Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer’s disease at various cognitive stages

Abstract Synaptic loss, plaques and neurofibrillary tangles are viewed as hallmarks of Alzheimer’s disease (AD). This study investigated synaptic markers in neocortical Brodmann area 9 (BA9) samples from 171 subjects with and without AD at different levels of cognitive impairment. The expression lev...

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Autores principales: Odile Poirel, Sébastien Mella, Catherine Videau, Lauriane Ramet, Maria Antonietta Davoli, Etienne Herzog, Pavel Katsel, Naguib Mechawar, Vahram Haroutunian, Jacques Epelbaum, Stéphanie Daumas, Salah El Mestikawy
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Publicado: Nature Portfolio 2018
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spelling oai:doaj.org-article:c7b90a287ba34fcc92a652b92c9be0452021-12-02T15:08:57ZModerate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer’s disease at various cognitive stages10.1038/s41598-018-19154-y2045-2322https://doaj.org/article/c7b90a287ba34fcc92a652b92c9be0452018-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-19154-yhttps://doaj.org/toc/2045-2322Abstract Synaptic loss, plaques and neurofibrillary tangles are viewed as hallmarks of Alzheimer’s disease (AD). This study investigated synaptic markers in neocortical Brodmann area 9 (BA9) samples from 171 subjects with and without AD at different levels of cognitive impairment. The expression levels of vesicular glutamate transporters (VGLUT1&2), glutamate uptake site (EAAT2), post-synaptic density protein of 95 kD (PSD95), vesicular GABA/glycine transporter (VIAAT), somatostatin (som), synaptophysin and choline acetyl transferase (ChAT) were evaluated. VGLUT2 and EAAT2 were unaffected by dementia. The VGLUT1, PSD95, VIAAT, som, ChAT and synaptophysin expression levels significantly decreased as dementia progressed. The maximal decrease varied between 12% (synaptophysin) and 42% (som). VGLUT1 was more strongly correlated with dementia than all of the other markers (polyserial correlation = −0.41). Principal component analysis using these markers was unable to differentiate the CDR groups from one another. Therefore, the status of the major synaptic markers in BA9 does not seem to be linked to the cognitive status of AD patients. The findings of this study suggest that the loss of synaptic markers in BA9 is a late event that is only weakly related to AD dementia.Odile PoirelSébastien MellaCatherine VideauLauriane RametMaria Antonietta DavoliEtienne HerzogPavel KatselNaguib MechawarVahram HaroutunianJacques EpelbaumStéphanie DaumasSalah El MestikawyNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-14 (2018)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Odile Poirel
Sébastien Mella
Catherine Videau
Lauriane Ramet
Maria Antonietta Davoli
Etienne Herzog
Pavel Katsel
Naguib Mechawar
Vahram Haroutunian
Jacques Epelbaum
Stéphanie Daumas
Salah El Mestikawy
Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer’s disease at various cognitive stages
description Abstract Synaptic loss, plaques and neurofibrillary tangles are viewed as hallmarks of Alzheimer’s disease (AD). This study investigated synaptic markers in neocortical Brodmann area 9 (BA9) samples from 171 subjects with and without AD at different levels of cognitive impairment. The expression levels of vesicular glutamate transporters (VGLUT1&2), glutamate uptake site (EAAT2), post-synaptic density protein of 95 kD (PSD95), vesicular GABA/glycine transporter (VIAAT), somatostatin (som), synaptophysin and choline acetyl transferase (ChAT) were evaluated. VGLUT2 and EAAT2 were unaffected by dementia. The VGLUT1, PSD95, VIAAT, som, ChAT and synaptophysin expression levels significantly decreased as dementia progressed. The maximal decrease varied between 12% (synaptophysin) and 42% (som). VGLUT1 was more strongly correlated with dementia than all of the other markers (polyserial correlation = −0.41). Principal component analysis using these markers was unable to differentiate the CDR groups from one another. Therefore, the status of the major synaptic markers in BA9 does not seem to be linked to the cognitive status of AD patients. The findings of this study suggest that the loss of synaptic markers in BA9 is a late event that is only weakly related to AD dementia.
format article
author Odile Poirel
Sébastien Mella
Catherine Videau
Lauriane Ramet
Maria Antonietta Davoli
Etienne Herzog
Pavel Katsel
Naguib Mechawar
Vahram Haroutunian
Jacques Epelbaum
Stéphanie Daumas
Salah El Mestikawy
author_facet Odile Poirel
Sébastien Mella
Catherine Videau
Lauriane Ramet
Maria Antonietta Davoli
Etienne Herzog
Pavel Katsel
Naguib Mechawar
Vahram Haroutunian
Jacques Epelbaum
Stéphanie Daumas
Salah El Mestikawy
author_sort Odile Poirel
title Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer’s disease at various cognitive stages
title_short Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer’s disease at various cognitive stages
title_full Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer’s disease at various cognitive stages
title_fullStr Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer’s disease at various cognitive stages
title_full_unstemmed Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer’s disease at various cognitive stages
title_sort moderate decline in select synaptic markers in the prefrontal cortex (ba9) of patients with alzheimer’s disease at various cognitive stages
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/c7b90a287ba34fcc92a652b92c9be045
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