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      Promising developments in neuropsychological approaches for the detection of preclinical Alzheimer’s disease: a selective review

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          Abstract

          Recently published guidelines suggest that the most opportune time to treat individuals with Alzheimer’s disease is during the preclinical phase of the disease. This is a phase when individuals are defined as clinically normal but exhibit evidence of amyloidosis, neurodegeneration and subtle cognitive/behavioral decline. While our standard cognitive tests are useful for detecting cognitive decline at the stage of mild cognitive impairment, they were not designed for detecting the subtle cognitive variations associated with this biomarker stage of preclinical Alzheimer’s disease. However, neuropsychologists are attempting to meet this challenge by designing newer cognitive measures and questionnaires derived from translational efforts in neuroimaging, cognitive neuroscience and clinical/experimental neuropsychology. This review is a selective summary of several novel, potentially promising, approaches that are being explored for detecting early cognitive evidence of preclinical Alzheimer’s disease in presymptomatic individuals.

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          Frequent amyloid deposition without significant cognitive impairment among the elderly.

          Howard Aizenstein, Robert Nebes, Judith Saxton … (2008)
          To characterize the prevalence of amyloid deposition in a clinically unimpaired elderly population, as assessed by Pittsburgh Compound B (PiB) positron emission tomography (PET) imaging, and its relationship to cognitive function, measured with a battery of neuropsychological tests. Subjects underwent cognitive testing and PiB PET imaging (15 mCi for 90 minutes with an ECAT HR+ scanner). Logan graphical analysis was applied to estimate regional PiB retention distribution volume, normalized to a cerebellar reference region volume, to yield distribution volume ratios (DVRs). University medical center. From a community-based sample of volunteers, 43 participants aged 65 to 88 years who did not meet diagnostic criteria for Alzheimer disease or mild cognitive impairment were included. Regional PiB retention and cognitive test performance. Of 43 clinically unimpaired elderly persons imaged, 9 (21%) showed evidence of early amyloid deposition in at least 1 brain area using an objectively determined DVR cutoff. Demographic characteristics did not differ significantly between amyloid-positive and amyloid-negative participants, and neurocognitive performance was not significantly worse among amyloid-positive compared with amyloid-negative participants. Amyloid deposition can be identified among cognitively normal elderly persons during life, and the prevalence of asymptomatic amyloid deposition may be similar to that of symptomatic amyloid deposition. In this group of participants without clinically significant impairment, amyloid deposition was not associated with worse cognitive function, suggesting that an elderly person with a significant amyloid burden can remain cognitively normal. However, this finding is based on relatively small numbers and needs to be replicated in larger cohorts. Longitudinal follow-up of these subjects will be required to support the potential of PiB imaging to identify preclinical Alzheimer disease, or, alternatively, to show that amyloid deposition is not sufficient to cause Alzheimer disease within some specified period.
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            Imaging beta-amyloid burden in aging and dementia.

            C Rowe, S Ng, U. Ackermann … (2007)
            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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              Alterations in memory networks in mild cognitive impairment and Alzheimer's disease: an independent component analysis.

              Kim Celone, Vince D. Calhoun, Bradford Dickerson … (2006)
              Memory function is likely subserved by multiple distributed neural networks, which are disrupted by the pathophysiological process of Alzheimer's disease (AD). In this study, we used multivariate analytic techniques to investigate memory-related functional magnetic resonance imaging (fMRI) activity in 52 individuals across the continuum of normal aging, mild cognitive impairment (MCI), and mild AD. Independent component analyses revealed specific memory-related networks that activated or deactivated during an associative memory paradigm. Across all subjects, hippocampal activation and parietal deactivation demonstrated a strong reciprocal relationship. Furthermore, we found evidence of a nonlinear trajectory of fMRI activation across the continuum of impairment. Less impaired MCI subjects showed paradoxical hyperactivation in the hippocampus compared with controls, whereas more impaired MCI subjects demonstrated significant hypoactivation, similar to the levels observed in the mild AD subjects. We found a remarkably parallel curve in the pattern of memory-related deactivation in medial and lateral parietal regions with greater deactivation in less-impaired MCI and loss of deactivation in more impaired MCI and mild AD subjects. Interestingly, the failure of deactivation in these regions was also associated with increased positive activity in a neocortical attentional network in MCI and AD. Our findings suggest that loss of functional integrity of the hippocampal-based memory systems is directly related to alterations of neural activity in parietal regions seen over the course of MCI and AD. These data may also provide functional evidence of the interaction between neocortical and medial temporal lobe pathology in early AD.
              Article 0 comments Cited 190 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Dorene M Rentz
                Mario A Parra Rodriguez
                Rebecca Amariglio
                Yaakov Stern
                Reisa Sperling
                Steven Ferris
                Journal
                Journal ID (nlm-ta): Alzheimers Res Ther
                Journal ID (iso-abbrev): Alzheimers Res Ther
                Title: Alzheimer's Research & Therapy
                Publisher: BioMed Central
                ISSN (Electronic): 1758-9193
                Publication date Collection: 2013
                Publication date (Electronic): 21 November 2013
                Publication date PMC-release: 21 November 2014
                Volume: 5
                Issue: 6
                Page: 58
                Affiliations
                [1 ]Center for Alzheimer Research and Treatment, Departments of Neurology, Brigham and Women’s Hospital and Massachusetts General Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, MA 02115, USA
                [2 ]Department of Psychology, University of Edinburgh, Centre for Cognitive Aging and Cognitive Epidemiology, Alzheimer Scotland Dementia Research Centre and Scottish Dementia Clinical Research Network, 7 George Square, Edinburgh EH8 9JZ, UK
                [3 ]Cognitive Neuroscience Division, Department of Neurology, Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032, USA
                [4 ]Alzheimer’s Disease Center, Comprehensive Center for Brain Aging, Department of Psychiatry, NYU Langone Medical Center, 145 East 32nd Street, New York, NY 10016, USA
                Article
                Publisher ID: alzrt222
                DOI: 10.1186/alzrt222
                PMC ID: 3978443
                PubMed ID: 24257331
                SO-VID: 9d6c5b3a-05aa-4dfd-8728-e05bbb34180f
                Copyright © Copyright © 2013 BioMed Central Ltd.
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                Subject: Review

                ScienceOpen disciplines: Neurology
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                ScienceOpen disciplines: Neurology

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