Rethinking the Cognitive Mechanisms Underlying Pantomime of Tool Use: Evidence from Alzheimer’s Disease and Semantic Dementia

2017 ◽  
Vol 23 (2) ◽  
pp. 128-138 ◽  
Author(s):  
Mathieu Lesourd ◽  
Josselin Baumard ◽  
Christophe Jarry ◽  
Frédérique Etcharry-Bouyx ◽  
Serge Belliard ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Problem Solving ◽  
Tool Use ◽  
Complex Problem ◽  
Semantic Dementia ◽  
Cognitive Mechanisms ◽  
Global Performance ◽  
And Control ◽  
Production Errors

AbstractObjectives: Pantomiming the use of familiar tools is a central test in the assessment of apraxia. However, surprisingly, the nature of the underlying cognitive mechanisms remains an unresolved issue. The aim of this study is to shed a new light on this issue by exploring the role of functional, mechanical, and manipulation knowledge in patients with Alzheimer’s disease and semantic dementia and apraxia of tool use. Methods: We performed multiple regression analyses with the global performance and the nature of errors (i.e., production and conception) made during a pantomime of tool use task in patients and control participants as dependent variables and tasks investigating functional, mechanical, and manipulation knowledge as predictors. Results: We found that mechanical problem solving, assessing mechanical knowledge, was a good predictor of the global performance of pantomime of tool use. We also found that occurrence of conception errors was robustly predicted by the task assessing functional knowledge whereas that of production errors was not explained by only one predictor. Conclusions: Our results suggest that both functional and mechanical knowledge are important to pantomime the use of tools. To our knowledge, this is the first demonstration that mechanical knowledge plays a role in pantomime of tool use. Although impairment in pantomime of tool use tasks (i.e., apraxia) is widely explained by the disruption of manipulation knowledge, we propose that pantomime of tool use is a complex problem-solving task. (JINS, 2017, 23, 128–138)

Mechanical problem-solving strategies in Alzheimer’s disease and semantic dementia.

2016 ◽  
Vol 30 (5) ◽  
pp. 612-623 ◽  
Author(s):  
Mathieu Lesourd ◽  
Josselin Baumard ◽  
Christophe Jarry ◽  
Frédérique Etcharry-Bouyx ◽  
Serge Belliard ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Problem Solving ◽  
Semantic Dementia ◽  
Mechanical Problem ◽  
Problem Solving Strategies

scholarly journals One Size Does Not Fit All: Face Emotion Processing Impairments in Semantic Dementia, Behavioural-Variant Frontotemporal Dementia and Alzheimer’s Disease Are Mediated by Distinct Cognitive Deficits

2012 ◽  
Vol 25 (1) ◽  
pp. 53-60 ◽  
Author(s):  
Laurie A. Miller ◽  
Sharpley Hsieh ◽  
Suncica Lah ◽  
Sharon Savage ◽  
John R. Hodges ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontotemporal Dementia ◽  
Emotion Processing ◽  
Semantic Dementia ◽  
Cognitive Mechanisms ◽  
Healthy Control ◽  
Patient Groups ◽  
Matching Performance ◽  
Selection Tasks

Patients with frontotemporal dementia (both behavioural variant [bvFTD] and semantic dementia [SD]) as well as those with Alzheimer's disease (AD) show deficits on tests of face emotion processing, yet the mechanisms underlying these deficits have rarely been explored. We compared groups of patients with bvFTD (n= 17), SD (n= 12) or AD (n= 20) to an age- and education-matched group of healthy control subjects (n= 36) on three face emotion processing tasks (Ekman 60, Emotion Matching and Emotion Selection) and found that all three patient groups were similarly impaired. Analyses of covariance employed to partial out the influences of language and perceptual impairments, which frequently co-occur in these patients, provided evidence of different underlying cognitive mechanisms. These analyses revealed that language impairments explained the original poor scores obtained by the SD patients on the Ekman 60 and Emotion Selection tasks, which involve verbal labels. Perceptual deficits contributed to Emotion Matching performance in the bvFTD and AD patients. Importantly, all groups remained impaired on one task or more following these analyses, denoting a primary emotion processing disturbance in these dementia syndromes. These findings highlight the multifactorial nature of emotion processing deficits in patients with dementia.

SPECIFIC PROPERTIES OF TUBULIN IN THE PREFRONTAL CORTEX IN CONTROL, SCHIZOPHRENIA AND VASCULAR DEMENTIA

2020 ◽  
pp. 65-71
Author(s):  
Burbaeva G.Sh. ◽  
Androsova L.V. ◽  
Vorobyeva E.A. ◽  
Savushkina O.K.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prefrontal Cortex ◽  
Vascular Dementia ◽  
Binding Activity ◽  
Nephelometric Method ◽  
Rate Of Polymerization ◽  
Mental Diseases ◽  
And Control ◽  
The Brain

The aim of the study was to evaluate the rate of polymerization of tubulin into microtubules and determine the level of colchicine binding (colchicine-binding activity of tubulin) in the prefrontal cortex in schizophrenia, vascular dementia (VD) and control. Colchicine-binding activity of tubulin was determined by Sherlinе in tubulin-enriched extracts of proteins from the samples. Measurement of light scattering during the polymerization of the tubulin was carried out using the nephelometric method at a wavelength of 450-550 nm. There was a significant decrease in colchicine-binding activity and the rate of tubulin polymerization in the prefrontal cortex in both diseases, and in VD to a greater extent than in schizophrenia. The obtained results suggest that not only in Alzheimer's disease, but also in other mental diseases such as schizophrenia and VD, there is a decrease in the level of tubulin in the prefrontal cortex of the brain, although to a lesser extent than in Alzheimer's disease, and consequently the amount of microtubules.

scholarly journals Distinct network topology in Alzheimer’s disease and behavioral variant frontotemporal dementia

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Adeline Su Lyn Ng ◽  
Juan Wang ◽  
Kwun Kei Ng ◽  
Joanna Su Xian Chong ◽  
Xing Qian ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontotemporal Dementia ◽  
Network Topology ◽  
Neuropsychiatric Symptoms ◽  
Brain Network ◽  
Salience Network ◽  
Behavioral Variant Frontotemporal Dementia ◽  
Control Networks ◽  
And Control

Abstract Background Alzheimer’s disease (AD) and behavioral variant frontotemporal dementia (bvFTD) cause distinct atrophy and functional disruptions within two major intrinsic brain networks, namely the default network and the salience network, respectively. It remains unclear if inter-network relationships and whole-brain network topology are also altered and underpin cognitive and social–emotional functional deficits. Methods In total, 111 participants (50 AD, 14 bvFTD, and 47 age- and gender-matched healthy controls) underwent resting-state functional magnetic resonance imaging (fMRI) and neuropsychological assessments. Functional connectivity was derived among 144 brain regions of interest. Graph theoretical analysis was applied to characterize network integration, segregation, and module distinctiveness (degree centrality, nodal efficiency, within-module degree, and participation coefficient) in AD, bvFTD, and healthy participants. Group differences in graph theoretical measures and empirically derived network community structures, as well as the associations between these indices and cognitive performance and neuropsychiatric symptoms, were subject to general linear models, with age, gender, education, motion, and scanner type controlled. Results Our results suggested that AD had lower integration in the default and control networks, while bvFTD exhibited disrupted integration in the salience network. Interestingly, AD and bvFTD had the highest and lowest degree of integration in the thalamus, respectively. Such divergence in topological aberration was recapitulated in network segregation and module distinctiveness loss, with AD showing poorer modular structure between the default and control networks, and bvFTD having more fragmented modules in the salience network and subcortical regions. Importantly, aberrations in network topology were related to worse attention deficits and greater severity in neuropsychiatric symptoms across syndromes. Conclusions Our findings underscore the reciprocal relationships between the default, control, and salience networks that may account for the cognitive decline and neuropsychiatric symptoms in dementia.

scholarly journals Anhedonia in Semantic Dementia—Exploring Right Hemispheric Contributions to the Loss of Pleasure

2021 ◽  
Vol 11 (8) ◽  
pp. 998
Author(s):  
Siobhán R. Shaw ◽  
Hashim El-Omar ◽  
Siddharth Ramanan ◽  
Olivier Piguet ◽  
Rebekah M. Ahmed ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Temporal Lobe ◽  
Rating Scale ◽  
Right Hemisphere ◽  
Semantic Knowledge ◽  
Semantic Dementia ◽  
Anterior Cingulate ◽  
Functional Impairments ◽  
Lobe Atrophy

Semantic dementia (SD) is a younger-onset neurodegenerative disease characterised by progressive deterioration of the semantic knowledge base in the context of predominantly left-lateralised anterior temporal lobe (ATL) atrophy. Mounting evidence indicates the emergence of florid socioemotional changes in SD as atrophy encroaches into right temporal regions. How lateralisation of temporal lobe pathology impacts the hedonic experience in SD remains largely unknown yet has important implications for understanding socioemotional and functional impairments in this syndrome. Here, we explored how lateralisation of temporal lobe atrophy impacts anhedonia severity on the Snaith–Hamilton Pleasure Scale in 28 SD patients presenting with variable right- (SD-R) and left-predominant (SD-L) profiles of temporal lobe atrophy compared to that of 30 participants with Alzheimer’s disease and 30 healthy older Control participants. Relative to Controls, SD-R but not SD-L or Alzheimer’s patients showed clinically significant anhedonia, representing a clear departure from premorbid levels. Overall, anhedonia was more strongly associated with functional impairment on the Frontotemporal Dementia Functional Rating Scale and motivational changes on the Cambridge Behavioural Inventory in SD than in Alzheimer’s disease patients. Voxel-based morphometry analyses revealed that anhedonia severity correlated with reduced grey matter intensity in a restricted set of regions centred on right orbitofrontal and temporopolar cortices, bilateral posterior temporal cortices, as well as the anterior cingulate gyrus and parahippocampal gyrus, bilaterally. Finally, regression and mediation analysis indicated a unique role for right temporal lobe structures in modulating anhedonia in SD. Our findings suggest that degeneration of predominantly right-hemisphere structures deleteriously impacts the capacity to experience pleasure in SD. These findings offer important insights into hemispheric lateralisation of motivational disturbances in dementia and suggest that anhedonia may emerge at different timescales in the SD disease trajectory depending on the integrity of the right hemisphere.

scholarly journals EAAT2 Expression in the Hippocampus, Subiculum, Entorhinal Cortex and Superior Temporal Gyrus in Alzheimer’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Jason H. Y. Yeung ◽  
Thulani H. Palpagama ◽  
Oliver W. G. Wood ◽  
Clinton Turner ◽  
Henry J. Waldvogel ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Entorhinal Cortex ◽  
Excitatory Amino Acid ◽  
Glutamate Uptake ◽  
Expression Patterns ◽  
Superior Temporal Gyrus ◽  
Altered Expression ◽  
And Control ◽  
Transporter Expression

Alzheimer’s disease (AD) is a neuropathological disorder characterized by the presence and accumulation of amyloid-beta plaques and neurofibrillary tangles. Glutamate dysregulation and the concept of glutamatergic excitotoxicity have been frequently described in the pathogenesis of a variety of neurodegenerative disorders and are postulated to play a major role in the progression of AD. In particular, alterations in homeostatic mechanisms, such as glutamate uptake, have been implicated in AD. An association with excitatory amino acid transporter 2 (EAAT2), the main glutamate uptake transporter, dysfunction has also been described. Several animal and few human studies examined EAAT2 expression in multiple brain regions in AD but studies of the hippocampus, the most severely affected brain region, are scarce. Therefore, this study aims to assess alterations in the expression of EAAT2 qualitatively and quantitatively through DAB immunohistochemistry (IHC) and immunofluorescence within the hippocampus, subiculum, entorhinal cortex, and superior temporal gyrus (STG) regions, between human AD and control cases. Although no significant EAAT2 density changes were observed between control and AD cases, there appeared to be increased transporter expression most likely localized to fine astrocytic branches in the neuropil as seen on both DAB IHC and immunofluorescence. Therefore, individual astrocytes are not outlined by EAAT2 staining and are not easily recognizable in the CA1–3 and dentate gyrus regions of AD cases, but the altered expression patterns observed between AD and control hippocampal cases could indicate alterations in glutamate recycling and potentially disturbed glutamatergic homeostasis. In conclusion, no significant EAAT2 density changes were found between control and AD cases, but the observed spatial differences in transporter expression and their functional significance will have to be further explored.

scholarly journals Surface-based analysis of cortical thickness and volume loss in Alzheimer’s disease

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Emily Iannopollo ◽  
Ryan Plunkett ◽  
Kara Garcia
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Magnetic Resonance ◽  
Cortical Thickness ◽  
Surface Matching ◽  
Cortical Surface ◽  
Volume Loss ◽  
Cortical Volume ◽  
Human Connectome Project ◽  
And Control

Background and Hypothesis: Magnetic resonance imaging (MRI) has become a useful tool in monitoring the progression of Alzheimer's disease. Previous surface-based analysis has focused on changes in cortical thickness associated with the disease1. The objective of this study is to analyze MRI-derived cortical reconstructions for patterns of atrophy in terms of both cortical thickness and cortical volume. We hypothesize that Alzheimer’s Disease progression will be associated with a more significant change in volume than thickness. Experimental Design or Project Methods: MRI data was obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI). All subjects with baseline and two-year 3T MRI scans were included. Segmentation of MRIs into gray and white matter was performed with FreeSurfer2,3,4,5. Subjects whose scans did not segment accurately were excluded. Surfaces were then registered to a common atlas with Ciftify6, and anatomically-constrained Multimodal Surface Matching (aMSM) was used to analyze longitudinal changes in each subject7. This produced continuous surface maps showing changes in cortical surface area and thickness. These maps were multiplied to create cortical volume maps8. Permutation Analysis of Linear Models (PALM) was used to perform two-sample t-tests comparing the maps of the Alzheimer’s and control groups9. Results: Preliminary analysis of nine Alzheimer’s subjects and nine control subjects produced surface maps displaying patterns that were expected given previous research findings10,11. There was increased volume and thickness loss in Alzheimer’s subjects relative to controls, with relatively high loss in structures of the medial temporal lobe. Future analysis of a larger sample will determine whether statistically significant differences exist between the Alzheimer’s and control groups in terms of thickness loss and volume loss. Conclusion and Potential Impact: If significant results are found, surface-based analysis of cortical volume may allow for detection of atrophy at an earlier stage in disease progression than would be possible based on cortical thickness.   References 1. Clarkson MJ, Cardoso MJ, Ridgway GR, Modat M, Leung KK, Rohrer JD, Fox NC, Ourselin S. A comparison of voxel and surface based cortical thickness estimation methods. NeuroImage. 2011 Aug 1; 57(3):856-65. 2. Dale AM, Fischl B, Sereno MI. Cortical surface-based analysis. I. Segmentation and surface reconstruction. Neuroimage. 1999;9:179194. 3. Fischl B, Sereno M, Dale A. Cortical surface-based analysis. II: Inflation, flattening, and a surface-based coordinate system. Neuroimage. 1999;9:195–207.  4. Fischl B, Salat DH, Busa E, Albert M, Dieterich M, Haselgrove C, van der Kouwe A, Killiany R, Kennedy D, Klaveness S, Montillo A, Makris N, Rosen B, Dale AM. Whole brain segmentation: automated labeling of neuroanatomical structures in the human brain. Neuron 2002;33:341-355. 5. Fischl B, Salat DH, van der Kouwe AJ, Makris N, Segonne F, Quinn BT, Dale AM. Sequence-independent segmentation of magnetic resonance images. Neuroimage 2004;23 Suppl 1:S69-84. 6. Glasser MF, Sotiropoulos SN, Wilson JA, Coalson TS, Fischl B, Andersson JL, Xu J, Jbabdi S, Webster M, Polimeni JR, Van Essen DC, Jenkinson M, WU-Minn HCP Consortium. The minimal preprocessing pipelines for the Human Connectome Project. Neuroimage. 2013 Oct 15;80:105-24. 7. Robinson EC, Garcia K, Glasser MF, Chen Z, Coalson TS, Makropoulos A, Bozek J, Wright R, Schuh A, Webster M, Hutter J, Price A, Cordero Grande L, Hughes E, Tusor N, Bayly PV, Van Essen DC, Smith SM, Edwards AD, Hajnal J, Jenkinson M, Glocker B, Rueckert D. Multimodal surface matching with higher-order smoothness constraints. Neuroimage. 2018;167:453-65. 8. Marcus DS, Harwell J, Olsen T, Hodge M, Glasser MF, Prior F, Jenkinson M, Laumann T, Curtiss SW, Van Essen DC. Informatics and data mining tools and strategies for the human connectome project. Front Neuroinform 2011;5:4. 9. Winkler AM, Ridgway GR, Webster MA, Smith SM, Nichols TE. Permutation inference for the general linear model. NeuroImage, 2014;92:381-397 10. Matsuda, H. MRI morphometry in Alzheimer’s disease. Ageing Research Reviews. 2016 Sep;30:17-24. 11. Risacher SL, Shen L, West JD, Kim S, McDonald BC, Beckett LA, Harvey DJ, Jack CR Jr, Weiner MW, Saykin AJ. Alzheimer's Disease Neuroimaging Initiative (ADNI). Longitudinal MRI atrophy biomarkers: relationship to conversion in the ADNI cohort. Neurobiol Aging. 2010 Aug;31(8):1401-18. 

Decreased α-Synuclein Serum Levels in Patients with Lewy Body Dementia Compared to Alzheimer’s Disease Patients and Control Subjects

2011 ◽  
Vol 31 (6) ◽  
pp. 413-416 ◽  
Author(s):  
Christoph Laske ◽  
Andreas J. Fallgatter ◽  
Elke Stransky ◽  
Katja Hagen ◽  
Daniela Berg ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Lewy Body Dementia ◽  
Serum Levels ◽  
Control Subjects ◽  
And Control
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