ArticleActa neuropathologica2018
Bidirectional modulation of Alzheimer phenotype by alpha-synuclein in mice and primary neurons.
Article in Acta neuropathologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Amyloid exacerbates tau and alpha-synuclein pathologies, behavioral impairments, and neuroinflammation in a mixed dementia model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Cell type transcriptomic modules reveal shared molecular mechanisms in Alzheimer's and Parkinson's disease.GigaScience · 2026Article
- Early Amyloid Formation and Neuroinflammatory Response in a Bigenic Mouse Model Expressing Human α-Synuclein and Aβ.Parkinson's disease · 2026Article
- Aβ42 promotes the aggregation of α-synuclein splice isoforms via heterogeneous nucleation.FEBS letters · 2025Article
- Research models to study lewy body dementia.Molecular neurodegeneration · 2025Review
- Associations between misfolded alpha-synuclein aggregates and Alzheimer's disease pathology in vivo.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Dysregulation of mTOR by tau in Alzheimer's disease.Cytoskeleton (Hoboken, N.J.) · 2024Review
- Functional and Pathological Effects of α-Synuclein on Synaptic SNARE Complexes.Journal of molecular biology · 2023Review
- Oligomerization by co-assembly of β-amyloid and α-synuclein.Frontiers in molecular biosciences · 2023Review
- SNCA genetic lowering reveals differential cognitive function of alpha-synuclein dependent on sex.Acta neuropathologica communications · 2022Article
- Comment on "Activation of the Omega-3 Fatty Acid Receptor GPR120 Protects against Focal Cerebral Ischemic Injury by Preventing Inflammation and Apoptosis in Mice".Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Loss of tau expression attenuates neurodegeneration associated with α-synucleinopathy.Translational neurodegeneration · 2022Article
- α-synuclein-assisted oligomerization of β-amyloid (1-42).Archives of biochemistry and biophysics · 2022Article
- Collusion of α-Synuclein and Aβ aggravating co-morbidities in a novel prion-type mouse model.Molecular neurodegeneration · 2021Article
- Amyloid Structural Changes Studied by Infrared Microspectroscopy in Bigenic Cellular Models of Alzheimer's Disease.International journal of molecular sciences · 2021Article
- Amyloid Oligomers: A Joint Experimental/Computational Perspective on Alzheimer's Disease, Parkinson's Disease, Type II Diabetes, and Amyotrophic Lateral Sclerosis.Chemical reviews · 2021Review
- Biophysical processes underlying cross-seeding in amyloid aggregation and implications in amyloid pathology.Biophysical chemistry · 2021Review
- Molecular subtyping of Alzheimer's disease using RNA sequencing data reveals novel mechanisms and targets.Science advances · 2021Article
- Immunotherapies for Aging-Related Neurodegenerative Diseases-Emerging Perspectives and New Targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- A three-dimensional dementia model reveals spontaneous cell cycle re-entry and a senescence-associated secretory phenotype.Neurobiology of aging · 2020Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
α-Synuclein (αSyn) histopathology defines several neurodegenerative disorders, including Parkinson's disease, Lewy body dementia, and Alzheimer's disease (AD). However, the functional link between soluble αSyn and disease etiology remains elusive, especially in AD. We, therefore, genetically targeted αSyn in APP transgenic mice modeling AD and mouse primary neurons. Our results demonstrate bidirectional modulation of behavioral deficits and pathophysiology by αSyn. Overexpression of human wild-type αSyn in APP animals markedly reduced amyloid deposition but, counter-intuitively, exacerbated deficits in spatial memory. It also increased extracellular amyloid-β oligomers (AβOs), αSyn oligomers, exacerbated tau conformational and phosphorylation variants associated with AD, and enhanced neuronal cell cycle re-entry (CCR), a frequent prelude to neuron death in AD. Conversely, ablation of the SNCA gene encoding for αSyn in APP mice improved memory retention in spite of increased plaque burden. Reminiscent of the effect of MAPT ablation in APP mice, SNCA deletion prevented premature mortality. Moreover, the absence of αSyn decreased extracellular AβOs, ameliorated CCR, and rescued postsynaptic marker deficits. In summary, this complementary, bidirectional genetic approach implicates αSyn as an essential mediator of key phenotypes in AD and offers new functional insight into αSyn pathophysiology.
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