ArticleAnnals of clinical and translational neurology2015
Network dysfunction in α-synuclein transgenic mice and human Lewy body dementia.
Article in Annals of clinical and translational neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
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- Longevity Factor Klotho and Resistance to Cognitive Deficits in Individuals with Parkinson's Disease and in an α-Synuclein Mouse Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Epilepsy and EEG abnormalities in neurodegenerative dementias: toward a system epilepsy framework.Frontiers in aging neuroscience · 2026Review
- Disrupting α-Synuclein-ClpP interaction restores mitochondrial function and attenuates neuropathology in Parkinson's disease models.Molecular neurodegeneration · 2025Article
- Late-onset unexplained epilepsy with dual amyloid and tau negativity: are alpha-synuclein seed amplification assays the next diagnostic step?Epilepsy & behavior reports · 2025Article
- Exploring biomarkers of neurodegeneration in epilepsy: Critical insights.Epileptic disorders : international epilepsy journal with videotape · 2025Review
- Alterations in non-REM sleep and EEG spectra precede REM-sleep deficits in a model of synucleinopathy.Journal of Parkinson's disease · 2025Article
- Resting-state EEG predicts cognitive decline in a neuropathologically diagnosed longitudinal community autopsied cohort.Parkinsonism & related disorders · 2024Article
- Delineating mechanisms underlying parvalbumin neuron impairment in different neurological and neurodegenerative disorders: the emerging role of mitochondrial dysfunction.Biochemical Society transactions · 2024Review
- Alteration of medial temporal lobe metabolism related to Alzheimer's disease and dementia with lewy bodies.Alzheimer's research & therapy · 2024Article
- Synchronous monitoring of brain-heart electrophysiology using heart rate variability coupled with rapid quantitative electroencephalography in orthostatic hypotension patients with α-synucleinopathies: Rapid prediction of orthostatic hypotension and preliminary exploration of brain stimulation therapy.CNS neuroscience & therapeutics · 2024Article
- Evidence for prodromal changes in neuronal excitability and neuroinflammation in the hippocampus in young alpha-synuclein (A30P) transgenic mice.Frontiers in dementia · 2024Article
- Latest advances in mechanisms of epileptic activity in Alzheimer's disease and dementia with Lewy Bodies.Frontiers in neurology · 2024Review
- Neurophysiological alterations in mice and humans carrying mutations in APP and PSEN1 genes.Alzheimer's research & therapy · 2023Article
- Antiseizure Medications in Alzheimer's Disease from Preclinical to Clinical Evidence.International journal of molecular sciences · 2023Review
- QEEG Signatures are Associated with Nonmotor Dysfunctions in Parkinson's Disease and Atypical Parkinsonism: An Integrative Analysis.Aging and disease · 2023Article
- A Mouse Model to Test Novel Therapeutics for Parkinson's Disease: an Update on the Thy1-aSyn ("line 61") Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Traditional and Innovative Anti-seizure Medications Targeting Key Physiopathological Mechanisms: Focus on Neurodevelopment and Neurodegeneration.Current neuropharmacology · 2023Article
- Article
- Emerging Electroencephalographic Biomarkers to Improve Preclinical to Clinical Translation in Alzheimer's Disease.Frontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveDementia with Lewy bodies (DLB) is associated with the accumulation of wild-type human α-synuclein (SYN) in neurons and with prominent slowing of brain oscillations on electroencephalography (EEG). However, it remains uncertain whether the EEG abnormalities are actually caused by SYN.
methodsTo determine whether SYN can cause neural network abnormalities, we performed EEG recordings and analyzed the expression of neuronal activity-dependent gene products in SYN transgenic mice. We also carried out comparative analyses in humans with DLB.
resultsWe demonstrate that neuronal expression of SYN in transgenic mice causes a left shift in spectral power that closely resembles the EEG slowing observed in DLB patients. Surprisingly, SYN mice also had seizures and showed molecular hippocampal alterations indicative of aberrant network excitability, including calbindin depletion in the dentate gyrus. In postmortem brain tissues from DLB patients, we found reduced levels of calbindin mRNA in the dentate gyrus. Furthermore, nearly one quarter of DLB patients showed myoclonus, a clinical sign of aberrant network excitability that was associated with an earlier age of onset of cognitive impairments. In SYN mice, partial suppression of epileptiform activity did not alter their shift in spectral power. Furthermore, epileptiform activity in human amyloid precursor protein transgenic mice was not associated with a left shift in spectral power.
interpretationWe conclude that neuronal accumulation of SYN slows brain oscillations and, in parallel, causes aberrant network excitability that can escalate into seizure activity. The potential role of aberrant network excitability in DLB merits further investigation.
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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.