scholarly journals Functional Connectivity Alterations of the Temporal Lobe and Hippocampus in Semantic Dementia and Alzheimer’s Disease

2020 ◽  
pp. 1-15
Author(s):  
Simon Schwab ◽  
Soroosh Afyouni ◽  
Yan Chen ◽  
Zaizhu Han ◽  
Qihao Guo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Functional Connectivity ◽  
Temporal Lobe ◽  
Semantic Dementia

scholarly journals Functional connectivity alterations of the temporal lobe and hippocampus in semantic dementia and Alzheimer’s disease

2018 ◽  
Author(s):  
Simon Schwab ◽  
Soroosh Afyouni ◽  
Yan Chen ◽  
Zaizhu Han ◽  
Qihao Guo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Functional Connectivity ◽  
Episodic Memory ◽  
Semantic Memory ◽  
Temporal Lobe ◽  
Orbitofrontal Cortex ◽  
Semantic Dementia ◽  
Common Pathway ◽  
The Right

AbstractThe severe semantic memory impairments in semantic dementia have been attributed to a pronounced atrophy and functional disruption of the anterior temporal lobes. In contrast, the medial and posterior temporal lobe damage predominantly found in patients with Alzheimer’s disease has been associated with episodic memory disturbance. However, the two dementia subtypes share hippocampal deterioration, despite a relatively spared episodic memory in semantic dementia. To gain more insight into the mutual and divergent functional alterations seen in Alzheimer’s disease and semantic dementia, we assessed the differences in intrinsic functional connectivity between temporal lobe regions in patients with Alzheimer’s disease (n = 16), semantic dementia patients from two international sites (n = 23), and healthy controls (n = 17). In an exploratory study, we used a functional parcellation of the temporal cortex to extract time series. The Alzheimer’s disease group showed a single connection with reduced functional connectivity as compared to the controls. This connection was located between the right orbitofrontal cortex and the right anterior temporal lobe. In contrast, functional connectivity was decreased in the semantic dementia group in six connections, mainly involving the hippocampus, lingual gyrus, temporal pole, and orbitofrontal cortex. We identified a common pathway with semantic dementia, since the functional connectivity between the right anterior temporal lobe and the right orbitofrontal cortex was reduced in both types of dementia. This might be related to social knowledge deficits as part of semantic memory decline. However, such interpretations are preferably made in the context of all disease-specific semantic impairments and functional connectivity changes. Despite some limitations owed to the two database sites, this study provides a first preliminary picture of the brain’s functional dysconnectivity in Alzheimer’s disease and semantic dementia. Future studies are needed to replicate findings of such a common pathway with matched diagnosis, neuropsychological, and data MRI acquisition procedures.

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.

Patterns of temporal lobe atrophy in semantic dementia and Alzheimer's disease

2001 ◽  
Vol 49 (4) ◽  
pp. 433-442 ◽  
Author(s):  
Dennis Chan ◽  
Nick C. Fox ◽  
Rachael I. Scahill ◽  
William R. Crum ◽  
Jennifer L. Whitwell ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Temporal Lobe ◽  
Semantic Dementia ◽  
Lobe Atrophy

scholarly journals Differential medial temporal lobe and default-mode network functional connectivity and morphometric changes in Alzheimer’s Disease

2017 ◽  
Author(s):  
Kamil A. Grajski ◽  
Steven L. Bressler ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Functional Connectivity ◽  
Temporal Lobe ◽  
Default Mode Network ◽  
Medial Temporal Lobe ◽  
Resting State Functional Connectivity ◽  
Default Mode

AbstractWe report group level differential detection of medial temporal lobe resting-state functional connectivity disruption and morphometric changes in the transition from cognitively normal to early mild cognitive impairment in an age-, education- and gender-matched 105 subjects Alzheimer’s Disease Neuroimaging Initiative dataset. In mild Alzheimer’s Disease, but not early mild cognitive impairment, characteristic brain atrophy was detected in FreeSurfer estimates of cortical thickness and subcortical and hippocampal subfield volumes. By contrast, functional connectivity analysis detected earlier significant changes. In early mild cognitive impairment these changes involved medial temporal lobe regions of transentorhinal, perirhinal and entorhinal cortices (associated with the earliest stages of neurofibrillary changes in Alzheimer’s Disease), hippocampus, parahippocampal gyrus and temporal pole, and cortical regions comprising or co-activated with the default-mode network, including rostral and medial prefrontal cortex, anterior cingulate cortex, precuneus and inferior temporal cortex. Key findings include: a) focal and bilaterally symmetric spatial organization of affected medial temporal lobe regions; b) mutual hyperconnectivity bilaterally involving ventral medial temporal lobe structures (temporal pole, uncus); and c) dorsal medial temporal lobe hypoconnectivity with anterior and posterior midline default-mode network nodes. These findings position medial temporal lobe resting state functional connectivity as a candidate biomarker of an Alzheimer’s Disease pathophysiological cascade, potentially in advance of clinical biomarkers, and coincident with biomarkers of the earliest stages of Alzheimer’s neuropathology. Our results indicate that medial temporal lobe resting-state functional connectivity should be further investigated as a potential biomarker in the diagnosis of Alzheimer’s Disease.HighlightsFunctional connectivity change seen before structural change in Alzheimer’s DiseaseMedial temporal lobes mutually hyper-connect in mild cognitive impairmentMedial temporal lobe and default mode network decouple in mild cognitive impairmentLoci of functional change in hippocampi are focal with bilaterally symmetric featuresNonmonotonic functional connectivity changes in Alzheimer’s Disease progression

scholarly journals Medial temporal lobe connectivity and its associations with cognition in early Alzheimer’s disease

Brain ◽  
2020 ◽  
Vol 143 (4) ◽  
pp. 1233-1248 ◽  
Author(s):  
David Berron ◽  
Danielle van Westen ◽  
Rik Ossenkoppele ◽  
Olof Strandberg ◽  
Oskar Hansson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Functional Connectivity ◽  
Temporal Lobe ◽  
Medial Temporal Lobe ◽  
Amyloid Β ◽  
Temporal System ◽  
Early Alzheimer’S Disease

Abstract Human episodic memory critically depends on subregions of the medial temporal lobe, which are part of functional brain systems such as the anterior-temporal and the posterior-medial system. Here we analysed how Alzheimer’s pathology affects functional connectivity within these systems. Data from 256 amyloid-β-negative cognitively unimpaired, 103 amyloid-β-positive cognitively unimpaired, and 83 amyloid-β-positive individuals with mild cognitive impairment were analysed. Amyloid-β and tau pathology were measured using the CSF amyloid-β42/40 ratio and phosphorylated tau, respectively. We found that amyloid-β-positive cognitively unimpaired individuals were mainly characterized by decreased functional connectivity between the medial temporal lobe and regions in the anterior-temporal system, most prominently between left perirhinal/entorhinal cortices and medial prefrontal cortex. Furthermore, correlation analysis in this group revealed decreasing functional connectivity between bilateral perirhinal/entorhinal cortices, anterior hippocampus and posterior-medial regions with increasing levels of phosphorylated tau. The amyloid-β-positive individuals with mild cognitive impairment mostly exhibited reduced connectivity between the medial temporal lobe and posterior-medial regions, predominantly between the anterior hippocampus and posterior cingulate cortex. In addition, they showed hyperconnectivity within the medial temporal lobe and its immediate proximity. Lower medial temporal-cortical functional connectivity networks resulting from the group comparisons of cognitively unimpaired individuals were associated with reduced memory performance and more rapid longitudinal memory decline as shown by linear mixed-effects regression analysis. Finally, we found that reduced medial temporal-cortical connectivity in mildly cognitively impaired individuals was related to reduced entorhinal thickness and white matter integrity of the parahippocampal cingulum and the fornix. No such relationships were found in cognitively unimpaired individuals. In conclusion, our findings show that the earliest changes in preclinical Alzheimer’s disease might involve decreased connectivity within the anterior-temporal system, and early changes in connectivity might be related to memory impairment, but not to structural changes. With disease progression and increased tau pathology, medial temporal functional connectivity with posterior-medial regions seems to be increasingly impaired. In individuals with mild cognitive impairment, reduced functional connectivity is associated with structural brain changes as well as the emergence of locally increased connectivity patterns. Thus, functional connectivity between the medial temporal lobe and the anterior-temporal and posterior-medial system could serve as stage-specific functional markers in early Alzheimer’s disease.

Sign in / Sign up

Export Citation Format

Share Document