Bilateral Symmetry of Cholinergic Deficits in Alzheimer's Disease

Gs, Zubenko; Moossy, John; Hanin, Israel; Aj, Martínez; Gr, Rao; Kopp, Ursula

doi:10.1001/archneur.1988.00520270029016

Cited by 30 publications

(6 citation statements)

References 24 publications

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“…However, only few post‐mortem studies have addressed the hemispheric asymmetry in pathology distribution, some reporting no asymmetries [Arnold et al, ], while others suggesting selective hemispheric asymmetries (L > R) of senile plaques and neurofibrillary tangles (tau) in AD [Moossy et al, ; Stefanits et al, ]. However, the reported asymmetries were limited to the entorhinal cortex and hippocampus but were not found in other cortical regions such as frontal and temporal cortex and basal nucleus of Meynert [Zubenko et al, ], and seemed to diminish with increasing disease severity [Moossy et al, ], pointing to their changing patterns during disease progression.…”

Section: Discussionmentioning

confidence: 99%

Gray matter asymmetries in aging and neurodegeneration: A review and meta‐analysis

Minkova

Habich

Peter

et al. 2017

Human Brain Mapping

153

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Inter-hemispheric asymmetries are a common phenomenon of the human brain. Some evidence suggests that neurodegeneration related to aging and disease may preferentially affect the left-usually language- and motor-dominant-hemisphere. Here, we used activation likelihood estimation meta-analysis to assess gray matter (GM) loss and its lateralization in healthy aging and in neurodegeneration, namely, mild cognitive impairment (MCI), Alzheimer's dementia (AD), Parkinson's disease (PD), and Huntington's disease (HD). This meta-analysis, comprising 159 voxel-based morphometry publications (enrolling 4,469 patients and 4,307 controls), revealed that GM decline appeared to be asymmetric at trend levels but provided no evidence for increased left-hemisphere vulnerability. Regions with asymmetric GM decline were located in areas primarily affected by neurodegeneration. In HD, the left putamen showed converging evidence for more pronounced atrophy, while no consistent pattern was found in PD. In MCI, the right hippocampus was more atrophic than its left counterpart, a pattern that reversed in AD. The stability of these findings was confirmed using permutation tests. However, due to the lenient threshold used in the asymmetry analysis, further work is needed to confirm our results and to provide a better understanding of the functional role of GM asymmetries, for instance in the context of cognitive reserve and compensation. Hum Brain Mapp 38:5890-5904, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

Gray matter asymmetries in aging and neurodegeneration: A review and meta‐analysis

Minkova

Habich

Peter

et al. 2017

Human Brain Mapping

153

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“…Several authors have described asymmetries in the neuronal number of the BFC. 21 , 28 - 32 Special focus was directed on Ayala’s nucleus whose asymmetry was explained by its cholinergic axons to Broca’s speech area. 6 , 17 We succeeded in visualizing size and shape differences of the periputaminal or lateral Ayala’s subnucleus by computer-assisted 3D reconstruction.…”

Section: Methodsmentioning

confidence: 99%

Computer-assisted 3D reconstruction of the human basal forebrain complex

Grinberg

Heinsen

2007

Dement. neuropsychol.

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The basal forebrain complex (BFC) is a small but intricate structure. Its organization and function is hard to investigate using conventional methods, especially in humans. By combining new methods of research we present a comprehensive overview of this complex, in order to better understand its function in normal and diseased brains.MethodsThe right and left BFC of a 29-year-old male were reconstructed from gallcocyanin (Nissl) stained 440 µm-thick serial horizontal sections by using advanced computer-assisted 3D reconstruction software.ResultsThe reconstructed components in the present case include Ch2, Ch3, Ch4am-al, Ch4i, Ch4p, juxtacommissural, Ayala’s medial (subpallidal) and lateral (periputaminal) subnuclei. These components are arranged in an arch-like course mainly beneath the anterior commissure. The bilateral volume of all subnuclei was 99.06 mm3, the left side accounting for 48.05 mm3. Some of the subnuclei exhibited volume asymmetry indices varying from 28.3 to 12.9%.The volume of Ayalas’ lateral or periputaminal nucleus was 9.7% higher on the right, than on the left side.ConclusionsOur methodological approach promises to be highly efficient and reproducible in studying morphofunctional correlations in complex cognitive features

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“…Our findings are consistent with early reports on the extent of left–right symmetry in the cholinergic deficits in AD brains, which was found to be symmetrically distributed compared to more asymmetrical morphological lesions. 47 , 48 …”

Section: Discussionmentioning

confidence: 99%

Genetic basis of anatomical asymmetry and aberrant dynamic functional networks in Alzheimer’s disease

Rubido,

Riedel,

Vuksanović

2023

Brain Communications

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Genetic associations with macroscopic brain networks can provide insights into healthy and aberrant cortical connectivity in disease. However, associations specific to dynamic functional connectivity in Alzheimer’s disease are still largely unexplored. Understanding the association between gene expression in the brain and functional networks may provide useful information about the molecular processes underlying variations in impaired brain function. Given the potential of dynamic functional connectivity to uncover brain states associated with Alzheimer’s disease, it is interesting to ask: How does gene expression associated with Alzheimer’s disease map onto the dynamic functional brain connectivity? If genetic variants associated with neurodegenerative processes involved in Alzheimer’s disease are to be correlated with brain function, it is essential to generate such a map. Here, we investigate how the relation between gene expression in the brain and dynamic functional connectivity arises from nodal interactions, quantified by their role in network centrality (i.e., the drivers of the metastability), and the principal component of genetic co-expression across the brain. Our analyses include genetic variations associated with Alzheimer’s disease and also genetic variants expressed within the cholinergic brain pathways. Our findings show that contrasts in metastability of functional networks between Alzheimer’s and healthy individuals can in part be explained by the two combinations of genetic co-variations in the brain with the confidence interval between 72% and 92%. The highly central nodes, driving the brain aberrant metastable dynamics in Alzheimer’s disease, highly correlate with the magnitude of variations from two combinations of genes expressed in the brain. These nodes include mainly the white matter, parietal and occipital brain regions, each of which (or their combinations) are involved in impaired cognitive function in Alzheimer’s disease. In addition, our results provide evidence of the role of genetic associations across brain regions in asymmetric changes in ageing. We validated our findings on the same cohort using alternative brain parcellation methods. This work demonstrates how genetic variations underpin aberrant dynamic functional connectivity in Alzheimer’s disease.

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Bilateral Symmetry of Cholinergic Deficits in Alzheimer's Disease

Cited by 30 publications

References 24 publications

Gray matter asymmetries in aging and neurodegeneration: A review and meta‐analysis

Gray matter asymmetries in aging and neurodegeneration: A review and meta‐analysis

Computer-assisted 3D reconstruction of the human basal forebrain complex

Genetic basis of anatomical asymmetry and aberrant dynamic functional networks in Alzheimer’s disease

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