ArticleNature communications2014
Pathological α-synuclein impairs adult-born granule cell development and functional integration in the olfactory bulb.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Role of α-Synuclein in the Prefrontal Cortex: From Physiological Synaptic Modulation to Synaptic Failure in Parkinson's Disease.Biomedicines · 2026Review
- Structural and molecular differentiation of cultured human neurons is accompanied by alterations of spontaneous and evoked calcium dynamics.Scientific reports · 2025Article
- Neural stem cells of the subventricular zone: A potential stem cell pool for brain repair in Parkinson's disease.Stem cell reports · 2025Review
- Cortical microstructural alterations in different stages of Parkinson's disease.Brain imaging and behavior · 2024Article
- Enhanced Spine Stability and Survival Lead to Increases in Dendritic Spine Density as an Early Response to Local Alpha-Synuclein Overexpression in Mouse Prefrontal Cortex.Cellular and molecular neurobiology · 2024Article
- Amelioration of olfactory dysfunction in a mouse model of Parkinson's disease via enhancing GABAergic signaling.Cell & bioscience · 2023Article
- Microstructural but not macrostructural cortical degeneration occurs in Parkinson's disease with mild cognitive impairment.NPJ Parkinson's disease · 2022Review
- Structural Plasticity of the Hippocampus in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- α-Synuclein aggregation in the olfactory bulb induces olfactory deficits by perturbing granule cells and granular-mitral synaptic transmission.NPJ Parkinson's disease · 2021Article
- Dendritic spine remodeling and plasticity under general anesthesia.Brain structure & function · 2021Review
- Review
- Local cortical overexpression of human wild-type alpha-synuclein leads to increased dendritic spine density in mouse.Neuroscience letters · 2020Article
- Dysregulated Plasma Membrane Turnover Underlying Dendritic Pathology in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2020Review
- Seeding and transgenic overexpression of alpha-synuclein triggers dendritic spine pathology in the neocortex.EMBO molecular medicine · 2017Article
- Disrupting GluA2-GAPDH Interaction Affects Axon and Dendrite Development.Scientific reports · 2016Article
- Increased Olfactory Bulb BDNF Expression Does Not Rescue Deficits in Olfactory Neurogenesis in the Huntington's Disease R6/2 Mouse.Chemical senses · 2016Article
- Elevated α-synuclein caused by SNCA gene triplication impairs neuronal differentiation and maturation in Parkinson's patient-derived induced pluripotent stem cells.Cell death & disease · 2015Article
- Neural stem cells in Parkinson's disease: a role for neurogenesis defects in onset and progression.Cellular and molecular life sciences : CMLS · 2015Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the role of noxious α-synuclein (α-SYN) in the degeneration of midbrain dopaminergic neurons and associated motor deficits of Parkinson's disease is recognized, its impact on non-motor brain circuits and related symptoms remains elusive. Through combining in vivo two-photon imaging with time-coded labelling of neurons in the olfactory bulb of A30P α-SYN transgenic mice, we show impaired growth and branching of dendrites of adult-born granule cells (GCs), with reduced gain and plasticity of dendritic spines. The spine impairments are especially pronounced during the critical phase of integration of new neurons into existing circuits. Functionally, retarded dendritic expansion translates into reduced electrical capacitance with enhanced intrinsic excitability and responsiveness of GCs to depolarizing inputs, while the spine loss correlates with decreased frequency of AMPA-mediated miniature EPSCs. Changes described here are expected to interfere with the functional integration and survival of new GCs into bulbar networks, contributing towards olfactory deficits and related behavioural impairments.
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