ArticleNPJ Parkinson's disease2023
Synaptic mechanisms underlying onset and progression of memory deficits caused by hippocampal and midbrain synucleinopathy.
Article in NPJ Parkinson's disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Sex- and Age-Dependent Neuroimmune Dysregulation and Early Neurodegenerative Signatures Following SARS-CoV-2 Infection in Golden Syrian Hamsters.Research square · 2026Article
- New insights into synaptic vesicle dysfunction in Parkinson's disease.Journal of Parkinson's disease · 2026Review
- Impairment in stimulus-response learning as a cognitive biomarker in a model of synucleinopathy.Translational psychiatry · 2026Article
- Engram cell vulnerability in neurodegeneration: from mechanistic insights to therapeutic horizons.Frontiers in aging neuroscience · 2026Review
- Glutamatergic synaptic resilience to overexpressed human alpha-synuclein.NPJ Parkinson's disease · 2025Article
- Integrating plasma circulating protein-centered multi-omics to identify potential therapeutic targets for Parkinsonian cognitive disorders.Journal of translational medicine · 2025Article
- Carvacrol attenuated haloperidol-induced Parkinson's disease via TNF/NFκβ-NLRP3-mediated pyroptosis.Laboratory animal research · 2025Article
- Brain and behavioural anomalies caused byLife science alliance · 2025Article
- Hippocampus and olfactory impairment in Parkinson disease: a comparative exploratory combined volumetric/functional MRI study.Neuroradiology · 2024Article
- Mild cognitive impairment in Parkinson's disease: current view.Frontiers in cognition · 2024Review
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cognitive deficits, including working memory, and visuospatial deficits are common and debilitating in Parkinson's disease. α-synucleinopathy in the hippocampus and cortex is considered as the major risk factor. However, little is known about the progression and specific synaptic mechanisms underlying the memory deficits induced by α-synucleinopathy. Here, we tested the hypothesis that pathologic α-Synuclein (α-Syn), initiated in different brain regions, leads to distinct onset and progression of the pathology. We report that overexpression of human α-Syn in the murine mesencephalon leads to late onset memory impairment and sensorimotor deficits accompanied by reduced dopamine D1 expression in the hippocampus. In contrast, human α-Syn overexpression in the hippocampus leads to early memory impairment, altered synaptic transmission and plasticity, and decreased expression of GluA1 AMPA-type glutamate receptors. These findings identify the synaptic mechanisms leading to memory impairment induced by hippocampal α-synucleinopathy and provide functional evidence of the major neuronal networks involved in disease progression.
Identifiers
What Socratic holds
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 Socratic graph.