ArticleJournal of Alzheimer's disease : JAD2023
Hippocampal Reduction of α-Synuclein via RNA Interference Improves Neuropathology in Alzheimer's Disease Mice.
Article in Journal of Alzheimer's disease : JAD, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 1 citations in OpenAlex.
- Time-Restricted Feeding Preserves Synaptic Function and Modulates Reelin andJournal of nutrition and metabolism · 2026Article
- Systemic delivery of anti-sense oligonucleotide targeting α-synuclein for treatment in a mouse model of multiple system atrophy.Frontiers in aging neuroscience · 2026Article
- Systemic delivery of anti-sense oligonucleotide targeting a-synuclein for the treatment of multiple system atrophy.Research square · 2025Article
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Authors and funding
8 authors at 3 institutions in 1 country.
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Abstract
backgroundAlzheimer's disease (AD) cases are often characterized by the pathological accumulation of α-synuclein (α-syn) in addition to amyloid-β (Aβ) and tau hallmarks. The role of α-syn has been extensively studied in synucleinopathy disorders, but less so in AD. Recent studies have shown that α-syn may also play a role in AD and its downregulation may be protective against the toxic effects of Aβ accumulation.
objectiveWe hypothesized that selectively knocking down α-syn via RNA interference improves the neuropathological and biochemical findings in AD mice.
methodsHere we used amyloid precursor protein transgenic (APP-Tg) mice to model AD and explore pathologic and behavioral phenotypes with knockdown of α-syn using RNA interference. We selectively reduced α-syn levels by stereotaxic bilateral injection of either LV-shRNA α-syn or LV-shRNA-luc (control) into the hippocampus of AD mice.
resultsWe found that downregulation of α-syn results in significant reduction in the number of Aβ plaques. In addition, mice treated with LV-shRNA α-syn had amelioration of abnormal microglial activation (Iba1) and astrocytosis (GFAP) phenotypes in AD mice.
conclusionOur data suggests a novel link between Aβ and α-syn pathology as well as a new therapeutic angle for targeting AD.
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Registered trials
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