Davide Bruno1, Chelsea Reichert Plaska2,3, Daniel P A Clark4, Henrik Zetterberg5,6,7,8, Kaj Blennow5,6, Marcel M Verbeek9, Nunzio Pomara2,10. 1. School of Psychology, Liverpool John Moores University, Liverpool, UK. 2. Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA. 3. Department of Psychology, the Graduate Center, City University of New York, New York City, NY, USA. 4. Department of Psychology, Liverpool Hope University, Liverpool, UK. 5. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. 6. Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden. 7. Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK. 8. UK Dementia Research Institute, London, UK. 9. Cognition and Behaviour, Departments of Neurology and Laboratory Medicine, Alzheimer Centre, Radboud University Medical Center, Donders Institute for Brain, Nijmegen, The Netherlands. 10. Department of Psychiatry, School of Medicine, New York University, New York City, NY, USA.
Abstract
Purpose/aim of the study: Major depressive disorder (MDD) in late life is linked to increased risk of subsequent dementia, but it is still unclear exactly what pathophysiological mechanisms underpin this link. A potential mechanism related to elevated risk of dementia in MDD is increased levels of α-synuclein (α-Syn), a protein found in presynaptic neuronal terminals.Materials and methods: In this study, we examined cerebrospinal fluid (CSF) levels of α-Syn in conjunction with biomarkers of neurodegeneration (amyloid-β 42, total and phospho tau) and synaptic dysfunction (neurogranin), and measures of memory ability, in 27 cognitively intact older individuals with MDD and 19 controls. Results: Our results show that CSF α-Syn levels did not significantly differ across depressed and control participants, but α-Syn was directly associated with neurogranin levels, and indirectly linked to poorer memory ability.Conclusions: All in all, we found that α-Syn may be implicated in the association between late life MDD and synaptic dysfunction, although further research is needed to confirm these results.
Purpose/aim of the study: Major depressive disorder (MDD) in late life is linked to increased risk of subsequent dementia, but it is still unclear exactly what pathophysiological mechanisms underpin this link. A potential mechanism related to elevated risk of dementia in MDD is increased levels of α-synuclein (α-Syn), a protein found in presynaptic neuronal terminals.Materials and methods: In this study, we examined cerebrospinal fluid (CSF) levels of α-Syn in conjunction with biomarkers of neurodegeneration (amyloid-β 42, total and phospho tau) and synaptic dysfunction (neurogranin), and measures of memory ability, in 27 cognitively intact older individuals with MDD and 19 controls. Results: Our results show that CSF α-Syn levels did not significantly differ across depressed and control participants, but α-Syn was directly associated with neurogranin levels, and indirectly linked to poorer memory ability.Conclusions: All in all, we found that α-Syn may be implicated in the association between late life MDD and synaptic dysfunction, although further research is needed to confirm these results.
Entities:
Keywords:
late-life major depressive disorder; memory; neurogranin; α-synuclein
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