ArticleNPJ Parkinson's disease2021
α-Synuclein aggregation in the olfactory bulb induces olfactory deficits by perturbing granule cells and granular-mitral synaptic transmission.
Article in NPJ Parkinson's disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- Localized amyloid-β oligomers in the lateral entorhinal cortex drives olfactory dysfunction through aberrant neuronal and network activity.Acta neuropathologica communications · 2026Article
- Gut-initiated alpha synuclein fibrils drive parkinsonism phenotypes: temporal mapping of REM sleep behavior disorder-like and other non-motor symptoms.Translational neurodegeneration · 2026Article
- Distribution and Levels of Insulin-like Growth Factor 2 Receptor Across Mouse Brain Cell Types.Receptors (Basel, Switzerland) · 2026Article
- Odor identity decoding by mitral/tufted cells in the olfactory bulb from large-scale pooled datasets.iScience · 2026Article
- Olfactory-to-Entorhinal Network Dysrhythmias Drive Parkinson's Cognitive Impairment Through Frequency-Specific Oscillatory Decoupling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Characterization of motor and non-motor features associated with bilateral nigral degeneration due to A53T alpha-synuclein in female rats.Scientific reports · 2026Article
- Capsaicin and nicotine alleviate MPTP induced olfactory dysfunction by suppressing cGAS/TBK1/STING and MAPK mediated neuroinflammation.NPJ Parkinson's disease · 2025Article
- Alpha-synuclein pathology and Parkinson's disease-related olfactory dysfunctions: an update on preclinical models and therapeutic approaches.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- Predicting CSF α-Synuclein Seed Amplification Assay Status From Demographics and Clinical Data.Neurology open access · 2025Article
- Anterior piriform cortex dysfunction underlies autism spectrum disorders-related olfactory deficits in Fmr1 conditional deletion mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Noradrenergic inputs from the locus coeruleus to anterior piriform cortex and the olfactory bulb modulate olfactory outputs.Nature communications · 2025Article
- Electrophysiological Signatures in Global Cerebral Ischemia: Neuroprotection Via Chemogenetic Inhibition of CA1 Pyramidal Neurons in Rats.Journal of the American Heart Association · 2024Article
- Optimization of Parkinson's disease therapy with plant extracts and nutrition's evolving roles.IBRO neuroscience reports · 2024Review
- Does COVID-19 Trigger the Risk for the Development of Parkinson's Disease? Therapeutic Potential of Vitamin C.Molecular neurobiology · 2024Review
- Odor representation and coding by the mitral/tufted cells in the olfactory bulb.Journal of Zhejiang University. Science. B · 2024Review
- Current Perspectives on Olfactory Loss in Atypical Parkinsonisms-A Review Article.Biomedicines · 2024Review
- Review
- Effect of host and strain factors on α-synuclein prion pathogenesis.Trends in neurosciences · 2024Review
- Genotype-phenotype correlation in PRKN-associated Parkinson's disease.NPJ Parkinson's disease · 2024Article
- Olfactory dysfunction and its related molecular mechanisms in Parkinson's disease.Neural regeneration research · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Olfactory dysfunction is an early pre-motor symptom of Parkinson's disease (PD) but the neural mechanisms underlying this dysfunction remain largely unknown. Aggregation of α-synuclein is observed in the olfactory bulb (OB) during the early stages of PD, indicating a relationship between α-synuclein pathology and hyposmia. Here we investigate whether and how α-synuclein aggregates modulate neural activity in the OB at the single-cell and synaptic levels. We induced α-synuclein aggregation specifically in the OB via overexpression of double-mutant human α-synuclein by an adeno-associated viral (AAV) vector. We found that α-synuclein aggregation in the OB decreased the ability of mice to detect odors and to perceive attractive odors. The spontaneous activity and odor-evoked firing rates of single mitral/tufted cells (M/Ts) were increased by α-synuclein aggregates with the amplitude of odor-evoked high-gamma oscillations increased. Furthermore, the decreased activity in granule cells (GCs) and impaired inhibitory synaptic function were responsible for the observed hyperactivity of M/Ts induced by α-synuclein aggregates. These results provide direct evidences of the role of α-synuclein aggregates on PD-related olfactory dysfunction and reveal the neural circuit mechanisms by which olfaction is modulated by α-synuclein pathology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.