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      Non-Alzheimer's disease—related memory impairment and dementia

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          Abstract

          Although Alzheimer's disease (AD) is a common cause of memory impairment and dementia in the elderly disturbed memory function is a widespread subjective and/or objective symptom in a variety of medical conditions. The early detection and correct distinction of AD from non-AD memory impairment is critically important to detect possibly treatable and reversible underlying causes. In the context of clinical research, it is crucial to correctly distinguish between AD or non-AD memory impairment in order to build homogenous study populations for the assessment of new therapeutic possibilities. The distinction of AD from non-AD memory impairment may be difficult, especially in mildly affected patients, due to an overlap of clinical symptoms and biomarker alterations between AD and certain non-AD conditions. This review aims to describe recent aspects of the differential diagnosis of AD and non-AD related memory impairment and how these may be considered in the presence of memory deficits.

          Translated abstract

          Aunque la Enfermedad de Alzheimer (EA) constituye una causa común de demencía y deterioro de memoria en la vejez, el trastorno de memoria es un síntoma generalizado objetivo ylo subjetivo en una variedad de situaciones médicas. La detección precoz y la correcta distinción entre la EA y el deterioro de memoria no-EA es muy importante para determinar causas subyacentes posiblemente tratables y reversibles. En el contexto de la investigation clínica es clave distinguir correctamente entre EA y deterioro de memoria no-EA para conformar poblaciones homogéneas de estudio para la evaluación de nuevas alternativas terapéuticas. La distinción entre EA y deterioro de memoria no-EA puede resultar difícíl, especialmente en pacientes con compromise leve, debido a una sobreposición de sintomas clínicos y alteraciones de biomarcadores entre la EA y ciertas condiciones no-EA. Esta revisóon tiene como objetivo describir aspectos recientes del diagnóstico diferencial de la EA y del deterioro de memoria no relacionado con la EA, y cómo estos pueden considerarse cuando hay presencia de déficit de memoria.

          Translated abstract

          La maladie d'Alzheimer (MA) est une cause fréquente de troubles de la mémoire et de démence chez les sujets âgés mais une fonction mnésique perturbée est un symptôme subjectif et/ou objectif très répandu dans de nombreuses pathologies. La détection précoce et une distinction correcte entre troubles mnésiques lies ou non à la MA sont primordiales pour diagnostiquer des causes sous-jacentes qui pourraient être réversibles et traitables. En recherche clinique, faire cette distinction est essentiel pour constituer des populations d'étude homogènes afin d'évaluer de nouveaux traitements. La superposition des symptômes cliniques et des modifications des biomarqueurs entre la MA et d'autres pathologies non-MA peut rendre difficile la différentiation selon I'étiologie, surtout chez les patients légèrement atteints. Dans cet article nous décrivons les caractéristiques récentes du diagnostic différentiel entre troubles mnésiques liés ou non à la MA et leur prise en compte en présence d'un déficit de la mémoire.

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          Most cited references57

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          Structural neuroimaging studies in major depressive disorder. Meta-analysis and comparison with bipolar disorder.

          Although differences in clinical characteristics exist between major depressive disorder (MDD) and bipolar disorder (BD), consistent structural brain abnormalities that distinguish the disorders have not been identified. To investigate structural brain changes in MDD using meta-analysis of primary studies; assess the effects of medication, demographic, and clinical variables; and compare the findings with those of a meta-analysis of studies on BD. The MEDLINE, EMBASE, and PsycINFO databases were searched for studies from January 1, 1980, to February 2, 2010. Two hundred twenty-five studies that used magnetic resonance imaging or x-ray computed tomography to compare brain structure in patients with MDD with that of controls were included in an online database, and 143 that measured common brain structures were selected for meta-analysis. Twenty-five variables, including demographic and clinical data, were extracted from each study, when available. For the meta-analysis, mean structure size and standard deviation were extracted for continuous variables, and the proportion of patients and controls with an abnormality in brain structure was extracted for categorical variables. Compared with the structure of a healthy brain, MDD was associated with lateral ventricle enlargement; larger cerebrospinal fluid volume; and smaller volumes of the basal ganglia, thalamus, hippocampus, frontal lobe, orbitofrontal cortex, and gyrus rectus. Patients during depressive episodes had significantly smaller hippocampal volume than patients during remission. Compared with BD patients, those with MDD had reduced rates of deep white matter hyperintensities, increased corpus callosum cross-sectional area, and smaller hippocampus and basal ganglia. Both disorders were associated with increased lateral ventricle volume and increased rates of subcortical gray matter hyperintensities compared with healthy controls. The meta-analyses revealed structural brain abnormalities in MDD that are distinct from those observed in BD. These findings may aid investigators attempting to discriminate mood disorders using structural magnetic resonance imaging data.
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            Imaging beta-amyloid burden in aging and dementia.

            To compare brain beta-amyloid (Abeta) burden measured with [(11)C]Pittsburgh Compound B (PIB) PET in normal aging, Alzheimer disease (AD), and other dementias. Thirty-three subjects with dementia (17 AD, 10 dementia with Lewy bodies [DLB], 6 frontotemporal dementia [FTD]), 9 subjects with mild cognitive impairment (MCI), and 27 age-matched healthy control subjects (HCs) were studied. Abeta burden was quantified using PIB distribution volume ratio. Cortical PIB binding was markedly elevated in every AD subject regardless of disease severity, generally lower and more variable in DLB, and absent in FTD, whereas subjects with MCI presented either an "AD-like" (60%) or normal pattern. Binding was greatest in the precuneus/posterior cingulate, frontal cortex, and caudate nuclei, followed by lateral temporal and parietal cortex. Six HCs (22%) showed cortical uptake despite normal neuropsychological scores. PIB binding did not correlate with dementia severity in AD or DLB but was higher in subjects with an APOE-epsilon4 allele. In DLB, binding correlated inversely with the interval from onset of cognitive impairment to diagnosis. Pittsburgh Compound B PET findings match histopathologic reports of beta-amyloid (Abeta) distribution in aging and dementia. Noninvasive longitudinal studies to better understand the role of amyloid deposition in the course of neurodegeneration and to determine if Abeta deposition in nondemented subjects is preclinical AD are now feasible. Our findings also suggest that Abeta may influence the development of dementia with Lewy bodies, and therefore strategies to reduce Abeta may benefit this condition.
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              The global cognitive impairment in schizophrenia: consistent over decades and around the world.

              Schizophrenia results in cognitive impairments as well as positive, negative, and disorganized symptomatology. The present study examines the extent to which these cognitive deficits are generalized across domains, potential moderator variables, and whether the pattern of cognitive findings reported in schizophrenia has remained consistent over time and across cultural and geographic variation. Relevant publications from 2006 to 2011 were identified through keyword searches in PubMed and an examination of reference lists. Studies were included if they (1) compared the cognitive performance of adult schizophrenia patients and healthy controls, (2) based schizophrenia diagnoses on contemporary diagnostic criteria, (3) reported information sufficient to permit effect size calculation, (4) were reported in English, and (5) reported data for neuropsychological tests falling into at least 3 distinct cognitive domains. A set of 100 non-overlapping studies was identified, and effect sizes (Hedge's g) were calculated for each cognitive variable. Consistent with earlier analyses, patients with schizophrenia scored significantly lower than controls across all cognitive tests and domains (grand mean effect size, g=-1.03). Patients showed somewhat larger impairments in the domains of processing speed (g=-1.25) and episodic memory (g=-1.23). Our results also showed few inconsistencies when grouped by geographic region. The present study extends findings from 1980 to 2006 of a substantial, generalized cognitive impairment in schizophrenia, demonstrating that this finding has remained robust over time despite changes in assessment instruments and alterations in diagnostic criteria, and that it manifests similarly in different regions of the world despite linguistic and cultural differences. © 2013.
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                Author and article information

                Contributors
                Department of Psychiatry and Psychotherapy, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
                Journal
                Dialogues Clin Neurosci
                Dialogues Clin Neurosci
                Dialogues Clin Neurosci
                Dialogues in Clinical Neuroscience
                Les Laboratoires Servier (France )
                1294-8322
                1958-5969
                December 2013
                December 2013
                : 15
                : 4
                : 465-473
                Affiliations
                Department of Psychiatry and Psychotherapy, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
                Author notes
                Article
                10.31887/DCNS.2013.15.4/sarlt
                3898684
                24459413
                ca6a7adf-323c-44ad-ade2-2920588fb6d3
                Copyright: © 2013 Institut la Conférence Hippocrate - Servier Research Group

                This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by-nc-nd/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Clinical Research

                Neurosciences
                alzheimer's disease,lewy body dementia,frontotemporal dementia,depression,differential diagnosis,biomarker

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