Hippocampal Proliferation Is Increased in Presymptomatic Parkinson’s Disease and due to Microglia

Besides dopamine-deficiency related motor symptoms, nonmotor symptoms, including cognitive changes occur in Parkinson's disease (PD) patients, that may relate to accumulation of α-synuclein in the hippocampus (HC). This brain region also contains stem cells that can proliferate. This is a well-...

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Main Authors: Karlijn J. Doorn, Benjamin Drukarch, Anne-Marie van Dam, Paul J. Lucassen
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2014/959154
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author Karlijn J. Doorn
Benjamin Drukarch
Anne-Marie van Dam
Paul J. Lucassen
author_facet Karlijn J. Doorn
Benjamin Drukarch
Anne-Marie van Dam
Paul J. Lucassen
author_sort Karlijn J. Doorn
collection DOAJ
description Besides dopamine-deficiency related motor symptoms, nonmotor symptoms, including cognitive changes occur in Parkinson's disease (PD) patients, that may relate to accumulation of α-synuclein in the hippocampus (HC). This brain region also contains stem cells that can proliferate. This is a well-regulated process that can, for example, be altered by neurodegenerative conditions. In contrast to proliferation in the substantia nigra and subventricular zone, little is known about the HC in PD. In addition, glial cells contribute to neurodegenerative processes and may proliferate in response to PD pathology. In the present study, we questioned whether microglial cells proliferate in the HC of established PD patients versus control subjects or incidental Lewy body disease (iLBD) cases as a prodromal state of PD. To this end, proliferation was assessed using the immunocytochemical marker minichromosome maintenance protein 2 (MCM2). Colocalization with Iba1 was performed to determine microglial proliferation. MCM2-positive cells were present in the HC of controls and were significantly increased in the presymptomatic iLBD cases, but not in established PD patients. Microglia represented the majority of the proliferating cells in the HC. This suggests an early microglial response to developing PD pathology in the HC and further indicates that neuroinflammatory processes play an important role in the development of PD pathology.
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spelling doaj-art-b5e673830aa1443abc35a87183937b2b2025-02-03T05:59:08ZengWileyNeural Plasticity2090-59041687-54432014-01-01201410.1155/2014/959154959154Hippocampal Proliferation Is Increased in Presymptomatic Parkinson’s Disease and due to MicrogliaKarlijn J. Doorn0Benjamin Drukarch1Anne-Marie van Dam2Paul J. Lucassen3Swammerdam Institute for Life Sciences (SILS), Center for Neuroscience, University of Amsterdam (UvA), Science Park 904, 1098 XH Amsterdam, The NetherlandsNeuroscience Campus Amsterdam (NCA), Free University (VU) Medical Center, Van der Boechorststraat 7, 1081 BT Amsterdam, The NetherlandsNeuroscience Campus Amsterdam (NCA), Free University (VU) Medical Center, Van der Boechorststraat 7, 1081 BT Amsterdam, The NetherlandsSwammerdam Institute for Life Sciences (SILS), Center for Neuroscience, University of Amsterdam (UvA), Science Park 904, 1098 XH Amsterdam, The NetherlandsBesides dopamine-deficiency related motor symptoms, nonmotor symptoms, including cognitive changes occur in Parkinson's disease (PD) patients, that may relate to accumulation of α-synuclein in the hippocampus (HC). This brain region also contains stem cells that can proliferate. This is a well-regulated process that can, for example, be altered by neurodegenerative conditions. In contrast to proliferation in the substantia nigra and subventricular zone, little is known about the HC in PD. In addition, glial cells contribute to neurodegenerative processes and may proliferate in response to PD pathology. In the present study, we questioned whether microglial cells proliferate in the HC of established PD patients versus control subjects or incidental Lewy body disease (iLBD) cases as a prodromal state of PD. To this end, proliferation was assessed using the immunocytochemical marker minichromosome maintenance protein 2 (MCM2). Colocalization with Iba1 was performed to determine microglial proliferation. MCM2-positive cells were present in the HC of controls and were significantly increased in the presymptomatic iLBD cases, but not in established PD patients. Microglia represented the majority of the proliferating cells in the HC. This suggests an early microglial response to developing PD pathology in the HC and further indicates that neuroinflammatory processes play an important role in the development of PD pathology.http://dx.doi.org/10.1155/2014/959154
spellingShingle Karlijn J. Doorn
Benjamin Drukarch
Anne-Marie van Dam
Paul J. Lucassen
Hippocampal Proliferation Is Increased in Presymptomatic Parkinson’s Disease and due to Microglia
Neural Plasticity
title Hippocampal Proliferation Is Increased in Presymptomatic Parkinson’s Disease and due to Microglia
title_full Hippocampal Proliferation Is Increased in Presymptomatic Parkinson’s Disease and due to Microglia
title_fullStr Hippocampal Proliferation Is Increased in Presymptomatic Parkinson’s Disease and due to Microglia
title_full_unstemmed Hippocampal Proliferation Is Increased in Presymptomatic Parkinson’s Disease and due to Microglia
title_short Hippocampal Proliferation Is Increased in Presymptomatic Parkinson’s Disease and due to Microglia
title_sort hippocampal proliferation is increased in presymptomatic parkinson s disease and due to microglia
url http://dx.doi.org/10.1155/2014/959154
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AT annemarievandam hippocampalproliferationisincreasedinpresymptomaticparkinsonsdiseaseandduetomicroglia
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