Source: McGill University.
A new study challenges conventional belief about Alzheimer’s, finding very minor neuronal and synaptic loss in patients at various stages of the disease.
The study implicitly suggests that dementia is associated with a synaptic dysfunction rather than the disappearance of synapses from the patient’s cortex. Identifying this dysfunction could lead to the development of effective treatments for this disease. NeuroscienceNews.com image is in the public domain.
Frequently encountered in the elderly, Alzheimer’s is considered a neurodegenerative disease, which means that it is accompanied by a significant, progressive loss of neurons and their nerve endings, or synapses. A joint French and Canadian study published in Scientific Reports now challenges this view.
Conducted among more than 170 subjects at various stages of Alzheimer’s disease, the study by the team led by Salah El Mestikawy (Douglas Mental Health University Institute, Canada) and Stéphanie Daumas (Université Pierre et Marie Curie, France) has shown instead that the disease is accompanied by a minor decline in neuronal and synaptic markers.
“Much to our surprise, in studying the fate of eight neuronal and synaptic markers in our subjects’ prefrontal cortices, we only observed very minor neuronal and synaptic losses. Our study therefore suggests that, contrary to what was believed, neuronal and synaptic loss is relatively limited in Alzheimer’s disease. This is a radical change in thinking,” explains El Mestikawy, an associate professor at McGill University.
The scientists also attempted to correlate all these minor synaptic losses with the subjects’ level of dementia. Their results show that the declines in synaptic biomarkers had little impact on the participants’ cognitive skills.
Towards other therapies
The study implicitly suggests that dementia is associated with a synaptic dysfunction rather than the disappearance of synapses from the patient’s cortex. Identifying this dysfunction could lead to the development of effective treatments for this disease.
“Until now, therapeutic interventions have been aimed at slowing synaptic destruction. Based on our study, we are going to have to change our therapeutic approach,” says El Mestikawy.
According to the Alzheimer Society of Canada, 564,000 Canadians currently have Alzheimer’s disease or another form of dementia. The figure will be 937,000 within 15 years. Presently, there is no truly effective treatment for this disease.
Funding: This research was funded by grants from the Canadian Institutes of Health Research, the Agence Nationale de la Recherche, the Fonds de recherche du Québec — Santé, the Douglas Institute Foundation, the Graham Boeckh Foundation, the Canada Foundation for Innovation, Canada Research Chairs, the Université Pierre-et-Marie-Curie, the Institut national de la santé et de la recherche médicale, the Centre national de la recherche scientifique, and the Fédération pour la Recherche sur le Cerveau.
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer’s disease at various cognitive stages” by 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 in Scientific Reports. Published online January 17 2018,
Abstract
Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer’s disease at various cognitive stages
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.
“Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer’s disease at various cognitive stages” by 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 in Scientific Reports. Published online January 17 2018 doi:10.1038/s41598-018-19154-y
http://neurosciencenews.com/neuron-loss-alzheimers-8326/
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