-induced amnesia. The hippocampal and prefrontal cortex tissues displayed anti-amnesic potential of aripiprazole. Aripiprazole seems to improved memory performance against scopolamine-induced memory impairment in mice. Keywords: Aripiprazole; Anti-amnesic; Scopolamine; Memory

scholarly journals APOE4 is associated with cognitive and pathological heterogeneity in patients with Alzheimer’s disease: a systematic review

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Sheina Emrani ◽  
Hirra A. Arain ◽  
Cassandra DeMarshall ◽  
Tal Nuriel
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Atrophy ◽  
Medial Temporal Lobe ◽  
Memory Impairment ◽  
Phenotypic Differences ◽  
Visuospatial Abilities ◽  
Parietal Lobes ◽  
Ε4 Allele ◽  
The Impact

Abstract Possession of the ε4 allele of apolipoprotein E (APOE) is the primary genetic risk factor for the sporadic form of Alzheimer’s disease (AD). While researchers have extensively characterized the impact that APOE ε4 (APOE4) has on the susceptibility of AD, far fewer studies have investigated the phenotypic differences of patients with AD who are APOE4 carriers vs. those who are non-carriers. In order to understand these differences, we performed a qualitative systematic literature review of the reported cognitive and pathological differences between APOE4-positive (APOE4+) vs. APOE4-negative (APOE4−) AD patients. The studies performed on this topic to date suggest that APOE4 is not only an important mediator of AD susceptibility, but that it likely confers specific phenotypic heterogeneity in AD presentation, as well. Specifically, APOE4+ AD patients appear to possess more tau accumulation and brain atrophy in the medial temporal lobe, resulting in greater memory impairment, compared to APOE4− AD patients. On the other hand, APOE4− AD patients appear to possess more tau accumulation and brain atrophy in the frontal and parietal lobes, resulting in greater impairment in executive function, visuospatial abilities, and language, compared to APOE4+ AD patients. Although more work is necessary to validate and interrogate these findings, these initial observations of pathological and cognitive heterogeneity between APOE4+ vs. APOE4− AD patients suggest that there is a fundamental divergence in AD manifestation related to APOE genotype, which may have important implications in regard to the therapeutic treatment of these two patient populations.

Hidden Disabilities in Multiple Sclerosis – The impact of Multiple Sclerosis on Patients and their Caregivers

2013 ◽  
Vol 8 ((Suppl.1)) ◽  
pp. 2 ◽  
Author(s):  
Gavin Giovannoni ◽  
John F Fole ◽  
David W Brandes ◽  
◽  
◽  
...  
Keyword(s):  
Quality Of Life ◽  
Multiple Sclerosis ◽  
Memory Impairment ◽  
Sexual Dysfunctions ◽  
Walking Ability ◽  
Pharmacological Treatments ◽  
Heterogeneous Condition ◽  
Hidden Disabilities ◽  
The Impact

Multiple sclerosis (MS) is a heterogeneous condition that presents with a large variety of symptoms. While motor functions including coordination, gait and walking ability are clearly visible to clinicians, including MS specialists. These are sometimes termed hidden disabilities and are often overlooked because patients do not mention them in consultations, either because they are embarrassed, do not want to disappoint their family and therefore do not mention the symptoms, or they have not linked the symptoms to their disease. Hidden disabilities in MS include cognition and memory impairment, depression, anxiety and pseudobulbar affect, pain, fatigue, sleep disorders, bowel, bladder and sexual dysfunctions, osteopenia and osteoporosis. These disabilities are associated with a reduced quality of life in patients, their families and caregivers, and affect the ability of patients to function in everyday life. Pharmacological treatments and other interventions are available to manage these symptoms; however, the effectiveness of these interventions in MS is variable. There is need for greater recognition and further research into therapeutic options to reduce the burden of hidden disabilities in MS.

scholarly journals The cognitive consequences of the COVID-19 epidemic: collateral damage?

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Karen Ritchie ◽  
Dennis Chan ◽  
Tam Watermeyer
Keyword(s):  
Neurological Disorders ◽  
Memory Impairment ◽  
Animal Studies ◽  
Epidemiological Studies ◽  
Neural Basis ◽  
Cognitive Difficulties ◽  
System A ◽  
Cognitive Consequences ◽  
The Impact

Abstract Recovery from coronavirus disease 2019 (COVID-19) will be principally defined in terms of remission from respiratory symptoms; however, both clinical and animal studies have shown that coronaviruses may spread to the nervous system. A systematic search on previous viral epidemics revealed that while there has been relatively little research in this area, clinical studies have commonly reported neurological disorders and cognitive difficulties. Little is known with regard to their incidence, duration or underlying neural basis. The hippocampus appears to be particularly vulnerable to coronavirus infections, thus increasing the probability of post-infection memory impairment, and acceleration of neurodegenerative disorders such as Alzheimer’s disease. Future knowledge of the impact of COVID-19, from epidemiological studies and clinical practice, will be needed to develop future screening and treatment programmes to minimize the long-term cognitive consequences of COVID-19.

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