Structural Changes in Thalamic Nuclei Across Prodromal and Clinical Alzheimer’s Disease

2021 ◽  
pp. 1-11
Author(s):  
Adam S. Bernstein ◽  
Steven Z. Rapcsak ◽  
Michael Hornberger ◽  
Manojkumar Saranathan ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Large Scale ◽  
Structural Changes ◽  
Thalamic Nuclei ◽  
Medial Temporal Lobes ◽  
Cognitive Changes ◽  
Temporal Lobes ◽  
Medial Geniculate ◽  
Healthy Control

Background: Increasing evidence suggests that thalamic nuclei may atrophy in Alzheimer’s disease (AD). We hypothesized that there will be significant atrophy of limbic thalamic nuclei associated with declining memory and cognition across the AD continuum. Objective: The objective of this work was to characterize volume differences in thalamic nuclei in subjects with early and late mild cognitive impairment (MCI) as well as AD when compared to healthy control (HC) subjects using a novel MRI-based thalamic segmentation technique (THOMAS). Methods: MPRAGE data from the ADNI database were used in this study (n = 540). Healthy control (n = 125), early MCI (n = 212), late MCI (n = 114), and AD subjects (n = 89) were selected, and their MRI data were parcellated to determine the volumes of 11 thalamic nuclei for each subject. Volumes across the different clinical subgroups were compared using ANCOVA. Results: There were significant differences in thalamic nuclei volumes between HC, late MCI, and AD subjects. The anteroventral, mediodorsal, pulvinar, medial geniculate, and centromedian nuclei were significantly smaller in subjects with late MCI and AD when compared to HC subjects. Furthermore, the mediodorsal, pulvinar, and medial geniculate nuclei were significantly smaller in early MCI when compared to HC subjects. Conclusion: This work highlights nucleus specific atrophy within the thalamus in subjects with early and late MCI and AD. This is consistent with the hypothesis that memory and cognitive changes in AD are mediated by damage to a large-scale integrated neural network that extends beyond the medial temporal lobes.

Structural MRI in Alzheimer’s Disease

2020 ◽  
pp. 208-240
Author(s):  
Briana S. Last ◽  
Batool Rizvi ◽  
Adam M. Brickman
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrovascular Disease ◽  
Cognitive Aging ◽  
Structural Mri ◽  
The Other ◽  
Aging Brain ◽  
Medial Temporal Lobes ◽  
Temporal Lobes ◽  
Magnetic Resonance Imaging Mri

Structural magnetic resonance imaging (MRI) is a powerful tool to visualize and quantitate morphological and pathological features of the aging brain. Most work that has used structural MRI to study Alzheimer’s disease (AD) focused on the spatial distribution of atrophic changes associated with disease. These studies consistently show focal atrophy beginning in medial temporal lobes in early and presymptomatic stages of AD before spreading globally throughout the cortical mantle. Normal cognitive aging—aging in the absence of major neurodegenerative disease—on the other hand follows and anterior-to-posterior gradient of atrophic change. In addition to atrophic changes, conventional structural MRI can be used to appreciate markers of small and large vessel cerebrovascular disease, including white matter hyperintensities (WMHs), cerebral microbleeds, and infarction. Studies that have examined cerebrovascular changes associated with AD also show a consistent relationship with risk and severity of clinical AD, particularly with regard to lobar microbleeds and posterior WMH. It is unclear whether cerebrovascular changes play an independent role in the clinical expression of AD or whether it is more mechanistically related, reflecting a core feature of the disease. This chapter reviews recent work on regional atrophy in AD and normal aging, as well as work on small and large cerebrovascular disease in AD.

6. Atrophy of the medial temporal lobes as early marker in Alzheimer's disease: a MRI study

1992 ◽  
Vol 94 (1) ◽  
pp. 82
Author(s):  
P. Scheltens ◽  
D. Leys ◽  
F. Barkhof ◽  
H.C. Weinstein ◽  
E.C. Wolters ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Medial Temporal Lobes ◽  
Temporal Lobes ◽  
Early Marker ◽  
Mri Study

scholarly journals Relationship between the Presence of the ApoE ε4 Allele and EEG Complexity along the Alzheimer’s Disease Continuum

Sensors ◽  
2020 ◽  
Vol 20 (14) ◽  
pp. 3849
Author(s):  
Víctor Gutiérrez-de Pablo ◽  
Carlos Gómez ◽  
Jesús Poza ◽  
Aarón Maturana-Candelas ◽  
Sandra Martins ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Brain Activity ◽  
Developed Countries ◽  
Brain Regions ◽  
Major Health Problem ◽  
Temporal Lobes ◽  
Clinical Onset ◽  
Healthy Control

Alzheimer’s disease (AD) is the most prevalent cause of dementia, being considered a major health problem, especially in developed countries. Late-onset AD is the most common form of the disease, with symptoms appearing after 65 years old. Genetic determinants of AD risk are vastly unknown, though, ε 4 allele of the ApoE gene has been reported as the strongest genetic risk factor for AD. The objective of this study was to analyze the relationship between brain complexity and the presence of ApoE ε 4 alleles along the AD continuum. For this purpose, resting-state electroencephalography (EEG) activity was analyzed by computing Lempel-Ziv complexity (LZC) from 46 healthy control subjects, 49 mild cognitive impairment subjects, 45 mild AD patients, 44 moderate AD patients and 33 severe AD patients, subdivided by ApoE status. Subjects with one or more ApoE ε 4 alleles were included in the carriers subgroups, whereas the ApoE ε 4 non-carriers subgroups were formed by subjects without any ε 4 allele. Our results showed that AD continuum is characterized by a progressive complexity loss. No differences were observed between AD ApoE ε 4 carriers and non-carriers. However, brain activity from healthy subjects with ApoE ε 4 allele (carriers subgroup) is more complex than from non-carriers, mainly in left temporal, frontal and posterior regions (p-values < 0.05, FDR-corrected Mann–Whitney U-test). These results suggest that the presence of ApoE ε 4 allele could modify the EEG complexity patterns in different brain regions, as the temporal lobes. These alterations might be related to anatomical changes associated to neurodegeneration, increasing the risk of suffering dementia due to AD before its clinical onset. This interesting finding might help to advance in the development of new tools for early AD diagnosis.

scholarly journals A biased competition account of attention and memory in Alzheimer's disease

2013 ◽  
Vol 368 (1628) ◽  
pp. 20130062 ◽  
Author(s):  
Kathrin Finke ◽  
Nicholas Myers ◽  
Peter Bublak ◽  
Christian Sorg
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Large Scale ◽  
Brain Networks ◽  
Memory Deficits ◽  
Attention And Memory ◽  
Biased Competition ◽  
Common View ◽  
Temporal Lobes ◽  
Age Related

The common view of Alzheimer's disease (AD) is that of an age-related memory disorder, i.e. declarative memory deficits are the first signs of the disease and associated with progressive brain changes in the medial temporal lobes and the default mode network. However, two findings challenge this view. First, new model-based tools of attention research have revealed that impaired selective attention accompanies memory deficits from early pre-dementia AD stages on. Second, very early distributed lesions of lateral parietal networks may cause these attention deficits by disrupting brain mechanisms underlying attentional biased competition. We suggest that memory and attention impairments might indicate disturbances of a common underlying neurocognitive mechanism. We propose a unifying account of impaired neural interactions within and across brain networks involved in attention and memory inspired by the biased competition principle. We specify this account at two levels of analysis: at the computational level, the selective competition of representations during both perception and memory is biased by AD-induced lesions; at the large-scale brain level, integration within and across intrinsic brain networks, which overlap in parietal and temporal lobes, is disrupted. This account integrates a large amount of previously unrelated findings of changed behaviour and brain networks and favours a brain mechanism-centred view on AD.

Dehydroepiandrosterone (DHEA) and its Sulphate (DHEAS) in Alzheimer’s Disease

2020 ◽  
Vol 17 (2) ◽  
pp. 141-157 ◽  
Author(s):  
Dubravka S. Strac ◽  
Marcela Konjevod ◽  
Matea N. Perkovic ◽  
Lucija Tudor ◽  
Gordana N. Erjavec ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Large Scale ◽  
Therapeutic Potential ◽  
Relevant Literature ◽  
Comprehensive Overview ◽  
Brain Functions ◽  
Specific Effects ◽  
And Behavior

Background: Neurosteroids Dehydroepiandrosterone (DHEA) and Dehydroepiandrosterone Sulphate (DHEAS) are involved in many important brain functions, including neuronal plasticity and survival, cognition and behavior, demonstrating preventive and therapeutic potential in different neuropsychiatric and neurodegenerative disorders, including Alzheimer’s disease. Objective: The aim of the article was to provide a comprehensive overview of the literature on the involvement of DHEA and DHEAS in Alzheimer’s disease. Method: PubMed and MEDLINE databases were searched for relevant literature. The articles were selected considering their titles and abstracts. In the selected full texts, lists of references were searched manually for additional articles. Results: We performed a systematic review of the studies investigating the role of DHEA and DHEAS in various in vitro and animal models, as well as in patients with Alzheimer’s disease, and provided a comprehensive discussion on their potential preventive and therapeutic applications. Conclusion: Despite mixed results, the findings of various preclinical studies are generally supportive of the involvement of DHEA and DHEAS in the pathophysiology of Alzheimer’s disease, showing some promise for potential benefits of these neurosteroids in the prevention and treatment. However, so far small clinical trials brought little evidence to support their therapy in AD. Therefore, large-scale human studies are needed to elucidate the specific effects of DHEA and DHEAS and their mechanisms of action, prior to their applications in clinical practice.

scholarly journals Commonalities between Copper Neurotoxicity and Alzheimer’s Disease

Toxics ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 4
Author(s):  
Roshni Patel ◽  
Michael Aschner
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Structural Changes ◽  
Copper Ion ◽  
Plaque Formation ◽  
Ion Concentration ◽  
Medical Community ◽  
Disease Etiology ◽  
Parent Protein ◽  
Lead Zinc

Alzheimer’s disease, a highly prevalent form of dementia, targets neuron function beginning from the hippocampal region and expanding outwards. Alzheimer’s disease is caused by elevated levels of heavy metals, such as lead, zinc, and copper. Copper is found in many areas of daily life, raising a concern as to how this metal and Alzheimer’s disease are related. Previous studies have not identified the common pathways between excess copper and Alzheimer’s disease etiology. Our review corroborates that both copper and Alzheimer’s disease target the hippocampus, cerebral cortex, cerebellum, and brainstem, affecting motor skills and critical thinking. Additionally, Aβ plaque formation was analyzed beginning from synthesis at the APP parent protein site until Aβ plaque formation was completed. Structural changes were also noted. Further analysis revealed a relationship between amyloid-beta plaques and copper ion concentration. As copper ion levels increased, it bound to the Aβ monomer, expediting the plaque formation process, and furthering neurodegeneration. These conclusions can be utilized in the medical community to further research on the etiology of Alzheimer’s disease and its relationships to copper and other metal-induced neurotoxicity.

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