ArticleJournal of Alzheimer's disease : JAD2024
Spatial and planar profiling of Rac1/Cdc42 signaling in Alzheimer's disease brain.
Article in Journal of Alzheimer's disease : JAD, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Neuronal Actin Remodeling and Its Role in Higher Nervous Activity.International journal of molecular sciences · 2025Review
- Mechanistic Role of Astrocytic Rac1 Protein in Alzheimer's Disease.Aging and disease · 2025Review
- Role of LIMK1-cofilin-actin axis in dendritic spine dynamics in Alzheimer's disease.Cell death & disease · 2025Review
- The role of small GTPases in Alzheimer's disease tau pathologies.Frontiers in cellular neuroscience · 2025Review
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4 authors.
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Abstract
backgroundA neuropathogenic hallmark of Alzheimer's disease (AD) is loss of neuronal synapses in selective brain regions. Small GTPases Rac1 and Cdc42, critical modulators of synaptic architecture and remodeling, are dysregulated in AD brains and are potential AD therapeutic targets. However, the exact contribution of their signaling to AD is still not clear.
objectiveWe intend to investigate the hypothesis that Rac1/Cdc42 activity changes in a spatial and planar dependent manner in relation to AD.
methodsWe applied anti-pRac/Cdc42 (Serine 71 phosphorylation), which recognizes an inactive form of Rac1/Cdc42, and anti-pPAK (Threonine 423 phosphorylation), which detects the active PAK, a positive downstream effector of Rac1/Cdc42 signaling. For this study, triple transgenic mouse model (3xTg-AD) brain and human AD brain samples were used.
resultspRac/Cdc42 expression was decreased in 3xTg-AD mouse cortex while pPAK expression increased compared to wild-type mouse cortex. Immunostaining of mouse brain serial sections revealed increased pRac/Cdc42 expression in the rostral region, decreased expression in the caudal region, and pPAK showed an overall opposite trend of pRac/Cdc42. There was also a brain plane specific nuclear to cytoplasmic redistribution of pRac/Cdc42. Human non-dementia and AD cortex and cerebellum showed differential expressions for pRac/Cdc42, Rac1, and Cdc42. Mouse whole transcriptome analysis demonstrated spatial dependent expression of Rac1/Cdc42 signaling-associated genes in neuronal and non-neuronal (astrocyte) populations of 3xTg-AD hippocampi.
conclusionsRac1/Cdc42 signaling is dysregulated in both 3xTg-AD mouse and AD human brain and Rac1/Cdc42 activity level changes along the spatial and planar dimensions.
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