Publication

GABA and glutamate moderate beta-amyloid related functional connectivity in cognitively unimpaired old-aged adults

Dimitri Nestor Alice Van De Ville, Maria Giulia Preti
2019
Journal Articles

Résumé

Background: Effects of beta-amyloid accumulation on neuronal function precede the clinical manifestation of Alzheimer's disease (AD) by years and affect distinct cognitive brain networks. As previous studies suggest a link between beta-amyloid and dysregulation of excitatory and inhibitory neurotransmitters, we aimed to investigate the impact of GABA and glutamate on beta-amyloid related functional connectivity. Methods: 29 cognitively unimpaired old-aged adults (age = 70.03 +/- 5.77 years) were administered 11CPittsburgh Compound B (PiB) positron-emission tomography (PET), and MRI at 7 Tesla (7T) including blood oxygen level dependent (BOLD) functional MRI (fMRI) at rest for measuring static and dynamic functional connectivity. An advanced 7T MR spectroscopic imaging (MRSI) sequence based on the free induction decay acquisition localized by outer volume suppression' (FIDLOVS) technology was used for gray matter specific measures of GABA and glutamate in the posterior cingulate and precuneus (PCP) region. Results: GABA and glutamate MR-spectra indicated significantly higher levels in gray matter than in white matter. A global effect of beta-amyloid on functional connectivity in the frontal, occipital and inferior temporal lobes was observable. Interactive effects of beta-amyloid with gray matter GABA displayed positive PCP connectivity to the frontomedial regions, and the interaction of beta-amyloid with gray matter glutamate indicated positive PCP connectivity to frontal and cerebellar regions. Furthermore, decreased whole-brain but increased fronto-occipital and temporo-parietal dynamic connectivity was found, when GABA interacted with regional beta-amyloid deposits in the amygdala, frontal lobe, hippocampus, insula and striatum. Conclusions: GABA, and less so glutamate, may moderate beta-amyloid related functional connectivity. Additional research is needed to better characterize their interaction and potential impact on AD.

Source officielle

https://infoscience.epfl.ch/entities/publication/0d04e8d3-bd6b-46d7-9caf-3cd83aeafe5f

Dimitri Nestor Alice Van De Ville, Maria Giulia Preti
2019
Journal Articles

Résumé

Source officielle

https://infoscience.epfl.ch/entities/publication/0d04e8d3-bd6b-46d7-9caf-3cd83aeafe5f

Concepts associés (32)

Lobe frontal

Le lobe frontal est une région du cerveau des vertébrés. Il est situé à l'avant des lobes pariétal et temporal. Dans le cerveau humain, le sillon central (ou scissure de Rolando) sépare le lobe frontal du lobe pariétal tout au long de la surface du cortex cérébral. Le sillon latéral (ou scissure de Sylvius) sépare le gyrus (ou circonvolution) frontal inférieur du lobe temporal.

Lobe pariétal

Le lobe pariétal (ou cortex pariétal) est une région du cerveau des vertébrés. Il est situé en arrière du lobe frontal, au-dessus des lobes temporal et occipital. D'un point de vue anatomique, le lobe pariétal est la partie du cortex cérébral délimitée par les sillons suivants : le sillon central (anciennement scissure de Rolando) sépare le lobe frontal du lobe pariétal en avant ; la limite postérieure du lobe pariétal avec le lobe occipital est marquée par le sillon pariéto-occipital (ancienne scissure perpendiculaire interne) qui n'est pas toujours bien visible ; le sillon latéral (ancienne scissure de Sylvius) marque la limite inférieure du lobe pariétal sous laquelle se trouve le lobe temporal.

Bêta-amyloïde

Le peptide amyloïde bêta ou β-amyloïde est un peptide (une petite protéine) appartenant à la famille des substances amyloïdes. Dans certaines circonstances, il est néfaste pour le système nerveux central (sous l’influence de différents facteurs génétiques et environnementaux encore mal compris). L'amyloïde bêta est au centre de l'hypothèse amyloïde qui est la théorie, formulée initialement par JA Hardy et GA Higgins en 1992, selon laquelle la maladie d'Alzheimer est causée par la présence de plaques amyloïdes dans le cerveau.

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