ArticleTranslational psychiatry2025
LRRK2 deficiency mitigates amyloid β deposition-mediated pathology in a murine Alzheimer's disease model by reprogramming microglia.
Article in Translational psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Review
- Tiaobu Xinshen Recipe Improves Cognitive Deficits by Alleviating Synaptic Ultrastructure Degradation and Reducing Amyloid β in Transgenic Mice of Alzheimer's Disease.Chinese journal of integrative medicine · 2026Article
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Abstract
Leucine-rich repeat kinase 2 (LRRK2), primarily expressed in microglia, is responsible for the modulation of innate immune responses and associated with various immunological disorders. Available evidence documents that though as the predominant etiological factor for familial Parkinson's disease, LRRK2 mutations rarely occur in Alzheimer's disease (AD) and that LRRK2 polymorphism is potentially associated with late-onset AD. However, the role of LRRK2 in AD immunopathogenesis remains unknown. In this study, we investigated the impact of LRRK2 deficiency on cognitive function, Aβ plaque accumulation, and plaque-associated neuropathology in AD mice. The results revealed that compared with the 5xFAD mice, the 8-month-old 5xFAD;LRRK2
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