ArticleNeurobiology of disease2020
Behavioral defects associated with amygdala and cortical dysfunction in mice with seeded α-synuclein inclusions.
Article in Neurobiology of disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 88 citations in OpenAlex.
- Knockout of Rab27b exacerbates neuropathology in alpha-synuclein mouse models.Acta neuropathologica communications · 2026Article
- Association between α-synuclein in plasma neuron-derived exosomes and clinical symptoms in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Imaging spatial transcriptomics reveals molecular patterns underlying accumulation of p-Ser129 α-synuclein in a transgenic mouse model.NPJ Parkinson's disease · 2026Article
- Uncovering the role of c-Fos in the bidirectional relationship between depression/anxiety behaviors and α-synuclein propagation in Parkinson's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- The extent of alpha-synuclein aggregate accumulation in neurons varies depending on the type of neurotransmitter they release.Scientific reports · 2025Article
- Modulation of O-GlcNAc cycling influences α-synuclein amplification, degradation, and associated neuroinflammatory pathology.Molecular neurodegeneration · 2025Article
- Oligomeric alpha-synuclein causes early synaptic dysfunction of the corticostriatal pathway associated with non-motor symptoms.NPJ Parkinson's disease · 2025Article
- Synaptic enrichment of pSer129 alpha-synuclein correlates with dopaminergic denervation in early-stage Parkinson's disease.Nature communications · 2025Article
- A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects.Biology open · 2025Article
- Early α-synuclein aggregation decreases corticostriatal glutamate drive and synapse density.Neurobiology of disease · 2025Article
- Phosphoproteome modifications and cortical circuit dysfunction are linked to the early-stage progression of alpha-synuclein aggregation.bioRxiv : the preprint server for biology · 2025Article
- Cognitive impairment in Parkinson's disease and other parkinsonian syndromes.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Motor cortical neuronal hyperexcitability associated with α-synuclein aggregation.NPJ Parkinson's disease · 2025Article
- Deciphering motor dysfunction and microglial activation in mThy1-Frontiers in molecular neuroscience · 2025Article
- Motor Cortical Neuronal Hyperexcitability Associated with α-Synuclein Aggregation.Research square · 2024Article
- Excitatory synaptic structural abnormalities produced by templated aggregation of α-syn in the basolateral amygdala.Neurobiology of disease · 2024Article
- Suppression of the JAK/STAT pathway inhibits neuroinflammation in the line 61-PFF mouse model of Parkinson's disease.Journal of neuroinflammation · 2024Article
- Motor Cortical Neuronal Hyperexcitability Associated with α-Synuclein Aggregation.bioRxiv : the preprint server for biology · 2024Article
- Review
- Suppression of the JAK/STAT Pathway Inhibits Neuroinflammation in the Line 61-PFF Mouse Model of Parkinson's Disease.Research square · 2024Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Parkinson's disease (PD) is defined by motor symptoms such as tremor at rest, bradykinesia, postural instability, and stiffness. In addition to the classical motor defects that define PD, up to 80% of patients experience cognitive changes and psychiatric disturbances, referred to as PD dementia (PDD). Pathologically, PD is characterized by loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and intracellular inclusions, called Lewy bodies and Lewy neurites, composed mostly of α-synuclein. Much of PD research has focused on the role of α-synuclein aggregates in degeneration of SNpc dopamine neurons because of the impact of loss of striatal dopamine on the classical motor phenotypes. However, abundant Lewy pathology is also found in other brain regions including the cortex and limbic brain regions such as the amygdala, which may contribute to non-motor phenotypes. Little is known about the consequences of α-synuclein inclusions in these brain regions, or in neuronal subtypes other than dopamine neurons. This project expands knowledge on how α-synuclein inclusions disrupt behavior, specifically non-motor symptoms of synucleinopathies. We show that bilateral injections of fibrils into the striatum results in robust bilateral α-synuclein inclusion formation in the cortex and amygdala. Inclusions in the amygdala and prefrontal cortex primarily localize to excitatory neurons, but unbiased stereology shows no significant loss of neurons in the amygdala or cortex. Fibril injected mice show defects in a social dominance behavioral task and fear conditioning, tasks that are associated with prefrontal cortex and amygdala function. Together, these observations suggest that seeded α-synuclein inclusion formation impairs behaviors associated with cortical and amygdala function, without causing cell loss, in brain areas that may play important roles in the complex cognitive features of PDD.
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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.